Letter from the insurance company

Claudia got this letter from her health insurance company:

Dear Ms. ------,

Based on a recent review of your cholesterol panel of January 12, 2011, we feel that you should strongly consider speaking to your doctor about cholesterol treatment.

Reducing cholesterol values to healthy levels has been shown to reduce heart attack risk . . .


Okay. So the health insurer wants Claudia to take a cholesterol drug in the hopes that it will reduce their exposure to the costs for her future heart catheterization, angioplasty and stent, or bypass surgery. This is understandable, given the extraordinary costs of such hospital services, typically running from $40,000 for a several hour-long outpatient catheterization procedure, to as much as $200,000 for a several day long stay for coronary bypass surgery.

So what's the problem?

Here are Claudia's most recent lipid values:

LDL cholesterol 196 mg/dl
HDL 88 mg/dl
Triglycerides 37 mg/dl
Total cholesterol 291 mg/dl

By the criteria followed by her health insurer, both total and LDL cholesterol are much too high. Note, of course, that LDL cholesterol was a calculated value, not measured.

Here are Claudia's lipoproteins, drawn simultaneously with her lipids:

LDL particle number 898 nmol/L
Small LDL particle number less than 90 nmol/L (Values less than 90 are not reported by Liposcience)

LDL particle number is, by far and away, the best measure of LDL particles, an actual count of particles, rather than a guesstimate of LDL particles gauged by measuring cholesterol in the low-density fraction of lipoproteins (i.e., LDL cholesterol). It is also measured and is highly reproducible.

To convert LDL particle number in nmol/L to an LDL cholesterol-like value in mg/dl, divide by ten (or just drop the last digit).

Claudia's measured LDL is therefore 89 mg/dl--54% lower than the crude calculated LDL suggests.

This is because virtually all of Claudia's LDL particles are large, with little or no small. This situation throws off the crude assumptions built into the LDL calculation, making it appear that she has very high LDL cholesterol.

Do you think that Big Pharma advertises this phenomenon?

Healthy smoothies

I've now seen several people who have either caused themselves to be diabetic or to have other phenomena associated with excessive consumption of carbohydrates, all by innocently indulging in a carbohydrate-packed smoothie every morning.

Kay, for instance, has a smoothie of a half-pint blueberries, a banana, a scoop of whey, low-fat yogurt, a cup of milk every morning. The rest of her diet was fairly healthy: salads with oil-based dressing for lunch, salmon and asparagus for dinner, only an occasional carbohydrate indulgence outside of her morning smoothie ritual. Yet she had a HbA1c (a reflection of prior 60 to 90 days average blood sugar) at the near-diabetic range of 5.9%.

The mistake most people make when making smoothies is relying too heavily on carbohydrates like fruit. A smoothie like the one made by Kay can easily top 50, 60, or 70 grams carbohydrates per serving, more than sufficient to send blood sugars up to 150 mg/dl or more.

So what can you put in your smoothie and not send you over the edge to diabetes, small LDL, and all the other undesirable phenomena of excessive carbohydrates? Here's a list:

--coconut milk, unsweetened almond milk. Less desirable: milk, full-fat soymilk
--ground flaxseed
--oils: flaxseed oil, coconut oil (melted), extra-light olive oil, walnut oil
--dried coconut
--extracts: vanilla, almond, coconut, cherry, hazelnut
--spices: cinnamon, nutmeg, ginger
--herbs: mint leaves, cilantro
--cocoa powder (unsweetened)
--nut or seed butters (peanut butter, almond butter, sunflower seed butter)
--tofu
--exotic ingredients (ingredients you wouldn't expect in a smoothie): spinach, kale, cucumber

How do you sweeten a smoothie? This is what trips up most people. If you resort to fruit like bananas, pineapple, or apple, you will readily send your blood sugar skyward. Honey, agave syrup, and sugar, of course, all increase blood sugar and/or have the adverse effects of fructose. Be careful of yogurt, also, for similar reasons.

Therefore, to sweeten your smoothie, consider:

--Small servings of berries, e.g., 8-10 blueberries, 2 strawberries, a few wedges of apple, half a kiwi
--Non-nutritive sweeteners like stevia, Truvia, sucralose, xylitol, erythritol. Also, sugar-free (sucralose-based) syrups like those from DaVinci and Torani are useful. (Just be aware that non-nutritive sweeteners can increase appetite--use sparingly.)

Also, note that, if you have divorced yourself from wheat, cornstarch, and sugars, your desire for sweet should be much reduced. Foods other people find just right will taste sickeningly sweet to you. You might therefore find that foods like peanut butter or coconut milk have a mild natural sweetness; added sweetness is only minimally necessary.

Coming next: I'll share a smoothie recipe or two of mine. Anyone want to share a recipe?

Insulin secretagogue

Dairy products have the peculiar property of triggering pancreatic release of insulin. The research group at Lund University in Sweden have contributed the most to documenting this phenomenon:




Mean (±SEM) incremental changes (?) in serum insulin in response to equal amounts of carbohydrate from a white-wheat-bread reference meal (x) and test meals of whey (?), milk (?), cheese (?), cod (?), gluten-low (?), and gluten-high (?) meals. From Nilsson 2004.

Note that it is the area under the curve (AUC), not the peak value, that assumes greatest importance.

Dairy products, especially milk, whey, and yogurt, are insulin secretagogues: they stimulate pancreatic release of insulin. The effect is likely due to amino acids and/or polypeptides in dairy products. (The effect is less prominent with cheese. Also see this study.)

By conventional wisdom, this may be a good thing, since the excess insulin will blunt the glucose rise after consumption. However, in my book, this is not such a good thing, since most of us have tired, beaten, overworked pancreatic beta cells from our decades of carbohydrate overconsumption. I fear that the effect of dairy products just take us a bit closer to beta cell failure: diabetes.

Good news: The effect is least with cheese.

Be gluten-free without "gluten-free"

While I've discussed this before, it is such a confusing issue that I'd like to discuss it again.

I advocate wheat elimination because consumption of products made from modern dwarf Triticum aestivum:

--Triggers formation of extravagant quantities of small LDL and LDL particle number (or apoprotein B)
--Triggers inflammatory phenomena like c-reactive protein, increases leptin resistance, and reduction of the protective adipocytokine, adiponectin.
--Encourages accumulation of deep visceral fat ("wheat belly") that is inflammatory and causes resistance to insulin
--Increases blood sugar more than nearly all other foods--higher than a Milky Way bar, higher than a Snickers bar, higher than table sugar.
--Is being linked to a growing number of immune-mediated diseases, including celiac disease (quadrupled over past 50 years), type 1 diabetes in children, and cerebellar ataxia and peripheral neuropathies.

This last group of wheat-related phenomena are primarily due to gluten, the collection of 50+ proteins found in each wheat plant. For this reason, people diagnosed with celiac disease are advised to eliminate gluten from wheat and other sources (barley, rye, triticale, bulgur) and to eat gluten-free foods.

Gluten-free has therefore come to be viewed as wheat-free and problem-free. It ain't so.

Among the few foods that increase blood glucose higher than wheat: cornstarch, rice starch, potato starch, and tapioca starch--Yup: the ingredients commonly used to replace wheat in gluten-free foods. They are also flagrant triggers of the small LDL pattern, along with increased triglycerides, reduced HDL, increased visceral fat, increased blood pressure. In short, gluten-free foods lack the immune and brain effects of wheat gluten, but still make you fat, hypertensive, and diabetic.

I tell patients to view gluten-free foods like jelly beans: Gluten-free pancakes, muffins, breads, etc. are indulgences, not healthy replacements for wheat. It's okay to have a few jelly beans now and then. But they should not be part of a frequent or daily routine. Same with gluten-free foods.

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.
All posts by william-davis

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.

Apo E4 and sterols: Lethal combination?

Phytosterols, or just "sterols" to its friends and neighbors, are a group of cholesterol-like compounds that are abundant in the plant world. Lately, however, sterols have proliferated in the processed food supply, thanks to the observation that sterols reduce LDL cholesterol when ingested by humans.

This must mean that sterols are good for you.

Uh oh. Wait a minute: There is a rare disease called sitosterolemia in which there is unimpeded intestinal absorption of all sterols ingested through diet. They must have really low LDL cholesterols! Nope. They develop coronary disease--heart attacks, angina, etc.--in their late teens and 20s. In other words, if sterols gain access to your bloodstream, they are bad. Very bad.

Conventional thinking is that only a modest quantity of dietary sterols gain access to the bloodstream. But there are two potentially fatal flaws in this overly simplistic line of thinking:

1) What happens when you load up your diet with "heart healthy" sterols, such as those in "heart healthy" margarines, mayonnaise, and yogurt, effectively increasing sterol intake 10-fold?

2) What happens in people with the genetic pattern, apo E4, that is carried by 25% of the general population that permits much greater intestinal absorption of sterols?

My prediction: Despite the fact that sterols reduce LDL, they may, in certain genetically-susceptible people, such as those with apo E4, increase risk for heart disease: heart unhealthy.

Here are two studies that suggest that greater sterol absorption in people without sitosterolemia are at higher risk for heart disease:

Alterations in cholesterol absorption/synthesis markers characterize Framingham offspring study participants with CHD

Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study

Glucomania

As I suggested in a previous Heart Scan Blog post, a glucose meter is your best tool to:

1) Lose weight
2) Cure diabetes
3) Reduce or eliminate small LDL particles
4) Achieve anti-aging or age-slowing effects


But it means getting hold of a glucose meter and applying it in a very different way.

Diabetics typically check fasting morning glucose and again several times during the day to assess medication effects. But you and I can measure blood glucose to assess the immediate effects of food choices--two very different approaches.

The concept is simple: Check a blood glucose just prior to a food or meal of interest, then one hour after finishing.

Let's take two hypothetical breakfasts. First, oatmeal, a so-called "low-glycemic index" food. Slow-cooked, stone ground oatmeal with skim milk, a handful of walnuts, just a few blueberries.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 175 mg/dl

I made those numbers up, but this is a fairly typical response for many adults. (This is why "low-glycemic index" is an absurd notion.) This kind of response causes 1) glycation, the adverse effects of glucose modification of proteins that leads to cataracts, kidney disease, cartilage damage and arthritis, atherosclerosis, skin wrinkles, etc., 2) high insulin response that cascades into fat deposition, especially visceral fat ("wheat belly"), and 3) glucotoxicity, i.e., direct damage to the pancreas that can, over years, lead to diabetes.

Next day, let's try a breakfast of 3-egg omelet made with green peppers, sundried tomatoes, and olive oil.

Blood glucose just prior: 95 mg/dl
Blood glucose one hour after finish: 93 mg/dl

This is a meal of virtually zero-glycemic index. This kind of response triggers none of the effects experienced following the oatmeal. Repeated over time and you fail to trigger glycation, you stop provoking insulin, and visceral fat mobilizes rather than accumulates: you lose weight, particularly around the middle.

We therefore aim to keep the one-hour blood glucose 100 mg/dl or less. If you start with a high fasting blood glucose of, say, 118 mg/dl, then we aim to keep the one-hour after-eating blood glucose no higher than the pre-meal.

It works. Plain and simple.

This makes the primary care docs crazy: "How dare you check your blood sugar! You're not diabetic." In truth, blood glucose meters are relatively simple devices to use. The test strips and lancets will cost a few bucks. (The meters themselves are either low-cost or free, just like Gillette sometimes sends you a beautiful new razor for free but expects you to buy the blades). These are direct-to-consumer products. While a prescription written by your doctor for a glucose meter and supplies helps insurance cover the costs, you can easily get these devices without a prescription. Some stores, like Target, keep their devices out on the shelves with the shampoo and bath soap.

Warning: Anyone taking diabetes drugs will have to consult with their doctors about the safety of such an approach. Because this approach can actually cure diabetes in some people, if you are taking some diabetes drugs, especially glyburide, glipidize, and glimepiride, you can experience dangerously low blood sugars, just as any non-diabetic taking these drugs would.

Diarrhea, runny noses, and rage: Poll results

Here are the results of the week-long poll asking the question:

Have you experienced a wheat re-exposure syndrome?
Yes, undesirable gastrointestinal effects 223 (41%)

Yes, asthma or sinus problems 51 (9%)

Yes, joint pains and/or swelling 85 (15%)

Yes, emotional or other nervous system effects 59 (10%)
No, nothing, nada  107 (19%)

No. Wheat is sacred and you're all nuts  13 (2%)


There are several interesting observations to make from this informal poll. First, as I have observed, the most common wheat re-exposure syndrome is gastrointestinal, usually involving cramps, diarrhea, and lame explanations to your dinner partner.

Second most common: joint pains and/or swelling.

Third: asthma or sinus congestion.

The incidence of emotional or nervous system effects surprised me a bit. I didn't expect 10% of people to share this effect. This is an effect I also experience personally, along with the gastrointestinal consequences.

To be sure, this is a skewed poll, since many people likely come to this blog in the first place because of such issues. But I was nonetheless impressed with the relatively modest proportion of people who did not share such a re-exposure syndrome: only 19%.

Beyond the interesting numbers provided by readers, a good many also provided some fascinating and graphic comments. Here's a sample:




Sassy said:

Reflux -- starts a day later and goes for up to a week. And Bloat:2-5 inches on my waistline in a day, lasting up to three. Miserable. And why, having experienced this once, have I done it often enough to verify the connection with certainty? I am working on that one.



Anonymous said:
Wheat increased hunger with even with only a small amount. Crackers in soup was enough to set it off.

Also, when I was trying to get off wheat, I noticed that 2 eggs and 2 bacon and I could go 5 hours before hunger, or 2 eggs and 2 bacon and toast was good for three hours before hunger. That was the final step to giving up wheat. Now three years and 59 Kg [130 lbs!] loss later, there is no doubt in my mind that wheat is evil, and I do not regard it as suitable for human food. I speculate that it increases ghrelin or cortisol.

Anna said:
For me, in the two years since I began eating Gluten-Free (Low Carb for 6 years), the few times I've had re-exposure to wheat, I've experienced fast onset and intense abdominal pain (known exposure during the daytime) and heartburn, indigestion, intense nausea, and disrupted sleep (exposures during evening meal not discovered until the next day).

My husband wants to think he's fine with wheat (though I know that he has at least one gene that predisposes to celiac), but IMO, he isn't. He eats no wheat at home because that's the default, and he's OK with that. But if he goes out to dinner at a restaurant that serves "good" artisan bread, he will indulge in a few bites (he does restrict his carb intake, so it's still a limited amount). More often than not, he will sleep fitfully on those nights, snore more, and wake in the night with indigestion. He wants to bury his head in the sand and will only acknowledge the discomfort being due to eating too many carbs, not the wheat itself. I notice he sleeps fine if he eats a small amount of potato or rice. Go figure.

Our 12 yo son has been eating GF for two years also. About 6 months into GF, he unknowingly ate wheat a number of times (licorice candy laces at a friend's house), which resulted in outbreaks of canker sores in his mouth each time. He also exhibits mood and behavior changes when he eats wheat, which is what prompted me to test him for gluten intolerance in the first place.

Mark said:
If I go for 3-4 days without wheat, grains or sugar and then go out and binge on a pizza and ice cream or something like that I become explosive within 20 minutes to an hour. It's like a wheat and sugar rage.(I'm not saying this is an excuse for rage, I'm saying it has happened to me and I believe partly do to re-exposure) It seems the combination of the wheat plus sugar can be the worst.

I get red rashes around my neck sometimes right away and sometimes up to a day or later and sometimes get bad diarrhea. 
I think it can be almost dangerous to cut things like gluten and sugar suddenly out of the diet without being very serious about keeping them out. I have found it very hard to cut out wheat without binging on it later after 4 or 5 days. I don't believe that my symptoms are just psychological either.

I was also diagnosed with ADHD as a young kid and then rediagnosed with adult ADHD by 3 different doctors. I also have bouts of mania at times too. I am considering trying to go completely gluten/refined carbohydrate free to see if it helps with the symptoms and gives me some relief.

I have never been tested for celiac or gluten intolerance but I would like to be. I think it would help explain to my girlfriend, family and friends why I can't go out and eat pizza or have a beer or ice cream. Right now they all think I'm a hypochondriac. At times I have experienced an intense fatigue the next day like I can't wake up and also sharp pains in my body and headaches.

Anonymous said:
I ditched wheat a year ago after my wife was diagnosed celiac. I immediately experienced a number of health improvements (blood lipids, sleep, allergies, etc.).

Fast forward: We all suffered some inadvertent wheat exposure yesterday via some chocolate covered Brazil nuts (of all things). This accidental A-B-A experimental design resulted in the following:

1. My celiac wife experienced what she calls "the flip" within an hour of exposure (i.e., intense GI distress).
2. My five-year old son went to bed with some wicked reflux.
3. I woke up with some twinges in my lower back and an ache in my football-weary left shoulder. I was also complaining to my wife about fuzzy-headedness that refused to respond to caffeine or hydration. I could only describe it as "carb flu"...

And then I read your post!

Anne said:
Depression, agitation and brain fog if I get glutened. Some times this comes with abdominal pain and a rash on my back - I think it is dose dependent. Cross contamination with wheat is a big issue when eating out. Needless to say, I eat out infrequently and then try to stick with the restaurants that are the most aware of gluten issues.

Terrence said:
Several weeks ago, I started Robb Wolf's 30 day challenge.

The first two weeks were brutal - calling it a withdrawal flu was a massive understatement. So, I thought I would try some wheat and see what happened (could not be worse, I thought). Well, it was.

I still felt extremely crappy, but I was now MASSIVELY GASSY - AMAZINGLY GASSY, for about 48 hours - flatulence on wheels, in spades. I did not go out at all in those 48 hours - when the gas came on, it went out, LONG, and QUICKLY and LOUDLY.

I am easing back into wheat and grain free. I am gluten free today and tomorrow (Sunday and Monday). I expect to try a small amount of wheat on Thursday, then maybe a little more the following Thursday.

Donald said:
I have limited wheat consumption severely over the last 8 months. I have lost 120 pounds, no longer have bouts of illness, asthma, depression, or low energy. I also take vitamin D and other supplements that have helped (many are from your blog recommendations).

Last week I ate a small piece of cake and dessert pizza. Shortly thereafter I started sneezing, had a scratchy throat, and runny nose. I called off sick the next day for fear of being contagious. My symptoms subsided quickly and I am now attributing them to the processed flour eaten at my work luncheon. I think it was an allergic reaction since I recall having much more severe symptoms fairly regularly in my wheat eating days. Those were attributed to an "allergy" of unknown origin back then.

John said:
I suffered from Ankylosing Spondylitis, Iritis, Plantar Fasciits, etc for a number of years. I restricted carbs, especially wheat and I've been symptom free for the past two years now.

Lori said:
I found wheat to be one of the worst things for giving me gas bloating and acid reflux, and I'd had sinus and nasal congestion my whole life. When I ate that cookie, it just re-introduced old problems. I can occasionally eat a gluten-free, grainy goody at my party place without any side effects. I also have a little sprouted rice protein powder every day.

Another odd thing about wheat: it was hard for me to stop eating it once I started. I could go through a whole box of cookies in one sitting, even though I wasn't a binge eater. But I can have a couple of gluten-free cookies and stop.

Paul said:
Except for one slip up this recently past holiday season, I've been sugar-grain-starch free since July 2008. Mental fog was the most noticable re-exposure symptom I had.

My mom has had the worst acid-reflux for 40-plus years. It had become so bad that she was on three medications just to deal with the symptoms. After much training and coaxing, I finally got across to her 
how to totally get off wheat. Not at all to my surprise, after being wheat free for a few weeks, she lost weight and her acid reflux was GONE!

But she had been addicted to wheat for so long, she relapsed, and the reflux fire soon returned. Wheat must be akin to heroin with some people. Even though they know it's very bad for them, they can't help themselves.

Onschedule said:
Re-exposure often leads to diarrhea for me, or such a heavy feeling of tiredness that all I can do is lay down and pass out. A local pizzeria makes a darn good pie, but since I started practicing wheat-avoidance, I can't keep my eyes open after eating there. I can't say for sure that it's the wheat causing it, but definitely something in the crust. Diarrhea, on the other hand, is definitely triggered by the wheat for me.

My mom complained of gastric reflux for years, but never filled the prescriptions that her doctors would give her. I suggested wheat-avoidance- gastric reflux disappeared within 3 days and hasn't returned (has been 6 months now). I've already commented elsewhere on this blog about how much weight and bloating she has lost...

Steve said:
Interesting that I should sit down, turn on my computer and find your poll. Having gone several weeks, maybe months, avoiding gluten, I took my daughter and her boyfriend out to eat because my wife has been working late at the office lately. Although I was thinking I would just eat my steak and chicken, I succumbed to the temptation of eating about a dozen greasy, breaded shrimp that my daughter and her boyfriend ordered. It's 1:39am and I still do not feel sleepy. My left nostril is completely blocked, my stomach feels bloated, really, really full and I've been burping. In your poll I checked sinus problems but could have chose gastrointestinal or nervous problems just as well. 


A few weeks ago my daughter brought home a pizza and, once again, despite my knowing that I shouldn't, I ate a couple of pieces. I was sick for two days. The pain in what I think was my transverse colon was so bad I thought I might have to go to ther emergency room. Before I ate the pizza I had never gone grain-free that long before. I did this after reading Robb Wolf's book. 


I AM CONVINCED. No more wheat for me! Please, Lord, give me strength.

LV said:
What don't I experience! I typically avoid wheat (and gluten for that matter) as I'm pretty sure it makes me sick, but when I slip (or someone else slips me some) I end up with massive amounts of joint swelling and tenderness, diarhea, cramping, gas, bloating and brain fog. I'm absolutely miserable. Just that alone is enough to keep me off gluten. I have RA, so if I have repeated exposures I'll have a flare which SUCKS!

The perfect Frankengrain

Pretend I'm a mad food scientist. I'd like to create a food that:

1) Wreaks gastrointestinal havoc and cause intractable diarrhea, cramps, and anemia.
2) Kills some people who consume it after a long, painful course of illness.
3) Damages the brain and nervous system such that some people wet their pants, lose balance, and lose the ability to feel their feet and legs.
4) Brings out the mania of bipolar illness.
5) Amplifies auditory hallucinations in people with paranoid schizophrenia.
6) Makes people diabetic by increasing blood sugars.
7) Worsens arthritis, such as osteoarthritis and rheumatoid arthritis.
8) Triggers addictive eating behavior.
9) Punishes you with a withdrawal process if you try to remove it from your diet.

I will develop a strain that is exceptionally hardy and tolerates diverse conditions so that it can grow in just about any climate. It should also be an exceptionally high yield crop, so that I can sell it cheaply to the masses.

Now, if my evil scheme goes as planned, I will then persuade the USDA that not only is my food harmless, but it is good for health. If they really take the bait, they might even endorse it, create a diet program around it.

Dag nabit! Such a plan has already been implemented. Another evil food scientist already beat me to the punch. The food is called wheat.

Diabetes: A study in aging

Diabetics experience long-term health difficulties, including atherosclerosis/heart attacks, peripheral vascular disease, hypertension, cataracts, kidney disease, neuropathies, male erectile dysfunction, osteoarthritis, and colorectal cancer. They also die, on average, 10 years earlier than non-diabetics.

In effect, diabetics compress their lives into a shorter period of time. They experience all the "complications" of aging at a younger age. People without diabetes, of course, can develop atherosclerosis, cataracts, kidney disease, etc., but they tend to do so later in life compared to diabetics.

One index of the rate of aging (but not chronologic age itself) is hemoglobin A1c, or HbA1c, a "moving average" of glycated hemoglobin, i.e., glucose-modified hemoglobin. Blood glucose glycates hemoglobin linearly and irreversibly; measuring HbA1c thereby provides an index of the last 60 or so days average blood glucose.

To put HbA1c values into perspective:

Average HbA1c of hunter-gatherers: 4.5%
Average HbA1c for Americans: 5.6%
American Diabetes Association definition of diabetes: 6.5% or greater
American Diabetes Association definition of adequate control of diabetes: 7.0% or less

Why do diabetics age faster? There are likely several reasons. One important reason is glycation, as indexed by HbA1c. Glycated proteins in the lens of the eye causes cataracts. Glycated proteins in cartilage leads to arthritis. Glycated LDL particles (apo B) leads to atherosclerosis. Glycated nerve cells causes neuropathy. And so on.

If glycation underlies many of the phenomena of aging, then we might surmise that:

1) The less you glycate, the slower you age.
2) The more you glycate, the faster you age.

Therefore, the higher the HbA1c, the faster you are aging.

What foods increase HbA1c? Carbohydrates. That bowl of slow-cooked, stone ground oatmeal? A one-hour after-eating blood sugar of 170 mg/dl is common. Your doctor says that's okay because it's below 200 mg/dl and you don't "need" medication yet.
All posts by william-davis

Dr. Cannell on vitamin D and cancer

Here is Dr. John Cannell's Vitamin D Council Newsletter reprinted in its entirety. It answers some of the questions that came up on The Heart Scan Blog about the recent release of a study of vitamin D and cancer



The Vitamin D Newsletter

December, 2007

Does vitamin D prevent cancer? If it does, will doctors who ignore the research end up with blood on their hands? The press makes it easy for doctors to believe what they want to believe. Below are six stories about the same scientific study; read the six different headlines. According to your a priori beliefs, you can choose the story you want to believe and read that one. Don't feel bad, we all do it. As Walter Lippman once said, "We do not see and then believe, we believe and then we see."


Vitamin D cuts colon cancer death risk



Study Finds No Connection Between Vitamin D And Overall Cancer Deaths



Vitamin D protects against colorectal cancer



Vitamin D May Not Cut Cancer Deaths



Vitamin D protects against colorectal cancer



Scientists advise a vitamin D downgrade as there is no real proof ...




Another option is to read the study yourself.


Freedman DM, et al. Prospective Study of Serum Vitamin D and Cancer Mortality in the United States. J Natl Cancer Inst. 2007 Oct 30; [Epub ahead of print]




What Dr. Freedman actually discovered is that when you take a very large group of people (16,818), some as young as seventeen, measure their vitamin D levels, and then wait about ten years to see who dies from cancer, you find 536 die and that a vitamin D level from ten years earlier is not a good predictor of who will die from cancer. However, even a level drawn ten years earlier predicted that those with the lowest level were four times more likely to die from colon cancer, suggesting, as Ed Giovannucci has, that colon cancer may be exquisitely sensitive to vitamin D. Furthermore, 28 women got breast cancer, 20 in the group with the lowest vitamin D level but only 8 in the highest. The breast cancer findings were not statistically significant - even during a very long breast cancer awareness month - but can you imagine what critics at the American Cancer Society would be telling women if the numbers were reversed, if the 20 women who got breast cancer were in the high vitamin D group?



Another large epidemiological study appeared about breast cancer the very next day. This time, the press passed on the story and the American Cancer Society was mum, no editorials by Dr. Lichtenfeld, their spokesman, in spite of breast cancer awareness month.



Abbas S, et al. Serum 25-hydroxyvitamin D and risk of postmenopausal breast cancer - results of a large case-control study. Carcinogenesis. 2007 Oct 31; [Epub ahead of print]



In the above study, 1,394 women with breast cancer were case-controlled with a similar number of women without breast cancer. The women with breast cancer were three times more likely to have low vitamin D levels. That is a lot of women who may be dying during next year's breast cancer awareness month.



Both of the above studies were epidemiological, not randomized controlled trials. Of course a randomized controlled trial has already shown a 60% reduction in internal cancers in women taking even a modest 1,100 IU per day of vitamin D.



Lappe JM, et al. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.



What is interesting is the difference in the response of the Canadian Cancer Society and the American Cancer Society. The Canadian Cancer Society has advised all Canadians to take 1,000 IU per day - not enough but a good first step - and for immediate additional large scale clinical trials. The Canadians simply performed a risk/benefit analysis. What is the risk of treating vitamin D deficiency versus what are the potential benefits? They quote the American Food and Nutrition Board, which says 2,000 IU/day is safe for anyone over the age on one to take, on their own, without being under the care of a physician. If there is little or no risk, then the next question is what are the potential benefits of treating vitamin D deficiency? This is not quantum mechanics.



Cancer society calls for major vitamin D trial



The Canadians acted because the Canadian government knows it could save billions of dollars by treating vitamin D deficiency.



Vitamin D Deficiency Drains $9 billion From Canadian Health Care ...



If wide spread treatment of vitamin D deficiency became the rule, ask yourself, "Who would be helped and who would be hurt." First ask yourself that question about Canada and then about the USA. Remember, in Canada, the government directly pays for its citizen's health insurance; in the USA, private insurance is the norm. In Canada, the government is realizing they could save billions if vitamin D deficiencies were treated. In the USA, a large segment of the medical industry would be hurt, some anti-cancer drug manufacturers would have to close their doors, thousands of patents would become worthless, lucrative consulting contracts between industry and cancer researchers would dry up.

Both Canadians and Americans are shocked to think their doctors care about money, are in the illness business. In some ways people think of their doctors like they do their local public schools. They know medicine is a business and know doctors do things for money but they don't think their own doctors do. Likewise they think public schools are in bad shape but think their local schools are above average. They think their doctor is above average, like their "Lake Woebegone" kids.

Lake Woebegone Effect

The fact is that doctors, hospitals, regional cancer centers, and the cancer drug manufacturers are all in business to make money and all of these businesses make money off the sick, not off the well. Just a fact, but, as Aldous Huxley once observed, "Facts do not cease to exist because they are ignored."



Vitamin D will save the Canadian government enormous amounts of money but will cause widespread economic disruption in the USA. Do the physicians leading the American Cancer Society have strong economic ties to the cancer industry in the form of patents, stock options, and consulting fees? If so, what do you expect them to do? What would you do? It's simple. You would believe what you have to believe, what you need to believe, that is, anything with the word "vitamin" in it is simply the latest Laetrile. Look to Canada, not the USA, to lead the way.



Vitamin D may fight cancer


What about American physicians? They are apparently waiting for the American trial lawyers to smell a tort. After all, the case is quite simple. Doctor, did you advise Mrs. Jones to avoid the sun? Doctor, did you tell her the sun is the source of 90% of circulating stores of vitamin D? Doctor, did you prescribe vitamin D to make up for what the sun would not be making? Doctor, did you measure her vitamin D levels? So you had no way of knowing if your sun-avoidance advice resulted in vitamin D deficiency? Doctor, do you know our expert tested her vitamin D level and it was less than 20? Doctor, did you tell her about any of the studies indicating vitamin D deficiency causes cancer? Doctor, did you know Mrs. Jones has terminal breast cancer and will be leaving behind a loving husband and two young children?

And what about the American Cancer Society? Dr. Lichtenfeld, their spokesman, quickly gave his opinion; from what I can tell the first time he ever commented on a vitamin D study. That is, he has ignored the hundreds of positive epidemiological studies, ignored the incredible randomized controlled trial, but he jumped on this one:

Maybe Vitamin D Isn't The Answer After All

Dr. Lichtenfeld, implied the Canadian Cancer Society has acted precipitously in recommending that all Canadians take 1,000 IU of vitamin D daily. He implied that Americans should placidly wait until more randomized controlled trials, such as Lappe JM, et al (above), accumulate before they address their vitamin D deficiency. That is, nothing should be done until more randomized controlled trials prove vitamin D prevents cancer, one randomized controlled trial is not enough; epidemiological studies are not enough, animal studies are not enough, multiple anti-cancer mechanisms of action are not enough? If that is his position, I challenge him to point to one human randomized controlled trial that proves smoking is dangerous?

If he cannot, then he must admit that the American Cancer Society's position on smoking is entirely derived from epidemiological studies, animal studies, and a demonstrable mechanism of action, not on human randomized controlled trials? Vitamin D not only has hundreds of epidemiological studies, thousand of animal studies, and at least four anti-cancer mechanisms of action, vitamin D deficiency has something smoking does not have, it has a high quality randomized controlled trial. If future randomized controlled trials fail to show vitamin D prevents cancer - and Dr. Lichtenfeld better hope they do - he can have the satisfaction of saying "I told you so." If future randomized controlled trials confirm vitamin D prevents cancer, then he needs to look at his hands, the red he sees is the blood of needless cancer deaths.

John Cannell, MD

The Vitamin D Council

9100 San Gregorio Road

Atascadero, CA 93422



This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know.

Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website. Send your tax-deductible contributions to:

The Vitamin D Council

9100 San Gregorio Road

Atascadero, CA 93422

"Yes, Johnnie, there really is an Easter bunny"

A Heart Scan Blog reader recently posted this comment:

You wouldn't believe the trouble I'm having trying to get someone to give me a CT Heart Scan without trying to talk me into a Coronary CTA [CT angiogram]. Every facility I've talked to keeps harping on the issue that calcium scoring only shows "hard" plaque...and not soft.

I also had a nurse today tell me that 30% of the people that end up needing a coronary catheterization had calcium scores of ZERO. That doesn't sound right to me. What determines whether or not someone needs a coronary catheterization anyway?



There was a time not long ago when I saw heart scan centers as the emerging champions of heart disease detection and prevention. Heart scans, after all, provided the only rational means to directly uncover hidden coronary plaque. They also offered a method of tracking progression--or regression--of coronary plaque. No other tool can do that. Carotid ultrasound (IMT)? Indirectly and imperfectly, since it measures thickening of the carotid artery lining, partially removed from the influences that create coronary atherosclerotic plaque. Cholesterol? A miserable failure for a whole host of reasons.

Then something happened. General Electric bought the developer and manufacturer of the electron-beam tomography CT scanner, Imatron. (Initial press releases were glowing: The Future of Electron Beam Tomography Looks Better than Ever.The new eSpeed C300 electron beam tomographic scanner features the industry’s fastest temporal resolution, and is now backed by the strength of GE Medical Systems. Imatron and GE have joined forces to provide comprehensive solutions for entrepreneurs and innovative medical practitioners.)

Within short order, GE scrapped the entire company and program, despite the development of an extraordinary device, the C-300, introduced in 2001, and the eSpeed, introduced in 2003, both yanked by GE. The C-300 and eSpeed were technological marvels, providing heart scans at incredible speed with minimal radiation.

Why would GE do such a thing, buy Imatron and its patent rights, along with the fabulous new eSpeed device, then dissolve the company that developed the technology and scrap the entire package?

Well, first of all they can afford to, whether or not the device represented a technological advancement. Second (and this is my reading-between-the-lines interpretation of the events), it was in their best financial interest. Not in the interest of the public's health, nor the technology of heart scanning, but they believed that focusing on the multi-detector technology to be more financially rewarding to GE.

GE, along with Toshiba, Siemens, and Philips, saw the dollar signs of big money with the innovations in multi-detector technology (MDCT). They began to envision a broader acceptance of these devices into mainstream practice with the technological improvements in CT angiography, a device (or several) in every hospital and major clinic.

Anyway, this represents a long and winding return to the original issue: How I once believed that heart scan centers would be champions of heart disease detection and reversal. This has, unfortunately, not proven to be true.

Yes, there are heart scan centers where you can obtain a heart scan and also connect with people and physicians who believe in prevention of this disease. I believe that Milwaukee Heart Scan is that way, as is Dr. Bill Blanchet's Front Range Preventive Imaging, Dr. Roger White's Holistica Hawaii, and Dr. John Rumberger's Princeton Longevity Center.

But the truth is that most heart scan centers have evolved into places that offer heart scans, but more as grudging lip service to the concept of early detection earned with sweat and tears by the early efforts of the heart scan centers. But the more financially rewarding offering of CT coronary angiograms, while a useful service when used properly, has corrupted the prevention and reversal equation. "Entry level" CT heart scans have been subverted in the quest for profit.

CT angiograms pay better: $1800-4000, compared to $100-500 for a heart scan (usually about $250). More importantly, who can resist the detection of a "suspicious" 50% blockage that might benefit from the "real" test, a heart catheterization? Can anyone honestly allow a 50% blockage to be without a stent?

CT angiograms not only yield more revenue, they also serve as an effective prelude to "downstream" revenue. By this equation, a CT angiogram easily becomes a $40,000 hospital procedure with a stent or two, or three, or occasionally a $100,000 bypass. Keep in mind that the majority of people who are persuaded that a simple heart scans are not good enough and would be better off with the "superior" test of CT angiography are asymptomatic--without symptoms of chest pain, breathelessness, etc. Thus, the argument is that people without symptoms, usually with normal stress tests, benefit from prophylactic revascularization procedures like stents and bypass.

There are no data whatsoever to support this practice. People who have no symptoms attributable to heart disease and have normal stress tests do NOT benefit from heart procedures like heart catheterization. They do, of course, benefit from asking why they have atherosclerotic plaque in the first place, followed by a preventive program to correct the causes.

So, beware: It is the heart scan I believe in, a technique involving low radiation and low revenue potential. CT angiograms are useful tests, but often offered for the wrong reasons. If we all keep in mind that the economics of testing more often than not determine what is being told to us, then it all makes sense. If you want a simple heart scan, just say so. No--insist on it.

Take trust out of the equation. Don't trust people in health care anymore than you'd trust the used car salesman with "a great deal."

Finally, in answer to the reader's last comment about 30% of people needing heart catheterizations having zero calcium scores, this is absolute unadulterated nonsense. I'm hoping that the nurse who said this was taken out of context. Her comments are, at best, misleading. That's why I conduct this Heart Scan Blog and our website, www.cureality.com. They are your unbiased sources of information on what is true, honest, and not tainted by the smell of lots of procedural revenue.

Diabetes: controlled or . . . cured?

Russ had a beer belly, a big protuberant, hanging-over-the belt-on-top-of-skinny-legs sort of beer belly. Except he didn't get it from beer (only). Yes, he did drink beer, up to 3 or 4 per day on weekends, rarely during the week.

Russ got his "beer belly" from snack foods, processed foods, and yes, wheat products.

He came to my office for consultation for unexplained breathlessness. His primary care physician was stumped and asked for an opinion.

So, part of Russ' evaluation included laboratory work. Russ proved to have a blood sugar (glucose) of 136 mg/dl, well into the diabetic range. His insulin level was 102 microunits/ml, way above the desirable range of <10. I interpreted this to mean that Russ had early diabetes but still maintained vigorous pancreatic function, since the pancreas is the abdominal organ responsible for insulin production. In pre-diabetes and early diabetes, insulin levels can be high, reflecting the revved up output of the pancreas. However, the pancreas eventually "burns out," unable to keep up with the demand to product enormous quantities of insulin. That's when blood sugar skyrockets.

Along with the blood sugar and insulin, Russ showed all the expected markers of this syndrome (the "metabolic syndrome"): low HDL of 34 mg/dl, high triglycerides of 257 mg/dl, severe small LDL (80% of total LDL), high c-reactive protein, and high blood pressure.

A heart scan showed a surprisingly small amount of coronary plaque with a score of only 4. Thus, Russ' symptoms were unlikely to represent a coronary issue ("ischemia"). Breathlessness was far more likely to be from 1) his obesity and protuberant abdomen, large enough to encroach on his chest and lung volume, and 2) high blood pressure (which can, in turn, lead to high heart pressure and breathlessness, often called "left ventricular diastolic dysfunction").

I persuaded Russ to eliminate his previously flagrant and abundant over-reliance on wheat products and snack foods. Two months later, 15 lbs lighter, and a modestly less protuberant beer belly, Russ' laboratory evealuation showed:

--Blood sugar 90 mg/dl--normal.

--Insulin 12 microunit/ml--darn near normal.

Blood pressure was down 20 points. Russ' breathlessness was now entirely gone. He has another 30-40 lbs to go, but he's off to a great start. He is now clearly, solidly, and confidently NON-diabetic.

I see experiences like this every day, as do committed diabetes fighters like Jenny at Diabetes Update.

Why isn't this common practice? If pre-diabetes and diabetes can be cured by such a simple approach, why isn't it more widely embraced? After all, what other devastating diseases can claim to have such a simple, straightforward way to achieve cure?

And why does the American Diabetes Association (ADA) actually condone the inclusion of abundant carbohydrates in diabetics? Their modified food pyramid shows the widest part of the pyramid filled with "breads, grains, and other starches."



How about this question taken from a Q&A on the ADA website:

Can I eat foods with sugar in them?

For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.


The answer is simple. Just as the American Heart Association focuses on ways to deliver the message of palliation, so does the ADA. So ADA diet advice is designed to help diabetics maintain a stable blood sugar on their medication. It is definitely not intended to reverse or eliminate diabetes. My patient Russ would be deep into diabetes on the ADA diet, enjoying his rolls, whole wheat bread, breakfast cereals, and birthday cake.

Once again, another example of the growing irrelevance of the "official" arbiters of health information for those of us looking for reversal of disease.

Study review: cerivastatin

I'd like to start an occasional series of blog posts on The Heart Scan Blog in which I review studies relevant to the whole heart scan score reversal experience.

In a previous post, Don't be satisfied with "deceleration,"I discussed the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), in which either atorvastatin (Lipitor), 80 mg, or pravastatin (Pravachol),40 mg, was given to 615 women. Both groups showed an average of 15% annual plaque growth, regardless of which agent was taken and regardless of the amount of LDL cholesterol reduction.

I cited another study in which 471 participants received either Lipitor, 80 mg, or Lipitor, 10 mg. The rate of annual score increase was 25-27%, regardless of drug dose or LDL lowering.

Here's yet another study, a small German experience in 66 patients, with a curious design and using the now-defunct statin drug, cerivastatin (Bayccol, pulled in 2001, nearly simultaneous with the publication of this study, due to greater risk of muscle damage, particularly when used in combination with gemfibrozil). Achenbach et al in Influence of lipid-lowering therapy on the progression of coronary artery calcification: A prospective evaluation reported on this trial in which all participants underwent heart scanning to obtain a heart scan score; no treatment was initiated based on the score. A second scan was obtained after the no treatment period, followed by treatment with cerivastatin, 0.3 mg per day. A third scan was finally obtained.

In year one without treatment, the average increase in heart scan scores was 25%. In year two with cerivastatin, the average increase in heart scan score was 8.8%. In 32 participants who achieved LDL<100 mg/dl on the drug, there was an average modest reduction in heart scan scores of 3.7% (i.e., -3.7%).

Now, that was eye-opening. Why did this small study achieve such startlingly different results from the other two studies that showed relentless progression despite even high doses of Lipitor? That remains unanswered. Was cerivastatin unique among statins? Did the unique two-phase trial design somehow change the outcome by triggering participants to change lifestyle habits after their first scan (since most exhibited an increase in score; they were not "blinded" to their scores). Those questions will remain unanswered, since the drug has been made unavailable. This smal l study had actually been intended to be larger, but was prematurely terminated because of cerivastatin's withdrawal.

This experience is unique, as you can see, compared to the two other studies. But it was also smaller. The results are also different than what I have seen in day-to-day practice when I've seen people treated with statin drugs alone (not cerivastatin, of course): rarely do heart scan scores stop increasing. While slowing does usually occur (18-24% per year rates of annual score increase are very common in people who do nothing but take a statin drug and make modest lifestyle changes), I have personally seen only two people stop their score with this strategy alone. Nobody has ever dropped their score taking a statin alone, in my experience.

You can also see the nature of clinical studies: single or limited interventions instituted in order to control for unexpected or complex effects. If three different treatments are used, then what desirable or undesirable effects, or lack of an effect, is due to which treatment agent?

My experience is that no single treatment stops or reduces heart scan scores. It requires a more rational effort that includes 1) identification of all causes of coronary plaque (e.g., low HDL, high triglycerides, Lp(a), small LDL, deficiency of vitamin D, etc, none of which are substantially affected by statin drugs), and 2) correction of all causes. That simple concept has served us well.

Dr. William Blanchet: A voice of reason

I don't mean to beat this discussion to a pulp, but looking back over the comments posted on www.theHeart.org forum, I am so deeply impressed with Dr. William Blanchet's grasp of the issues, that I posted his articulate and knowledgeable comments again.

Here is one post in which Dr. Blanchet, in response to accusations of trying to profit from heart scans, provides a wonderful summary of the logic and evidence behind the use of heart scans as the basis for heart disease prevention.


Yes, I have seen a dramatic reduction in coronary events.

Of 6,000 active patients, 48% being Medicare age and over, I have seen 4 heart attacks over the last 3+ years. 2 in 85 year old diabetics undergoing cancer surgery, one in a 90 year old with known disease and one in a 69 year old with no risk factors, who was healthy, and had never benefited from a heart scan.

The problem with coronary disease is that we rely on risk factors. Khot et al in JAMA 2003 showed that of 87,000 men with heart attacks, 62% had 0 or 1 major risk factor prior to their MI. According to ATP-III, almost everyone with 0-1 risk factors is low risk and most do not qualify for preventive treatment. EBT calcium imaging could identify 98% of these individuals as being at risk before their heart attack and treatment could be initiated to prevent their MI.

Treating to NCEP cholesterol goals prevents 30-40% of heart attacks. Treating to a goal of coronary calcium stability prevents 90% of heart attacks. Where I went to school, a 40% was an F. Why are we defending this result instead of striving to improve upon it? I am not making this up, look at Raggi's study in Arteriosclerosis, Thrombosis, and Vascular Biology 2004;24:1272, or Budoff Am J Card.[I believe it's the study Dr. Blanchet was referring to.]

I strongly disagree with the assertion that the stress test is a great risk stratifier. Laukkanen et al JACC 2001 studied 1,769 asymptomatic men with stress tests. Although failing the stress test resulted in an increased risk of future heart attack, 83% of the total heart attacks over the next 10 years occurred in those men who passed the stress test. Falk E, Shah PK, Fuster V Circulation 1995;92:657-671 demonstrated that 86% of heart attacks occur in vessels with less than 70% as the maximum obstruction. A vast majority of
patients with less than 70% vessel obstruction will pass their stress test.

Regarding [the] question of owning or referring for EBT imaging, I would be amused if it were not insulting. The mistake that is often made is that EBT imaging is a wildly profitable technology. It is not nearly as profitable as nuclear stress imaging. Indeed there are few EBT centers in the country that are as profitable as any random cardiologist's stress lab.

How can we justify not screening asymptomatic patients? Most heart attacks occur in patients with no prior symptoms and according to Steve Nissen, 150,000 Americans die each year from their first symptom of heart disease. My daughter is at this moment visiting with a friend who lost her father a few years ago to his first symptom of heart disease when she was 8 years old. That is not OK! We screen asymptomatic women for breast cancer risk. Women are 8 times more likely to die from heart disease than breast cancer. We do mass screening for colon cancer and we are over 10 times more likely to die from heart attacks than colon cancer. An EBT heart scan costs 1/8th the cost of a colonoscopy.

So what say we drop the sarcasm and look at this technology objectively. Read the literature, not just the editorial comments. This really does provide incredibly valuable information that saves lives.

Yes, a 90% reduction in heart attacks in my patients compared to the care I could provide 5 years ago when I was doing a lot of stress testing and referring for revascularization. Much better statistics than expected national or regional norms. I welcome your scrutiny.



That's probably the best, most concise summary of why heart scanning makes sense that I've ever heard. And it comes from a primary care physician in the trenches. With just a few paragraphs, Dr. Blanchet, in my view, handily trumps the arguments of my colleagues arguing to maintain the status quo of cholesterol testing, stress tests, and hospital procedures.


Note:
Dr. Blanchett talks openly about his affiliation with an imaging center in Boulder, Colorado, Front Range Preventive Imaging. I'm no stranger to the accusations Dr. Blanchet receives about trying to profit from the heart scan phenomenon. Ironically, heart scanning loses money. It is a preventive test, not a therapeutic, hospital-based procedure. Free-standing heart scan centers that do little else (perhaps virtual colonoscopies) usually manage to pay their bills but make little profit. Hospitals that offer heart scans usually do so as a "loss-leader," i.e., an inexpensive test that brings you in the door in the hopes that you will require more testing.

Accusations of profiteering off heart scans are, to those in the know, ridiculous and baseless. On the contrary, heart scans are both cost-saving and life-saving.

Vitamin D2 rip-offs

Here's a sampling of prescription vitamin D2/ergocalciferol products available:






Prescription ergocalciferol (vitamin D2) (Drisdol brand), 50 caps for $130.84.










Alfcip brand of erogocalciferol (vitamin D), 30 capsules for $28.20.









Ergocalciferol (vitamin D2) as Drisdol oral solution, 1 bottle $146.26.










How about vitamin D3/cholecalciferol?



Carlson's brand cholecalciferol (vitamin D3), 120 capsules $5.09.









Cholecalciferol, vitamin D3, is far less expensive than ergocalciferol, vitamin D2. Cholecalciferol is available as a supplement without prescription. Ergocalciferol is available only by prescription.

The price difference must mean that the plant-based form, ergocalciferol, must be far superior to the naturally-occurring human form, vitamin D3.

Of course, that's not true. Dr. Robert Heaney's study is just one of several documenting the inferiority of D2/ergocalciferol, Vitamin D2 Is Much Less Effective than Vitamin D3 in Humans. D2 exerted less than a third of the effect of D3.

In my experience, D2/ergocalciferol often exerts no effect whatsoever. One woman I consulted on came into the office having been prescribed Drisdol capsules, 50,000 units every day for the past 18 months (by mistake by her physician). Blood level of active 25-OH-vitamin D3: Zero.

But the pharmacy and drug manufacturer collected $1413 for her 18-month course. Cost for a 4000 unit per day dose of D3/cholecalciferol: $45--and it would have actually worked.

In my view, prescription vitamin D2 is yet another example of drug manufacturer scams, a product that provides no advantages, costs more, but yields bigger profits.

Yet this wonderful supplement called cholecalciferol, among which Carlson's is an excellent choice, is available to you inexpensively, without prescription, and actually provides the benefits you desire.

Stenosis detection vs. plaque detection

One of the most common misunderstandings encountered by both physicians and the public is that, to create an effective heart disease prevention program, we need tools for atherosclerotic plaque detection. What we do not need is a tool for stenosis detection. (Stenosis means percent blockage. A 50% stenosis means 50% of the diameter of an artery is reduced by atherosclerosis.)

This issue came to mind recently with the ongoing conversation at Heart.org forum, in which the conversation predictably degenerated into a "what good are heart scans when there are better tests to detect blockage" sort of mentality.
They are right: There are better tests to detect stenoses or blockages, such as stress tests, heart catheterization, and CT coronary angiography. If someone is having chest pain or breathlessness, these tests are useful to help understand why. These tests are preludes to stents, bypass surgery, and the like. They are the popular tools in hospitals, the ones that provide entry into the revenue-yielding world of heart disease procedures.

Plaque detection, on the other hand, is principally a tool for the person without symptoms. In this regard, it is more like cholesterol testing. I doubt my colleagues would bash cholesterol because it doesn't reveal blockages. Plaque detection identifies the person who has already started developing atherosclerosis.

Dr. William Blanchett of Colorado articulates this idea well:

EBT calcium imaging not only identifies the vast majority of individuals at risk, it also identifies individuals with minimal risk. In other words, it distinguishes those who are likely to benefit from treatment . . .and it identifies those unlikely to benefit from treatment. Furthermore, the greatest value of EBT calcium imaging is that with serial imaging you can determine who is and who is not responding to treatment.

Those patients not responding to the initial treatment are identified by progression of their calcified plaque on a subsequent scan are then placed on additional therapies. The net result is a remarkable reduction in heart attack rates.

Ahh, the voice of reason. Plaque detection empowers you in your prevention program. If you know how much plaque your begin with, you can track that value to know whether you have having a full effect or not. Stenosis detection, on the other hand, empowers your doctor and provides the irresistible impulse to stent.

Another common objection raised to plaque detection is "why bother if you're going to give everybody a statin anyway?" We know the origins of that argument, don't we? If the only strategy known to your doctor is cholesterol reduction with statin drugs, then perhaps that's right. But, with awareness of all the things that go beyond statin drugs, often make them unnecessary, then knowledge of who should engage in an intensive program of prevention or not is enabled by plaque detection.

Is an increase in heart scan score GOOD?

In response to an earlier Heart Scan Blog post, I don't care about hard plaque!, reader Dave responded:

Hello Dr Davis,

Interesting post about hard and soft plaque. I recently had a discussion with my GP regarding my serious increase in scan score (Jan 2006 = 235, Nov 2007 = 419).

After the first scan we started aggressively going after my LDL, HDL and Trig...196,59,221

And have them down to 103, 65, 92 - we still have a way to go to 60/60/60 [The Track Your Plaque target values]-

So the increase is a surprise, but my doctor said that the increase could in part be cause some of the soft plaque had been converted to hard plaque and the scan would show that conversion.



Dave's doctor then responded to him with this comment:

"Remember that although your coronary calcium score has gone up, this does not mean that you are at greater risk than you were a year ago. Remember that the most dangerous plaque is the not-yet calcified soft plaque, which will not show up on an EBT [i.e., calcium score]. It is only the safe, calcified plaque that can be measured with the EBT. [Emphasis mine.] For your score to go up like it did, while your lipids came down so much, what had to happen was that lots of dangerous unstable plaque was converted to stable, calcified plaque. There are no accepted guidelines for interpreting changes in calcium scores over time, because the scores tend to go up as treatment converts dangerous plaque to safer plaque. We do know that aggressively lowering LDL reduces both unstable and stable plaque, and we know that risk can be further lowered by adjuvant therapy such as I listed above."


Huh?

This bit of conventional "wisdom" is something I've heard repeated many times. Is it true?

It is absolutely NOT true. In fact, the opposite is true: Dave's substantial increase in heart scan score from 235 to 419 over 22 months, representing a 78% increase, or an annualized rate of increase of 37%. This suggests a large increase in his risk for heart attack, not a decrease. Big difference!

Dr. Paulo Raggi's 2004 study, Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy in 495 participants addresses this question especially well. Two heart scans were performed three years apart, with a statin drug initiated after the first scan, regardless of score.

During the period of study, heart attacks occurred in 41 participants. When these participants were analyzed, it was found that the average annual increase in score over the three year period was 42%. The average annual rate of increase in those free of heart attack was 17%. The group with the 42% annual rate of increase--all on statin drugs--the risk of heart attack was 17.2-fold greater, or 1720%.

The report made several other important observations:

--20% of the heart attack-free participants showed reduction of heart scan scores, i.e., reversal. None of the participants experiencing heart attack had a score reduction.
--Only 2 of the 41 heart attacks occurred in participants with <15% per year annual growth, while the rest (39) showed larger increases.
--The intensity of LDL reduction made no difference in whether heart attacks occurred or not. Those with LDL<100 mg/dl fared no better than those with LDL>100 mg/dl.

Dr. Raggi et al concluded:

"The risk of hard events [heart attack] was significantly higher in the presence of CVS [calcium volume score] progression despite low LDL serum levels, although the interaction of CVS change and LDL level on treatment was highly significant. The latter observation strongly suggests that a combination of serum markers and vascular markers [emphasis mine] may constitute a better way to gauge therapeutic effectiveness than isolated measurement of lipid levels."

This study demonstrates an important principle: Rising heart scan scores signal potential danger, regardless of LDL cholesterol treatment. Yes, LDL reduction does achieve a modest reduction in heart attack, but it does not eliminate them--not even close.

These are among the reasons that, in the Track Your Plaque program, we aim to correct more than LDL cholesterol. We aim to correct ALL causes of coronary plaque, factors that can be responsible for continuing increase in heart scan score despite favorable LDL cholesterol values.

So, Dave, please forgive your doctor his misunderstanding of the increase in your heart scan score. He is not alone in his ignorance of the data and parroting of the mainstream mis-information popular among the statin-is-the-answer-to-everything set.

Just don't let your doctor's ignorance permit the heart attack that is clearly in the stars. Take preventive action now.

The Heart.org online debate

There's a fascinating and vigorous debate going on at the Heart.org website among Dr. Melissa Shirley-Walton, the recently publicized proponent of "a cath lab on every corner": Dr. William Blanchet, a physician in northern Colorado; and a Track Your Plaque Member who calls himself John Q. Public.

John Q. has been trying to educate the docs about the Track Your Plaque program. Unfortunately, Dr. Shirley-Walton essentially pooh-poohs his comments, preferring to lament her heavy work load. In her last post, when she discovered that John Q. was not a physician, she threatened to block his posts and delete all prior posts.

However, Dr. Blanchet has emerged as a champion of heart scanning, intensive lipid management, and lipoproteins, much similar to our program. In fact, many of Dr. Blanchet's comments were so similar to mine that John Q. asked me if it was really me! (It is definitely not.)


Here's a sampling of some of the discussion going on now:


Dr. Blanchett started out the discussion by saying:

Stent Insanity
I have no trouble agreeing with the argument that we have initiated the widespread use of DES without adequate study regarding outcomes. Shame on us.

That said, we are ingoring the DATA that shows that most heart attacks occur as a result of non-obstructing plaque and all the talk about which stent to use ignors the majority of individuals at risk. In addition, for a decade we have known that stenting does not improve net outcomes anyway.

What ever happened to effective primary prevention? We discarded EBT calcium imaging like moldy cabbage without even looking at the outcomes DATA. With direction provided by EBT calcium imaging and effective primary prevention, I have been able to reduce myocardial infarction by 90% in my very large Internal Medicine practice. Through effectively identifying patients at risk and measuring success or failure of treatment with serial EBT, I have made the argument as to which stent to use moot. No symptomatic angina and rare infracts equals little need for any stent.

Is anybody listening? Certainly not the cardiologists whose wealth and fortunes are based on nuclaer imaging, angiography and stenting.



Dr. Shirley-Walton, skeptical of Dr. Blanchet's claim of >90% reduction of heart attacks using a prevention program starting with a heart scan:

To rely soley upon a calcium score will deprive you of a lot of information that could be otherwise helpful in the management of your patients.

Without seeming sarcastic, I must refute : "of 6,000 patients I've seen 4 heart attacks in 3 years". Although I certainly hope your statistics are accurate, I will suggest the following:

You've not seen all of the heart attacks since up to 30% of all heart attacks are clinically silent. So unless you are echo'ing or nuclear testing all of these patients in close followup, you aren't certain of your stats.

Secondly, in order to attribute this success to your therapy, you would have to have nearly 100% compliance. In the general population, compliance is often less than 50% with any regimen in any given year of treatment. If you can tell us how you've achieved this level of compliance, we could all take a lesson.




Dr. Blanchett, commenting on his use of heart scanning as a primary care physician:

CAC [coronary artery calcium] is an inexpensive and low radiation exam to identify who is at increased risk for heart attacks.

A study of 222 non-diabetic patients admitted with their first MI found 75% of them did not qualify for cholesterol modifying therapy prior to their initial MI (JACC 2003:41 1475-9). In another study of 87,000 men with heart attacks, 62% had 0 or 1 major risk factors (Khot, et al. JAMA. 2003). Almost all individuals with 0 or 1 risk factor are Framingham "Low risk" and therefore will not qualify for cholesterol lowering therapies. (JAMA. 2001;285:2486-2497)


Risk factors alone are not sufficient. In my practice, of the last 4 patients who have died from heart attacks, none qualified for preventive therapies by NCEP guidelines.

Studies have shown that CAC by EBT provides an independent and incremental predictor of heart attack risk. (1. Kondos et al, Circulation 2003;107:2571-2176, 2. Am Heart J 141. 378-382, 2001, 3. St Francis Heart Study Journal of the American College of Cardiology July, 2005) The old saw that CAC simply reflects risk factors and age is just wrong.


Although CT angiography shows great promise to reduce unnecessary conventional angiography and is helpful in emergency room chest pain evaluation, I do not see CT angiography as a screening study in asymptomatic individuals. 10 times more radiation than EBT calcium imaging plus the risk of IV dye exposure makes CT angiography inconsistent with the principles of a screening test. Taken in the context of a primary care physician's evaluation of heart attack risk, EBT calcium imaging has great value.

Coronary calcium changes management by: 1. Identifying those at risk who do not show up with standard risk stratification (St Francis Heart Study: Journal of the American College of Cardiology July, 2005). 2. Motivating patients to be compliant with therapies (Atherosclerosis 2006; 185:394-399). 3. By measuring serial calcium, we can see who is and who is not responding to our initial treatment so that we can further refine our therapeutic goals (Atherosclerosis, 2004;24:1272).

When used in the primary care preventive setting, CAC imaging is indeed of great incremental value. In my practice, in improves my outcomes so greatly that it compels Melissa Walton-Shirley to question my veracity.



Dr. Melissa Walton-Shirley:

Ahhhhhh.......the aroma of profit making, I thought I smelled it. [Accusing Dr. Blanchett of referring patients for heart scans for personal profit.]

I will tell you that I was a little hurt when I was called "a typical cardiologist with a butcher block mentality" after my primary pci piece for med-gen Med was reviewed by the track your placque [sic] folks.

Though, it's clear that they misunderstood and thought I was cathing for dollars, instead my intention was to "push" for primary PCI for AMI, it left me seething until the blessing of a busy schedule and a forgetful post menopausal brain took its toll.
None the less, an honest open discussion is always welcome here but I would appreciate it if everyone would just divulge their affiliations up front so that the context of their opinions could be better understood.

I also insist that the compliance described by you William B. is rather astounding and a bit unbelieveable, however if it's accurate, you are to be congratulated.




Dr. Blanchett, in response to Dr. Shirley-Walton's statement that she relies on stress testing:

I think that the threshold of comfort you get from stress test stratification is different than what I consider acceptable. It is hard for me to tell a bereaved spouse that the departed did everything I suggested and still died from a MI. Coronary calcium imaging provides me the tool that I need.

Are you aware that there are a number of studies that show a dramatic increase in risk of MI in individuals with an annualized increase in calcified plaque burden of >14%? I consider this to be a valuable measure of inadequacy of medical management. A stress test does not become positive until we have catastrophically failed in medical management. Consequently, even in the patient with “high risk” stratification, one can justify a calcium score to establish a baseline to measure adequacy of primary prevention. Calcium scores by EBT cost about 1/5th the cost of a nuclear stress test and subject the patient to 1/10th the radiation of nuclear imaging and provides more precise information.

Regarding John Q, I do not think that non-medical prospective should be excluded from this blog. I think we as physicians benefit from hearing how the non-physician public views medicine. I have become much better at what I do by listening to my patients and learning from them.


Dr. Blanchett continues:

Yes, I have seen a dramatic reduction in coronary events. Of 6,000 active patients, 48% being Medicare age and over, I have seen 4 heart attacks over the last 3+ years. 2 in 85 year old diabetics undergoing cancer surgery, one in a 90 year old with known disease and one in a 69 year old with no risk factors, who was healthy, and had never benefited from a heart scan.

The problem with coronary disease is that we rely on risk factors. Khot et al in JAMA 2003 showed that of 87,000 men with heart attacks, 62% had 0 or 1 major risk factor prior to their MI. According to ATP-III, almost everyone with 0-1 risk facto is low risk and most are do not qualify for preventive treatment. EBT calcium imaging could have identify 98% of these individuals as being at risk before their heart attack and treatment could be initiated to prevent their MI.

Treating to NCEP cholesterol goals prevents 30-40% of heart attacks. Treating to a goal of coronary calcium stability prevents 90% of heart attacks. Where I went to school a 40% was an F. Why are we defending this result instead of striving to improve upon it? I am not making this up, look at Raggi's study in Ateriosclerosis, Thrombosis, and Vascular Biology 2004;24:1272, or Budoff Am J Card


Melissa, I strongly disagree with the assertion that the stress test is a great risk stratifier. Laukkanen et al JACC 2001 studied 1,769 asymptomatic men with stress tests. Although failing the stress test resulted in an increased risk of future heart attack, 83% of the total heart attacks over the next 10 years occurred in those men who passed the stress test.
Falk E, Shah PK, Fuster V Circulation 1995;92:657-671 demonstrated that 86% of heart attacks occur in vessels with less than 70% as the maximum obstruction. A vast majority of patients with less than 70% vessel obstruction will pass thier stress test.


William, regarding your question of owning or referring for EBT imaging, I would be amused if it were not insulting. The mistake that is often made is that EBT imaging is a wildly profitable technology. It is not nearly as profitable as nuclear stress imaging. Indeed there are few EBT centers in the country that are as profitable as any random cardiologists stress lab.

How can we justify not screening asymptomatic patients? Most heart attacks occur in patients with no prior symptoms and according to Steve Nissen, 150,000 Americans die each year from their first symptom of heart disease. My daughter is at this moment visiting with a friend who lost her father a few years ago to his first symptom of heart disease when she was 8 years old. That is not OK! We screen asymptomatic women for breast cancer risk. Women are 8 times more likely to die from heart disease than breast cancer. We do mass screening for colon cancer and we are over 10 times more likely to die from heart attacks than colon cancer. An EBT heart scan costs 1/8th the cost of a colonoscopy.

So what say we drop the sarcasm and look at this technology objectively. Read the literature, not just the editorial comments. This really does provide incredibly valuable information that saves lives.

Yes, a 90% reduction in heart attacks in my patients compared to the care I could provide 5 years ago when I was doing a lot of stress testing and referring for revascularization. Much better statistics than expected national or regional norms. I welcome your scrutiny.



John Q. Public jumps into the fray with:

Fascinating, isn't it, that there appear to be two doctors, William Blanchet in this forum and Dr. William Davis, FACC, of cureality.com that both claim to have dramatically reduced risk of heart attack among their patients and/or actual calcium plaque score regression and BOTH are ardent proponents of CT Calcium Scoring?


Despite Dr. Blanchet's persuasive arguments backed up with numerous scientific citations and John Q.'s support, I sense they had no effect whatsoever on Shirley-Walton's way of thinking.

Such are the deeply-entrenched habits of the cardiology community. It will be many years and impassioned pleas to see things in a different light before the wave of change seizes hold.

To learn how to eat . . . try fasting

Curious thing about fasting: It teaches you how to eat.

In previous posts, I've discussed the potential benefits of fasting: reduction of blood pressure, reduction of inflammatory responses, drop in blood sugar, weight loss, and reduced heart attack risk. In my recent Heart Scan Blog post, Fasting and Heart Disease, I discussed the just-released results of a study in people who fast for religious reasons and experience less heart disease.

Fasting can mean going entirely without food and just making do with (plenty of) water, or it can mean variations on "fasting" such as vegetable juice fasts, soy milk fasts, etc.

How can fasting teach you any lessons about food and eating?

People who fast will tell you that the experience:

--Helps you appreciate food tastes when you resume eating. After a fast, flavors are stronger; sensations like sweet, sweet, or salty are sharper; you become reacquainted with the variety of wonderful food textures.

--Makes you realize how you ate too much before your fast. After a fast, you are satisfied with less. You will eat more for taste and enjoyment, less for satiety and mindless indulgence.

--Makes you more mindful of the act of eating. For many of us, eating is an automatic activity that provides fleeting satisfaction. After a fast, each bite of food brings its own special enjoyment.

--Reveals to you how awful you felt when many foods were eaten. For example, many people are physically slightly ill after eating pancakes, pizza, or other highly processed foods but cease to recognize it. Remove the offensive foods entirely and you might realize just how bad you felt.

--Takes away fear of hunger. Many people have a gut-wrenching fear of hunger. It's probably partly instinctive, that animal-like fear of not knowing when your next meal is coming, partly the abnormal, artificial drive to eat ignited by processed foods like wheat and corn syrup.

--Makes you realize just how much of your day is spent in some activity associated with food. Shopping, eating, cleaning up afterwards, thinking and talking about food all occupy an extraordinary portion of everyone's life. A fast can open your eyes to just how much time is spent in these pursuits. Sometimes, gaining an awareness of a mindless, repetitive behavior can provide the first step towards changing direction.


Most people consider a fast for rapid weight loss. But fasting is far more than that. Perhaps fasting has become an integral part of many religious practices because of its capacity for enlightenment, reawakening, revelation, but not of only the spiritual, but also of how far many of us have strayed in diet.

Fasting is what Omnivore's Dilemma author Michael Pollen might describe as looking the pig you're about to eat in the eye, an opportunity to open your eyes to what it is you 've been doing all these years.