Can I eat quinoa?

. . . or beans, or brown rice, or sweet potatoes? Or how about amaranth, sorghum, oats, and buckwheat? Surely corn on the cob is okay!

These are, of course, non-wheat carbohydrates. They lack several crucial undesirable ingredients found in our old friend, wheat, including no:

Gliadin--The protein that degrades to exorphins, the compound from wheat digestion that exerts mind effects and stimulates appetite to the tune of 400 additional calories (on average) per day.
Gluten--The family of proteins that trigger immune diseases and neurologic impairment.
Amylopectin A--The highly-digestible "complex" carbohydrate that is no better--worse, in fact--than table sugar.

So why not eat these non-wheat grains all you want? If they don't cause appetite stimulation, behavioral outbursts in children with ADHD, addictive consumption of foods, dementia (i.e., gluten encephalopathy), etc., why not just eat them willy nilly?

Because they still increase blood sugar. Conventional wisdom is that these foods trend towards having a lower glycemic index than, say, table sugar, meaning it raises blood glucose less.

That's true . . . but very misleading. Oats, for instance, with a glycemic index of 55 compared to table sugar's 59, still sends blood sugar through the roof. Likewise, quinoa with a glycemic index of 53, will send blood sugar to, say, 150 mg/dl compared to 158 mg/dl for table sugar--yeah, sure, it's better, but it still stinks. And that's in non-diabetics. It's worse in diabetics.

Of course, John Q. Internist will tell you that, provided your blood sugars after eating don't exceed 200 mg/dl, you'll be okay. What he's really saying is "There's no need for diabetes medication, so you're okay. You will still be exposed to the many adverse health consequences of high blood sugar similar to, though less quickly than, a full diabetic, but that's not my problem."

In reality, most people can get away with consuming some of these non-wheat grains . . . provided portion size is limited. Beyond limiting portion size, there are two ways to better manage your carbohydrate sensitivity to ensure that metabolic distortions, such as high blood sugar, glycation, and small LDL particles, are not triggered.

More on that in the future.


Lipoproteins . . . zero!

With the recent refinements in our approach to correction of the lipoprotein abnormalities that lead to coronary plaque and heart disease risk, I have been witnessing more and more people achieve:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L



For instance, Ted, a 58-year old man I saw in the office today started with:

Small LDL 1673 nmol/L
Lipoprotein(a) 219 nmol/L


In other words, both small LDL particles and lipoprotein(a) are being knocked down to zero values.

Incidentally, the combination of lipoprotein(a) with small LDL is among the most atherogenic (atherosclerotic plaque-causing) patterns known. Despite his athletic, slender build and avoidance of unhealthy habits, Ted's heart scan score was 922--very high.

So Ted followed the diet I advocate, i.e., wheat elimination followed by elimination of cornstarch, oats, and sugars; high-dose fish oil (total daily EPA + DHA of 6000 mg/day); vitamin D supplementation sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml; iodine supplementation; and thyroid normalization which, in Ted's case, required supplementation with the T3 thyroid hormone, liothyronine, at a small dose.

The result:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L


Not everybody, of course, is achieving these incredible--and previously impossible--results. But the numbers are growing. Ted is the third person to achieve zeroes all around, in fact, over the past 10 days.

Heart disease prevention is getting better and more powerful every day. And it ain't all about Lipitor and low-fat.


Chocolate almond biscotti

Biscotti are twice-baked biscuits or cookies that are perfect for dipping into coffee, latté, or espresso. These wheat-free, low-carb biscotti are rich with the taste of chocolate and almonds.

Yield: approximately 15 biscotti



Ingredients:

2 cups almond meal
½ cup chopped walnuts
1/4 cup cocoa powder (undutched)
½ cup dark chocolate chips
Sweetener equivalent to ½ cup sugar (e.g., liquid stevia, Truvia)
½ cup ricotta cheese, room temperature (replace with coconut milk if lactose intolerant)
4 tablespoons butter, melted (replace with coconut oil if lactose intolerant)
2 large eggs
¼ cup milk, unsweetened almond milk, or soy milk
¼ cup almond, peanut, or sunflower seed butter, room temperature

Preheat oven to 350º F.

Mix almond meal, walnuts, sweetener, cocoa powder, and chocolate chips in bowl. Mix in ricotta, butter, eggs, milk, and nut butter and blend by hand thoroughly.

Pour mix onto baking pan lined with parchment paper or greased with coconut oil or other oil. Shape into loaf approximately 1 inch deep and 3½ to 4 inches in width. Place in oven and bake for 40 minutes.

Remove loaf and allow to cool 15 minutes. Slice into approximately ¾-inch widths and lay each biscotto on its side on baking pan. Put back in oven for 10 minutes.

Remove pan and flip biscotti over. Place back in oven and bake an additional 5 minutes. Remove and cool.

Optional: For a little dark chocolate "icing":
Melt 3-4 oz semisweet or dark chocolate in microwave (in 15 second increments until melted) or in metal bowl placed in heated water. Stir in 1-2 teaspoons butter.
Dip each biscotti into melted chocolate mix or drizzle chocolate mixture over top of each biscotto.

Sun green tea

Here's a great way to enjoy the health benefits of green tea during the summer: sun green tea.


I dropped two green tea bags into approximately one-half gallon of cold water in a clear glass jar. I placed the jar in the sun (with top on) for four hours, then brought it into the kitchen. I served it as iced tea with a slice of lemon and mint leaf.

The sun green tea was a smoother than standard green tea brewed with hot water. Ordinarily, if you brew hot green tea for more than 3-5 minutes, it becomes more bitter or tannic. This sun green tea, despite steeping for four hours, was not the least bit bitter or tannic.

The green tea lasted well for about 48 hours, more than enough to enjoy several glasses per day.

Calling all super-duper weight losers!






Have you lost at least 1/2 your weight, e.g., 300 lbs down to 150 lbs? If you have, I have a major national magazine editor looking to talk to you.

If you have gone wheat-free and/or followed the dietary advice offered here in The Heart Scan Blog or through the Track Your Plaque program and would be willing to share your story, please let me know by commenting below. While losing half your body weight is not necessarily a requirement for health, it makes an incredibly inspiring story for others.

If we use your story, I will set aside a copy of my soon-to-be-released book, Wheat Belly.

Lp(a): Be patient with fish oil

High-dose omega-3 fatty acids from fish oil has become the number one strategy for reduction of lipoprotein(a), Lp(a), in the Track Your Plaque program for gaining control over coronary plaque and heart disease risk.

The original observations made in Tanzanian Bantus in the Lugalawa Study by Marcovina et al first suggested that higher dietary exposure to fish and perhaps omega-3 fatty acids from fish were associated with 40% lower levels of Lp(a). Interestingly, higher omega-3 exposure was also associated with having the longer apo(a) "tails" on Lp(a) molecules, a characteristic associated with more benign, less aggressive plaque-causing behavior.

Of course, the 600+ fish- consuming Bantus in the study consumed fish over a lifetime, from infancy on up through adulthood. So what is the time course of response if us non-Bantus take higher doses of fish oil to reduce Lp(a)?

We have been applying this approach in the Track Your Plaque program and in my office practice for the past few years. To my surprise, the majority of people taking 6000 mg per day of omega-3 fatty acids, EPA and DHA, will drop Lp(a) after one year.  Some have required two years.  Therefore checking Lp(a) after, say, 3 or 6 months, is nearly useless. (An early response does, however, appear to predict a very vigorous 1-2 year response.)

I'm sure that there is an insightful lesson to be learned from the incredibly slow response, but I don't currently know what it is.  But this strategy has become so powerful, despite its slow nature, that it has allowed many people to back down on niacin.

Baby your pancreas

There it is, sitting quietly tucked under your diaphragm, nestled beneath layers of stomach and intestines, doing its job of monitoring blood sugar, producing insulin, and secreting the digestive enzymes that allow you to convert a fried egg, tomato, or dill pickle into the components that compose you.

But, if you've lived the life of most Americans, your pancreas has had a hard life. Starting as a child, it was forced into the equivalent of hard labor by your eating carbohydrate-rich foods like Lucky Charms, Cocoa Puffs, Hoho's, Ding Dongs, Scooter Pies, and macaroni and cheese. Into adolescent years and college, it was whipped into subservient labor with pizza, beer, pretzels, and ramen noodles. As an adult, the USDA, Surgeon General's office and other assorted purveyors of nutritional advice urged us to cut our fat, cholesterol, and eat more "healthy whole grains"; you complied, exposing your overworked pancreas to keep up its relentless work pace, spewing out insulin to accommodate the endless flow of carbohydrate-rich foods.

So here we are, middle aged or so, with pancreases that are beaten, worn, hobbling around with a walker, heaving and gasping due to having lost 50% or more of its insulin-producing beta cells. If continued to be forced to work overtime, it will fail, breathing its last breath as you and your doctor come to its rescue with metformin, Actos, Januvia, shots of Byetta, and eventually insulin, all aimed at corralling the blood sugar that your failed pancreas was meant to contain.

What if you don't want to rescue your flagging pancreas with drugs? What if you want to salvage your poor, wrinkled, exhausted pancreas, eaking out whatever is left out of the few beta cells you have left?

Well, then, baby your pancreas. If this were a car with 90,000 miles on it, but you want it to last 100,000, then change the oil frequently, keep it tuned, and otherwise baby your car, not subjecting it to extremes and neglect to accelerate its demise. Same with your pancreas: Allow it to rest, not subjecting it to the extremes of insulin production required by carbohydrate consumption. Don't expose it to foods like wheat flour, cornstarch, oats, rice starch, potatoes, and sucrose that demand overtime and hard labor out of your poor pancreas. Go after the foods that allow your pancreas to sleep through a meal like eggs, spinach, cucumbers, olive oil, and walnuts. Give your pancreas a nice back massage and steer clear of "healthy whole grains," the nutritional equivalent of a 26-mile marathon. Pay your pancreas a compliment or two and allow it to have occasional vacations with a brief fast.

Bread equals sugar

Bread, gluten-free or gluten-containing, in terms of carbohydrate content, is equivalent to sugar.

Two slices of store-bought whole grain bread, such as the gluten-free bread I discussed in my last post, equals 5- 6 teaspoons of table sugar:








 

 

 

 

 

 

 

 

Some breads can contain up to twice this quantity, i.e., 10-12 teaspoons equivalent readily-digestible carbohydrate.

Gluten-free carbohydrate mania

Here's a typical gluten-free product, a whole grain bread mix. "Whole grain," of course, suggests high-fiber, high nutrient composition, and health.



 

 

 

 

 

 

 

 

What's it made of? Here's the ingredient list:
Cornstarch, Tapioca Starch, Whole Grain Sorghum Flour, Whole Grain Teff Flour, Whole Grain Amaranth Flour, Soy Fiber, Xanthan Gum, Soy Protein, Natural Cocoa and Ascorbic Acid

In other words, carbohydrate, carbohydrate, carbohydrate, carbohydrate and some other stuff. It means that a sandwich with two slices of bread provides around 42 grams net carbohydrates, enough to send your blood sugar skyward, not to mention trigger visceral fat formation, glycation, small LDL particles and triglycerides.

Take a look at the ingredients and nutrition facts on the label of any number of gluten-free products and you will see the same thing. Many also have proud low-fat claims.

This is how far wrong the gluten-free world has drifted: Trade the lack of gluten for a host of unhealthy effects.

Gluten-free is going DOWN

The majority of gluten-free foods are junk foods.

People with celiac disease experience intestinal destruction and a multitude of other inflammatory conditions due to an immune response gone haywire. The disease  is debilitating and can be fatal unless all gliadin/gluten sources are eliminated, such as wheat, barley, and rye.

A gluten-free food industry to provide foods minus gliadin/gluten has emerged, now large enough to become an important economic force. Even some Big Food companies are getting into the act, like Kraft, that now lists foods they consider gluten-free.

So we have gluten-free breads, cupcakes, scones, pretzels, breakfast cereals, crackers, bagels, muffins, pancake mixes and on and on. All are made with ingredients like brown rice flour, cornstarch, tapioca starch, and potato starch. Occasionally, they are made with amaranth, teff, or quinoa, other less popular, but gluten-free, grains.

Problem: These gluten-free ingredients, while lacking gliadin and gluten, make you fat and diabetic. They increase visceral fat, cause blood sugar to skyrocket higher than nearly all other foods (even higher than wheat, which is already pretty bad), trigger formation of small LDL and triglycerides, and are responsible for exaggerated postprandial (after-eating) lipoprotein distortions. They cause heart disease, cataracts, arthritis, and a wide range of other conditions, all driven by the extreme levels of glycation they generate.

Eliminating all things wheat from the diet is one of the most powerful health strategies I have ever witnessed. But replacing lost wheat with manufactured gluten-free foods is little better than replacing your poppyseed muffin with a bowl of jelly beans.

Whenever we've relied on the food industry to supply a solution, they've managed to bungle it. Saturated fat was replaced with hydrogenated fat and polyunsaturates; sucrose replaced with high-fructose corn syrup. Now, they are replacing wheat gluten-containing foods with junk carbohydrates.

For this reason, I am bringing out a line of recipes and foods that will be wheat gliadin/gluten-free, do NOT contain the junk carbohydrates that gluten-free foods are made of, and are genuinely healthy. They are tasty, to boot.

The gluten-free industry needs to smarten up. Having a following that is free of cramps and diarrhea but are obese, diabetic, and hobbling on arthritic knees and hips is good for nobody.
All posts by william-davis

Family lessons

Lou was recovering from his 3rd bypass operation. This third go-round left him weaker, slower, less quick on the rebound. In fact, he was lucky to have survived.

At 71 years old, Lou went a good 15 years since his second bypass, another 10 years prior to his first bypass at age 46.

In the days immediately following Lou's bypass, I had a chance to talk to his son, who stayed at his Dad's bedside while Lou struggled through post-op recovery.

"Did your Dad tell you about why this has happened, what caused his heart disease?" I asked.

"Sort of. He just said I should get checked," Lou's son, Aaron, replied.

"Did he mention the lipoprotein(a) pattern he has?"

"No. He never mentioned anything like that. He just said to get checked."

That's how it gets played out more often than not: Mom or Dad has a heart attack, stents, or (3rd) bypass, the children are told to get checked. Getting "checked" assumes that the doctor knows what to check for.

In Lou's case, the reason why he was in the hospital getting his 3rd (and final) bypass was lipoprotein(a), along with genetically-determined small LDL particles, low HDL, a postprandial (after-eating) disorder, hypertension, and borderline diabetes, not to mention vitamin D deficiency, omega-3 fatty acid deficiency, and marginal thyroid function. (Lou, a retired city employee, had showed only marginal interest in correcting these patterns. While he accepted medications, he proved unwilling to engage in the diet and nutritional supplement strategies required to correct his patterns.)

So Lou's 3rd bypass operation provided a moment of reflection for Aaron to ask: "Could I share the fate of my Dad?" With Lou's combination of genetic patterns, there was at least a 75% likelihood that he did. Sadly, going to his doctor would likely yield little more than a cholesterol panel, a question about smoking, and a prescription for Lipitor.

Just getting "checked" would be, more than likely, a recipe for disaster for Aaron: heart disease in his 40s or 50s. That's why you need to take control over this sad state of affairs and ask--no, insist--that an effort be made to determine whether you might share your parents' fate.

Look like Jimmy Stewart


"This diet works great," Don declared. "But I think I've lost too much weight."

At 67 years old and 5 ft. 11 inches, Don began the program weighing 228 lbs (BMI 31.9). Because of high triglycerides, high blood sugar, high c-reactive protein, and excessive small LDL, I instructed Don to eliminate all wheat products from his diet, along with cornstarch and sweets. His intake of lean meats, eggs, vegetables, oils, raw nuts, etc. was unlimited.

Don now weighed 194 lbs, down 34 lbs over 6 months (BMI 27.1). Triglycerides, blood sugar, blood pressure, and well-being had improved dramatically; small LDL, however, had dropped only 30%--still room for improvement.

"My friends say I'm too skinny. They ask if I have cancer!"

I've heard this many times: Someone loses weight in a relatively short period of time and friends and family tell you you're too skinny. "It must be cancer. Nobody loses weight like that."

Unfortunately, many Americans have forgotten what normal looks like. Normal is certainly not a 190-lb, 5 ft 4 in woman, nor is it a 228 lb, 5 ft 11 inch man. But Americans have put on so much weight that the prevailing view of what constitutes "normal" weight has been revised upward. Normal is closer to what we see in old movies from the 1940s and '50s with people like Jimmy Stewart and Donna Reed. That's what we are supposed to look like.

So Don actually remains mildly overweight but is judged as "too skinny," or even cancer-ridden, by friends and family.

Ignore such comments. As you lose pounds and approach a truly desirable weight, realize that you are returning to the normal state, not the vision of "normal" now held by most Americans.

Getting vitamin D right

Vitamin D is, without a doubt, the most incredible "vitamin"/prohormone/neurosteroid I have ever encountered. Frankly, I don't know how we got anything accomplished in health pre-D.

Unfortunately, people I meet rarely take their vitamin D in a way that accomplishes full restoration of vitamin D blood levels. It really isn't that tough.

Here's a list of common tripping points with vitamin D:

"I take vitamin D: 1000 units a day."
This is probably the most common mistake I see: Taking a dose that is unlikely to yield a desirable blood level. (We use 60-70 ng/ml of 25-hydroxy vitamin D as our target.) Most men and women require 6000 units per day to achieve this level. There is substantial individual variation, however, with an occasional person needing much more, a rare person requiring as little as 1000 units.


"I bought some vitamin D on sale. They were white tablets."
Time and again, patients in my office who initially have had successful vitamin D replacement, despite being reminded that only oil-based forms should be taken, switch to tablets. While they initially showed a 25-hydroxy vitamin D blood level, for instance, of 67 ng/ml on 8000 units per day with an oil-based capsule, they switch to a tablet form and the next blood level is 25 ng/ml. In other words, tablets are very poorly or erratically absorbed.

I have had people use tablets successfully, however, by taking their vitamin D tablets with a teaspoon of oil, e.g., olive oil. Oil is necessary for full absorption.


"I'm going to Florida. I'll stop my vitamin D because I'm going to lay in the sun."
Wrong. 90% of adults over 40 years old have lost the majority of their ability to activate vitamin D in the skin. A typical response might be an increase in blood level from 25 to 35 ng/ml--a 10 ng increase with a dark brown tan.

There is an occasional person who, with sun exposure, increases blood levels substantially. This can occur in both fair-skinned and dark-skinned people, though I've never seen it happen in an African-American person. The occasional person who maintains the ability to convert vitamin D with sun exposure, or young people, should seasonally adjust their vitamin D dose, e.g., 6000 units winter, 3000 units summer, or some other regimen that maintains desirable blood levels. You can see that monitoring blood levels (we check levels every 6 months for the first 2 years) is crucial: You cannot know what your vitamin D needs are unless you assess 25-hydroxy vitamin D levels.


"I drink plenty of milk. I don't think I need to take vitamin D."
Oh, boy. This is so wrong on so many levels.

First of all, no adult should be drinking plenty of cow's milk. (A discussion for another day.) Second of all, cow's milk averages 70 units of vitamin D, often the D2 form (ergocalciferol), per 8 oz. Even if the FDA-mandated 100 units per day were present, an average adult dose of 6000 units would require 60 glasses of milk per day. Can you say "diarrhea"?

Likewise, other food sources of vitamin D, such as fish (300-400 units per serving) and egg yolks (20 units per yolk), are inadequate. This makes sense: Humans are not meant to obtain vitamin D from food, but from sun exposure over a large body surface area. And this is a phenomenon that is meant to occur only in the youthful, ensuring that nature takes its course and us older folks get old and make way for the young (i.e., unless we intervene by taking vitamin D supplements).


"My doctor said that my vitamin D blood level was fine. It was 32 ng/ml."

Let's face it: By necessity, your overworked primary care physician, who manages gout, hip arthritis, migraine headaches, stomach aches, prostate enlargement, H1N1, depression, etc., is an amateur at nearly everything, expert in nothing. Nobody can do it all and get it right. Likewise vitamin D. The uncertain primary care physician will simply follow the dictates of the laboratory form that specifies "30-100 ng/ml" as the "normal" or "reference range." Unfortunately, the laboratory often quotes population distributions of a lab measure, not an ideal or desirable level.

To illustrate the folly of population distributions of a measure, imagine you and I want to know what women weigh. We go to a local mall and weigh several thousand women. We tally up the results and find that women weigh 172 lbs +/- 25 lbs (the mean +/- 2 standard deviations). (That's true, by the way.) Is that desirable? Of course it isn't. Population average or population distribution does not necessarily mean ideal or desirable.


"My husband's doctor said he should take 4000 units per day. So I just take the same dose."
That would be fine if all adults required the same dose. However, individual needs can vary enormously. A dose that is grossly insufficient for one person may be excessive for another. Once again, vitamin D dose needs can be individualized by assessing 25-hydroxy vitamin levels in the blood.


"I don't need to take vitamin D. I already take fish oil."
I suspect this mistaken belief occurs either because people confuse fish oil with cod liver oil, which does contain some vitamin D. (Cod liver oil is not the best source of vitamin D, mostly because of the vitamin A content; also a discussion for another time), or because they've heard that eating fish provides vitamin D. However, fish oil capsules do not contain vitamin D unless it is added, in which case it should be prominently and explicitly stated on the label.


"I don't have to take vitamin D. It's summer."

For most people I know, if it's a bright, sunny July day, where are they likely to be? In an office, store, or home--NOT lying in the sun with a large body surface area exposed. Also, most people expose no more than 5-10% of surface area in public. I doubt you cut the grass in a bathing suit. Because of modern indoor lifestyles and fashion, the majority of adults need vitamin D supplementation year-round.


I advise everyone that gelcap vitamin D is preferable. Some, though not all, liquid drop forms have also worked. Take a dose that yields desirable blood levels. And blood levels of 25-hydroxy vitamin D are ideally checked every 6 months: in summer and in winter to provide feedback on how much sun activation of D you obtain.

If your doctor is unwilling or unable to perform vitamin D testing, fingerstick vitamin D test kits can be obtained from Track Your Plaque.

Jimmy Moore's thyroid adventure

My friend, Jimmy Moore of Living La Vida Low Carb, describes his thyroid experience here.

As Jimmy points out, he was looking for a way to jump-start a 50-lb weight loss. In my experience, low thyroid hormone levels ("hypothyroidism") are an exceptionally common cause for weight gain. Correcting even marginal hypothyroidism can facilitate weight loss, often resulting in 10 or more pounds of weight loss within the first month.

Unfortunately, Jimmy's thyroid hormone panel proved normal: TSH 1.3, thyroid hormones free T3 and free T4 in the mid- to upper-half of the reference range.

I say "unfortunately" because it is really an easy, inexpensive, and benign solution for losing weight. (I don't, of course, wish that Jimmy or anyone else develops a thyroid condition. But it really can provide gratifying weight loss results when thyroid function is low.) Jimmy might consider taking his oral temperature first thing in the morning as another means of assessing the adequacy of thyroid function.

Perhaps you will be luckier than Jimmy and have thyroid dysfunction that can be corrected and jump-start your weight loss program. Fingerstick thyroid test kits like the one Jimmy used are available here from Track Your Plaque.

What's that in your mouth?




Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

De Novo Lipo-what?

Humans have limited capacity to store carbohydrates. Beyond the glucose and glycogen in our blood and tissues, we have relatively little carbohydrate to draw from in time of energy need. That's why long-distance runners and triathletes have to carry sugar sources to keep blood sugar from plummeting.

Fat, of course, is different. We have virtually unlimited capacity to store energy as fat.

Because we have limited carbohydrate storage capacity, what can the body do with the excessive quantities of carbohydrates that Americans ingest? What becomes of a bagel for breakfast, wheat crackers for snacks, a whole wheat sandwich for lunch, pretzels, and whole wheat pasta that many people eat every day, not to mention the chips, soft drinks, and juices?

Excess carbohydrates are diverted to an interesting metabolic pathway called de novo lipogenesis (DNL). This refers to the liver's ability to make triglycerides from excessive carbohydrates in the diet. Triglycerides are packaged for release into the blood as VLDL. VLDL, in turn, interacts with other lipoproteins, creating small LDL particles, reduced HDL and smaller, less protective HDL. High VLDL will be measured on a standard cholesterol panel as higher triglycerides.

A University of California (Berkeley, San Francisco) group has done much of the work describing DNL.

A diet weighed towards carbohydrates, especially if 50% or greater calories are carbohydrate, is sufficient to provoke plenty of DNL, even in slender people. DNL is a big part of the reason why low-fat (and, thereby, high-carbohydrate) diets result in higher triglycerides. DNL really gets turned on many-fold if the carbohydrates are "simple," rather than "complex."

Overweight people, however, can demonstrate five-fold greater DNL even with lesser quantities of carbohydrate intake (e.g., 40% fat, 46% carbohydrate, 14% protein):





From Schwarz et al 2003. Mean (± SEM) fractional de novo lipogenesis in lean normoinsulinemic (NI), obese NI, and obese hyperinsulinemic (HI) subjects after 5 d of consuming a high-fat, low-carbohydrate diet and in different lean NI and obese HI subjects after 5 d of consuming a low-fat, high-carbohydrate diet. Values with different superscript letters are significantly different.


Excessive carbohydrates, a la standard low-fat diets, are good for nobody. The concept of de novo lipogenesis fills in a theoretical hole that now explains why people who eat carbohydrates have higher triglycerides, VLDL, and, eventually, insulin resistance and diabetes.

Gretchen's postprandial diet experiment II

I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

A wheat-free 2010

A Heart Scan Blog reader sent this fascinating description of his wheat-free adventure.

Whenever I discuss this notion of going wheat-free and the incredible health effects that develop, I invariably receive comments or emails saying something like "I eat wheat and feel fine. That can't be true." The problem is that not everybody needs to go wheat-free. 20-30% of people can include wheat in their diet and suffer little more than weight gain, some not at all.

But stories like Michael's (below) are commonplace in my experience. I've had many patients who, at first, refused to believe that wheat exposure might be the underlying cause for health struggles. But they finally give it a try and find that rashes, arthritis, acid reflux, irritable bowel symptoms, mood swings, anger, etc. are miraculously improved or gone.

Anyway, hear what Michael has to tell us:


Dr. Davis,

I want to thank you. I was browsing the web a while back and happened to stumble upon your blog post about wheat belly. The first thing that caught my attention was that I thought you had somehow gotten a photograph of me. The young man you posted an image of looked exactly like me. So I read what you had to say. After reading, I thought "Four weeks isn’t so bad. I think I can handle this."

It has now been nine weeks and all I can say is that I am completely amazed. Let me say first that twice in the past twenty years I have been tested for allergies. The first time I was tested I showed a slight reaction to Timothy Grass, but not enough to cause me any problems. The second testing I did not show a reaction to anything. So, I have always assumed that my chronic sinus problem were due to sensitivities to environmental pollutions. Now I am not so sure. I would like to list for you everything that has happened to me since I eliminated wheat from my diet.

1. I have lost a total of 12 pounds in the last 9 weeks.
2. I have lost 1 ¼ inches of belly fat
3. I have lost a tremendous amount of fat from my neck.
4. My entire life I have had problems with oily hair. I could wash my hair and three hours later I looked as if I hadn’t washed in a week. Now my hair stays clean and soft for two to three days without shampoo.
5. My hair was always flat and stringy. Now it has lots of body.
6. I used to have thick layers of dry skin on my scalp. It would come loose in chunks as large as a fingernail. That dry scalp is gone.
7. I used to have dry flaky skin that seemed to secrete oil. That no longer happens. My skin is now soft and smooth.
8. I have lived with bad acne for at least 35 years. Now it is hard to find a pimple on my body.
9. I have always had to fight dehydration. That is no longer a problem.
10. I used to drink two large cups of coffee every morning just to be able to function. I now have enough energy that I have eliminated caffeine from my diet.
11. I sleep more soundly than ever before and my dreams are clear and vivid.
12. My thought processes are more active and clear than they have ever been.
13. My chronic sinus issue is now a thing of the past.
14. I used to have problems with getting the “shakes” if I had gone more than a couple of hours without eating. It was as if I was suffering from low blood sugar. I would even be afraid that I would pass out. Now all I feel is hunger. I can go all day without eating and never feel in danger of losing consciousness.


Today is Thursday. This past Monday my wife and I were eating out and I ordered a burger without a bun. What I didn’t realize was that the burger would arrive covered in onion rings. I knocked the mountain of onion rings onto the plate but there were still a couple that were embedded in the cheese. I decided, what the hell, a couple of onion rings shouldn’t make that much of a difference. I will not make that mistake again anytime soon. Within 30 minutes I felt like there was a steel spike going through my left eye socket. I don’t remember ever being in that much pain. My sinuses were exploding. This morning, as I write this, I still feel the vestiges of that pain. Just enough that I know it is there. But after two and a half days, I am at least able to function again.

I owe you a debt of gratitude. You may have just saved my life. In the very least you have given me the means to improve my life in ways that I never thought possible.

Thank you so much,
Michael B.



Now, if wheat exposure can do that in Michael, what damage can it do in other people?

Personally, I previously experienced many of the same symptoms that Michael suffered, all gone with wheat elimination.

My advice: If you have any inkling that you might have a wheat sensitivity, make a New Year's resolution to stay wheat-free for 4 weeks and see whether you can feel any difference. Not everybody will, but many will be telling us about the dramatic health turnarounds they experienced.

Lipoprotein lipase and you

Lipoprotein lipase can make the difference between having heart disease and not having it. Having sky-high triglycerides or normal triglycerides. It can mean dinner hanging around for over 12 hours in the bloodstream, rather than the usual 4-6 hours.

If you take niacin, you must exercise

We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.


But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:





From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.
All posts by william-davis

Vitamin D and autism

This has nothing to do with coronary plaque reversal, nor directly with the Track Your Plaque program, but I found Dr. John Cannell's discussion about the possible relationship between vitamin D and autism so compelling that I thought I just had to pass it on.

So, below are Dr. Cannell's latest thoughts. He takes some criticisms along with praise. I think we owe him a lot for continuing to doggedly promote the benefits of vitamin D.




Vitamin D Newsletter


August, 2007



Dear Dr. Cannell:

I saw an article from a Toronto newspaper about autism and vitamin D. I am currently searching for a vitamin D specialist in the Washington D.C. area to perform a medical work up on my daughter to look for vitamin D-related disorders. The reason I am in search of a vitamin D specialist is that I believe I have stumbled upon a complex relationship in my daughter involving her foot pain, vitamin D, and her autism.

In April 2006, a few weeks after my 3-year-old profoundly autistic daughter began refusing her daily PediaSure drink, she began having excruciating foot spasms lasting from 10-30 minutes at a time, several times a week. She would throw herself on the floor, curl her toes, slam her heels against the floor, and rub the tops of her feet against the carpet, all while screaming the entire time. These were horrible for her to endure, and horrible for my wife and myself to watch. This went on for a year.

From what I read, the symptom was perhaps like foot spasms associated with carpopedal syndrome or tetany. But her blood work did not support that at all. Calcium level was normal (10.2 mg/dL); 25-Hydroxy-vitamin D low (23.5 ng/ml); 1,25 dihydroxy-vitamin D normal (24.7). Despite some vitamin D deficiency, I was assured by medical professionals that nothing supported a vitamin D cause of these particular spasms, so vitamin D was dismissed. Because her calcium level was normal, they told me she did not have tetany, and vitamin D could not be the cause of the pain.

All medical consultants were stymied. I made another research effort and found a 2003 article on WebMD that stated vitamin D has been found to have some link to basic, unexplained muscle and bone pain. By chance, vitamin D was the next supplement we had at home to begin giving my daughter to treat her autism. So, in April 2007 we began giving my 4 year-old profoundly autistic daughter Vitamin D supplements. Her foot spasms which had plagued her for a year diminished within days and disappeared within three weeks. She has not had a spasm in over two months.

In addition, we noted clear improvements in her autistic condition which appear to be from the vitamin D supplements. Eye contact went from zero to fantastic. Her vocalizations increased markedly (still only babbling; she remains completely nonverbal). She appears even happier than previously (she has always been a somewhat happy child). (Please note that my wife and I have tried many dietary supplements over the past 1.5 years guided by a doctor and dietician who both specialize in autism. We honestly state that this is the only thing that has ever had a positive effect on my daughter. We have seen nothing else work.)

My daughter and vitamin D have a complicated relationship. By all counts, looking at her lab work and general condition, vitamin D should have played no role in those excruciating foot fits. And yet it is apparently exactly what is involved in them. And, my wife and I believe at the same time her autistic condition has improved from the vitamin D. The foot fits and her autism appear linked; it was not just a coincidence that this autistic child has those mysterious foot spasms, and the link appears to be vitamin D.

And so I wonder if this is just the tip of the iceberg, if perhaps there is more to know about my child's relationship with vitamin D and what that might mean for her autism. Does she have a specific vitamin D-related disorder? If so, might direct treatment of it also improve her autism further? These are the questions I would like to pose to a vitamin D specialist who could perform a medical work up on my daughter. Please let me know if you know of anyone in the Northern Virginia/Washington DC area. Also, where is the best place to get vitamin D? Thank you for your time.

Sincerely,
Paul, Washington, D.C.




Dear Paul:

I know of no such specialist in the Washington area, indeed no vitamin D/autism expert exists in the world. As far as a specific "vitamin D disorder," linking her spasms, autism, and vitamin D, the world's English language medical literature contains no description of such a disorder. From your daughter's case, it sounds as if PediaSure was her only regular source of vitamin D. If so, her spasms began two weeks after stopping the small amount of vitamin D contained in PediaSure. The spasms continued for a year, ending a few days after you started giving her vitamin D again, this time in the form of a supplement. Several weeks after restarting vitamin D, both you and your wife noticed an improvement in her autism. To my knowledge, this "case report" - your daughter's - is the first ever published.

As no medical literature has ever been published on any of this, all you can do is give her enough vitamin D to get her 25-hydroxy-vitamin D, known as 25(OH)D, into high normal ranges and then wait and hope. Vitamin D's extraordinary mass-action pharmacology implies that simply providing more substrate ([25(OH)D] will help children with low enzyme activity produce more activated vitamin D (calcitriol) in their brains. The vitamin D theory of autism is not simply that vitamin D deficiency in gestation or early childhood causes the disorder. Instead, the theory holds that a quantitative or qualitative abnormality exists in the enzyme system that activates vitamin D.

It could as simple as the normal variation in the enzyme, an enzyme whose activity would vary in a normal or Gaussian distribution, much like height. Some people are tall, some are short, most are in the middle. The same may be true of the enzyme that forms activated vitamin D (calcitriol), some children have a lot of enzyme and some only a little; most are in the middle. As the substrate [25(OH)D] the enzyme metabolizes fell over the last 20 years with sun-avoidance, more and more children on the low end of the enzyme curve are effected by marginally low 25(OH)D levels, explaining both its genetic basis and exploding incidence.

At this point, all your daughter needs is a physician willing to periodically measure her 25(OH)D. Then you can safely supplement your daughter with doses higher than the current Upper Limit for children (2,000 IU/day). You did not tell me your daughter's weight but, assuming she weighs about 30 pounds, even without 25(OH)D blood tests, you can safely give her 50 mcg/day which is 2,000 IU per day. In fact, the U.S. government says this dose is safe for children over the age of one. Life Extension Foundation sells 250 of the 1,000 IU capsules for about ten bucks with powdered vitamin D inside. The powder is tasteless and dissolves easily in juice. Bio Tech Pharmacal, of Fayetteville, Arkansas, told me they were going to be making a 1,000 IU capsule. Or you can get 1,000 IU capsules in a pharmacy or at Costco and crush them. A Canadian firm is now making vitamin D liquid, called Ddrops, with 1,000 IU per drop, but their mail order web site is not yet easily accessed. Beware of cod liver oil; do not use it because vitamin A inhibits the actions of activated vitamin D, and due to the potential for low-grade vitamin A toxicity.

Remember, more and more researchers now believe autism is a progressive, inflammatory, disorder. That is, the inflammation probably progressively destroys brain tissue as the child ages. As I said in my recent paper, I think there is a chance that vitamin D may have a treatment effect in young autistic children if given in adequate doses, due to its anti-inflammatory properties, and its ability to upregulate glutathione, the master antioxidant that also chelates (binds) and then helps excrete heavy metals like mercury. Unfortunately, I see no way, even if the vitamin D/autism theory turns out to be true, that vitamin D can regenerate brain tissue. However, if it stops the inflammation, and cell death, the brain could then begin to develop and learn. These are big ifs. However, you have nothing to lose by trying, the worst that will happen is that it will not help and vitamin D will be added to the long list of false-hope treatments.

Actually, there is a worse possibility. Say the parents of a three-year-old autistic child decide today that vitamin D is nonsense, another false hope, and that I'm a quack. They decide not to give vitamin D supplement their autistic child, who is probably - like your child - vitamin D deficient. Then, it turns out five years from now that scientific evidence shows vitamin D does indeed help. By that time, the child will be eight and will have suffered additional, irreparable, brain damage. In my mind, that is more tragic than another false hope.



Dear Dr. Cannell:

After that article appeared in the Toronto paper, I started my four-year-old son on 1,000 IU of vitamin D two weeks ago. So far the only thing I noticed is that after about ten days, he didn't seem so miserable. The thing that has always broken my heart is that look of sadness and suffering on his face. After about two weeks of vitamin D, I noticed he seemed less miserable. I wouldn't say he looks happy now but that look of misery seems to be gone. Will it come back? I'm not sure I can take it if it comes back. What else might happen? Also, last summer we noticed he seemed to get better, but then he got worse in the fall. We never thought about it until we read about vitamin D.

Susan, Toronto, Canada




Dear Susan:

I don't know. I think all parents have had their heart pierced by that look at one time or another. I would advise increasing the dose to 2,000 IU per day, making sure it is cholecalciferol and not ergocalciferol, and having your doctor order a 25(OH)D every two months to see if he needs higher doses. You want to get his blood level up to between 50 ng/ml and 80 ng/ml (In many countries outside of the USA, that would be reported as between 125 and 200 nmol/L.) and keep it there, summer and winter, and that may take more than 2,000 IU/day in the winter. If vitamin D has a treatment effect, it will take many months to see its full effect. As you noted, if the theory is correct, autistic children who spend time outdoors in the summer should show some seasonal improvements - if they don't wear sunblock and they expose enough of their skin to generate significant amounts of vitamin D.



Dear Dr. Cannell:

I resent you calling autism a tragedy. My son is not a tragedy and I'm glad he was born and is in our lives. He is our joy. Autism is not a tragedy.

Emma, London, England.





Dear Emma:

I'm glad he is your joy and I believe you. I'm new to the autism field and was not aware how much thought and speech control exists in the discussion of the disease. Nevertheless, I have a few politically incorrect questions. If autism is a joy, I assume you would like other parents to have an autistic child? If autism is such a joy, why is there a huge industry forming to prevent and treat it? At the risk of sounding insensitive - apparently one of the most serious charges leveled in the autism debate - autism is a tragedy. As I pointed out in my paper, research shows that having an autistic child, puts the family under more emotional stress than having a child with a fatal illness.



Dear Dr. Cannell:

Who are you to write an article on autism? You didn't even publish it in a medical journal. You are not with a university. You have not published very much. You have no expertise on autism. No autism experts support your theory. There is no evidence to support the theory. Shouldn't you leave this to experts before you give parents more false hopes?

Mary, Trenton, New Jersey.




Dear Mary:

You are right, I am a nobody; just ask my ex-wife. In the Toronto Globe, I explained why I have not yet submitted the paper. As far as giving false hopes, I've thought about that charge. Right now, regardless of what advocacy groups say, autism is rather hopeless. That is, no treatment, including vitamin D, has been shown to materially affect the clinical course of autism. As a psychiatrist, my observation is that people would rather live with a false hope than with no hope.

Furthermore, if autistic children began taking vitamin D, the worse that can happen is that a period of false hope will followed by dashed hopes and then parents will be back to hopelessness. In the meantime, they will have made their child vitamin D sufficient. Vitamin D deficiency is a serious problem in childhood.
Postgrad Med J. 2007 Apr;83(978):230-5.

The Telegraph, Why is Vitamin D So Vital?

As far as the theory having no support from experts, Dr. Richard Mills, research director of the National Autistic Society in England, was quoted in the Telegraph article on the autism/vitamin D theory: "There has been speculation in the past about autism being more common in high-latitude countries that get less sunlight and a tie-up with rickets has been suggested - observations which support the theory."

Finally, you said there is no evidence to support the theory. I assume you meant there is no proof. The first statement is absolutely false, the second absolutely true. As I detailed in my paper, there is a lot of evidence to support the theory. In fact, if anyone can come up with an autism fact, that the theory cannot explain, I'd like to know about it. Even the announcement of a link between television viewing and autism supports the theory. Furthermore, the TV/autism link is actually evidence of a treatment effect. That is, if autistic children who play outside in the sunshine more - watching less TV - have less severe illness, it may be due to the Sun-God, who bestows her precious gift of calcitriol into the brains of children playing outside in her sunlight but not into the brains of children watching TV inside in the darkness.
Natl Bur Econ Res Bull Aging Health. 2007 Winter;(18):2-3.

As far as proof the theory is true, there is, of course, none. In medicine, proof means randomized controlled human trials, the gold standard for proof. However, proof is the last step, not the first. First comes evidence, then comes a theory, then comes researchers disproving those theories. It works that way. Sometimes we never get to the last step, proof. For example, please point me to a single randomized controlled human trial proving cigarette smoking is dangerous? Instead, the convincing evidence of smoking's dangerousness lies in epidemiological studies, not randomized controlled trials. Proof, or disproof, of the autism vitamin D theory will take years, years during which young autistic brains will continue to suffer irreparable damage. Perhaps vitamin D' powerful anti-inflammatory actions will help prevent that damage, perhaps not.

It's something of a Pascal's wager, betting on vitamin D instead of the existence of God, risking your child's brain instead of eternal damnation. "If you believe vitamin D helps autism and turn out to be incorrect, you have lost nothing -- but if you don't believe in vitamin D and turn out to be incorrect, your child will suffer irreparable brain damage."

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. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

Michael Pollan Podcast

I just found this great podcast of an April, 2006 National Public Radio (NPR) interview with Omnivore's Dilemma author, Michael Pollan:

Author Michael Pollan: 'The Omnivore's Dilemma'

available at http://www.npr.org/templates/story/story.php?storyId=5342514

The Science Friday segment is a great encapsulation of all the fascinating spins this wonderfully insightful author has on human eating habits and the developing distortions of food choices, much magnified by the food manufacturing industry.

One of my favorite comments from Pollan: "The USDA should be called "The Department of Corn," referring to the ubiquitous dissemination of corn products into livestock and human foods that has increasingly led to the enormous health problems we're all facing in 2007.

Are you addicted to fructose?

Try a little experiment:

Side by side, try a yogurt made with fructose or high fructose corn syrup as one of the first ingredients on the label along with a yogurt made without fructose.

Yoplait and Dannon brands, for instance, fit the bill for fructose. Several brands do not use fructose products. Many of these are the unflavored or unsweetened versions. You may therefore have to add some blueberries, strawberries, or some other fruit for some flavor. ( I doubt that you would add high fructose corn syrup.) Add nuts, seeds, flaxseed, or oat bran to either.

Many people who do this will notice a peculiar effect: The fructose or high fructose corn syrup containing product is, to most, delicious. It also triggers a desire for more. You can't have just one--you've got to have another, or you've got to eat something else.

The non-fructose containing product is more likely to generate satiety, a feeling that you've had enough.

If you experience this effect, the solution is simple: avoid fructose and high fructose corn syrup. I believe that the most worrisome health effect of fructose is this hunger-increasing aspect, difficult to document, perhaps impossible to measure, but a great boon to the food industry who practice an "eat more" philosophy to increase revenues year after year.

Perhaps you will also see weight drop (since you will be more satisfied), see triglycerides drop (since fructose raises triglycerides), and maybe obtain all the downstream benefits of reduced triglycerides (higher HDL, less small LDL, less VLDL, more rapid clearance of post-prandial lipoproteins).

Most people who follow this idea gain better control over appetite, lose weight, and do better in health, including in their Track Your Plaque program.

Chicken Little

Clinical studies can be designed in a number of ways. The ease and cost of these studies differ dramatically, as does the confidence of the findings.

The most confident way to design a clinical study is to tell neither the participants nor the investigator(s) what treatment is being offered, then to administer treatment or placebo. Neither the people doing the research nor the participants know what they are receiving. Of course, there needs to be some way to find out what was given at the end of the study in order to analyze the outcome.

This is called a “double-blind, placebo-controlled” clinical study. While not perfect since it tends to examine a treatment phenomenon in isolation (e.g., the effects of a single drug in a select group of people), it is the best sort of study design that is most likely to yield confident results, both negative and positive. This sort of design is followed, for instance, for most prescription drugs.

There are pitfalls in such studies, of course, and some have made headlines lately. For instance, beyond tending to examine single conditions in a select group of participants, a double-blind, placebo-controlled study can also fail to uncover rare effects. If a study contains 5000 participants, for instance, but a rare complication develops in 1 person out of 20,000, then it’s unlikely such an ill-effect will be observed until larger numbers of people are exposed to the agent.

Another pitfall (though not so much of study design, but of human greed) is that study outcomes that are not favorable can be suppressed by simply failing to publish the results. This has undoubtedly happened numerous times over the years. For this reason, a registry has been created for all human clinical trials as a means to enforce publication of outcomes, both favorable and unfavorable.

Despite its weaknesses, the double-blind, placebo-controlled study design remains the most confident way to show whether or not some treatment does indeed yield some effect. It is less prone to bias from either the participant or the investigator. Human nature being what it is, we tend to influence results just to suit our particular agenda or interests. An investigator who knows what you are given, drug or placebo, but owns lots of stock in the company, or is hoping for special favors from the pharmaceutical company sponsor, for instance, is likely to perceive events in a light favorable to the outcome of the study.

Now, most studies are not double-blind, placebo-controlled studies. These are notoriously difficult studies to engineer; raise lots of ethical questions (can you not treat a person with an aggressive cancer, for instance, and administer a placebo?); often require substantial numbers of participants (thousands), many of whom may insist on payment for devoting their time, bodies, and perhaps even encountering some risk; and are tremendously expensive, costing many tens of millions of dollars.

For this reason, many other study designs are often followed. They are cheaper, quicker, may not even require the active knowledge or participation of the group being studied. That’s not to say that the participants are being tricked. It may simply be something like trying to determine if there are more heart attacks in people who live in cities compared to rural areas by comparing death rates from heart attack from public records and population demographic data. Or, a nutritional study could be performed by asking people how many eggs they eat each week and then contacting them every month for 5 years to see if they’ve had a heart attack or other heart event. No treatment is introduced, no danger is added to a person’s established habits. Many epidemiologic studies are performed this way.

The problem is that these other sorts of study designs, because they generate less confident results, are not generally regarded as proof of anything. They can only suggest the possibility of an association, an hypothesis. For real proof to occur, a double-blind, placebo-controlled may need to follow. Alternatively, if an association suggested by a study of lesser design might, by reasons of a very powerful effect, be sufficient. But this is rare. Thalidomide and catastrophic birth defects are an example of an association between a drug and fetal limb malformation that was so clear-cut that no further investigation was required to establish a causative association. Of course, no one in their right mind would even suggest a blinded study.

Where am I going with this tedious rambling? Lately, the media has been making a big to-do about several studies, none of which are double-blind, placebo-controlled, but were cross-sectional sorts of observations, the sorts of studies which can only suggest an effect. This happened with Dr. Steve Nissen’s study of Avandia (rosiglitazone) for pre-diabetes and risk for heart attack and the recent study suggesting that cancer incidence is increased when LDL cholesterol is low. Both were observations that suggested such associations.

Now, those of you following the Heart Scan Blog or the www.cureality.com website know that we do not defend drug companies nor their drugs. In fact, we’ve openly and repeatedly criticized the drug industry for many of its practices. Drugs are, in my opinion, miserably overused and abused.

But, as always, I am in the pursuit of truth. Neither of these studies, in my view, justified the sort of media attention they received. They are hypothesis-generating efforts—that’s it. You might argue that the questions raised are so crucial that any incremental risk of a drug is simply not worth it.

Despite the over-reaction to these studies, good will come of the fuss. I do believe that heightened scrutiny of the drug industry will result. Many people will seek to avoid prescription drugs and opt for healthy changes in lifestyle, thus reducing exposure to costs and side-effects.

But beware of the media, acting as our Chicken Little, reporting on studies that prove nothing but only raise questions.

200 point drop in heart scan score

Some of the math-savvy will have noticed that we often report drops in CT heart scan scores on a percentage basis. Unfortunately, it this were a competition (which, of course, it is not), this would be unfair.

A score of 50, for instance, that drops "only" 25 points would represent a 50% drop in score.

But someone with a score of 1050 who drops his or her score the same quantity, or 25, will have dropped their score less than 5%.

In other words, the magnitude of your starting score determines how large a percentage drop you achieve, even when the absolute, or real, quantity of plaque reversal is the same as someone who begins with a lower score.

I qualify this discussion in this vein because of Grady's story. Grady, a soon-to-retire attorney, started with a heart scan score of 1151. On the Track Your Plaque program, he saw his score drop nearly 200 points--200 points!

But, if we gauged Grady's success just on a percentage basis, he dropped his score only a measly 17% or so. (Imagine the headlines if this program were sponsored by a drug manufacturer. The Track Your Plaque program proudly has nothing to do with the drug industry.)

Of course, the Track Your Plaque program is not a competition. It is an effort to help everyone possible, the more the better. Even if Grady failed to set a new Track Your Plaque record gauged on a percentage basis, he will have achieved an extraordinary advantage in health: the virtual elimination of the dangers of heart disease.

With this drop in score, Grady's risk for heart attack plummets from a spine-chilling 25% per year to nearly zero. (I know of NO other program that can claim such a track record.)

Grady's full story will be reported in the August, 2007 Track Your Plaque newsletter. To subscribe or to just view when it is posted, go to www.cureality.com website, click on the upper right hand corner What Does My Heart Scan Show? graphic, which then takes you to the page to view the newsletter. Or, Track Your Plaque Members can just go to the Library and click on newsletter archives.

How tough is the Track Your Plaque 60-60-60 target?

One of the basic requirements that stack the odds in your favor of stopping or dropping your CT heart scan score is to achieve basic lipid targets of 60-60-60.

In other words, we generally see best results when LDL is reduced to 60 mg/dl, HDL raised to 60 mg/dl, triglycerides reduced to 60 mg/dl. Now, these are not absolute requirements. Someone can have a spectacular drop in heart scan score even with an HDL of 56, LDL of 71. But the "Rule of 60" provides a useful target that is easy to remember, packs real power, and is clearly beyond that achieved with conventional approaches.

People often ask, "Just how tough is it to get to these targets?"

It's really not that tough. Interestingly, whenever I tell my cardiologist or primary care colleagues that I advocate these 60-60-60 targets, they declare that it's tough, perhaps impossible, except for the most highly motivated.

I agree that it requires motivation. A cigarette-smoking, TV-addicted, 70-lb overweight, chip- and pretzel-eating couch potato is not going to achieve them.

On the other hand, you don't have to be a marathon running vegetarian to do it, either.

Most people, in fact, engaged in the Track Your Plaque program achieve the 60-60-60 targets---or exceed them. It's not uncommon, for instance, for HDL to skyrocket to 80 or 90 mg/dl with many of our strategies. (Of course, if your starting HDL is 20 or 25 mg/dl, 80 or 90 is not possible with current technology.)

But it certainly does require more than the "Take Lipitor and stick to your low-fat diet" approach that is the mantra repeated in the vast majority of medical offices across the U.S. For instance, reducing LDL to 60 mg/dl when starting at 170 mg/dl will require addition of oat bran and other soluble or viscous fibers; raw almonds and walnuts; perhaps the use of Benecol butter substitute; reduction or elimination of wheat products if small LDL comprises a substantial proportion of LDL particles. Reducing triglycerides requires the generous use of omega-3 fatty acids from fish oil. Attention to vitamin D must be a part of the effort.

So, yes, it is not as simple as the conventional approach. But the results are far superior in reducing or eliminating heart attack and in dropping your heart scan score.

But it can be done. We do it every day.

Vitamin D2 belongs in the garbage

It happened yet again.

Mel came to the office. CT heart scan score: 799--quite high, enough to pose a real threat very soon. Thus, no time to lose in instituting an effective prevention program.

We do the usual--identify the six causes of coronary plaque; begin fish oil, show him how to correct his plaque causes. You've heard it before.

Vitamin D blood level in March: 17 ng/ml--severe deficiency.

Vitamin D replacement needs to be a part of his coronary plaque control program. So I suggested 6000 units per day of an oil-based preparation of vitamin D3 (cholecalciferol). Conveniently, there is a Vitamin Shoppe outlet across the street from my office. I just point and tell people to go across the street.

Mel did just that. However, he also informed his primary care physician about his vitamin D deficiency. His primary physician promptly told him he needed to take a prescription form of vitamin D and not to bother with just a supplement.

So Mel stopped his vitamin D capsules and started taking vitamin D prescription "medication." Mel figured, naturally, that if it requires a prescription, it must be better. Unfortunately, Mel and his doctor failed to pass the change in strategy onto us.

So, four months later, Mel got repeat vitamin D blood level: 19 ng/ml.

I've seen this too many times. The prescription form of vitamin D is nonsense. There's hardly any effect on blood levels of vitamin D3 at all. The body's conversion of this non-human form of D is extremely inefficient and therefore virtually useless. While it raises the blood level of vitamin D2 (ergocalciferol) and thereby total D (D3 + D2), there is negligible effect on the real human and active form, D3.

How and why this preparation got through the FDA process to obtain approval as a drug is beyond me, though I am not a defender of FDA practices and politics.

This notion that "if it's a prescription, it must be better" is a fiction perpetuated by the drug industry. The same principle gets tossed around with fish oil, hormones like estrogens and testosterone, and others. Often, the principal difference between prescription and non-prescription is patent protection. Patent protection provides profit protection. Selling a product without patent protection can be risky business. It's certainly less profitable.

As always, getting at the truth is sometimes the most difficult job of all. Prescription vitamin D belongs in the garbage. Vitamin D capsules (gelcaps) do the job and do it well, over and over, with reliable, consistent and substantial rises in blood levels of 25-OH-vitamin D3. I take 6000 units per day (3 2000 unit capsules) that cost me $5.99 for a bottle of 120 capsules, or about $4.50 a month.

And nobody--nobody--pays me to say this. I say it because I believe it's true.

Angioplasty vs. Track Your Plaque

What does angioplasty have over the Track Your Plaque program?

Well, first of all, the Track Your Plaque program has a lot to boast about. What other approach can claim to have reduced heart disease 30, 40, 51, and now 63%? That's as close to a cure that's ever--EVER--been achieved. Statin drug manufacturers can talk about an occasional 1, 2, or 5% reversal. We're talking 10 times more.

The Track Your Plaque program also uses as little prescription medication as necessary. Fish oil, vitamin D, coenzyme Q10, niacin--some of the frequent tools used for plaque reversal in our program. Yes, we do use prescription medications, but only when there is truly a benefit and nutritional strategies have failed to achieve the goals we're seeking. We do not endorse shotgun prescription approaches conceived of by some marketing department at a pharmaceutical company.

So what possible advantage can coronary angioplasty have? Why don't more people embrace a program like Track Your Plaque that has already proven itself enormously effective?

Because angioplasty is easy. There's little worrying ahead of time. Just wait for the symptoms or other problem to appear, go to the hospital and get your procedure. You can live the free and easy life beforehand--no exercise, no diet efforts, no nutritional supplements. Just be sure to go to the hospital when suspicious symptoms strike. (Of course, you gamble that you survive the appearance of symptoms, a process 30-50% of people fail to survive.)

That means you can eat all you want, drink all you want, save the money you otherwise might have thrown away on supplements, pocket the monthly costs of an exercise club membership, etc. Go to the hospital when you experience the sensation of an anvil on your chest or of suffocation, let the emergency room do their thing, meet your cardiologist, go to the catheterization laboratory, get two or three stents, go home the next day!

Why bother with a prevention program, especially one that requires involvement, learning, and effort like Track Your Plaque?

Because it's your way to stack the odds enormously in your favor of 1) surviving the appearance of symptoms, 2) avoiding the prospect of heart procedures, which are not as clean and easy as they often seem, 3) have a longer lasting durability than a stent which could buy you a couple of years before your next procedure or heart catastrophe, and 4) it's the right thing to do for the sake of the huge societal cost of heart disease.

Many of you have the equivalent of a cure for heart disease at your fingertips. Unless you have a soft spot in your heart for hospitals, cardiologists, or the pharmaceutical or medical device industry, there isn't a choice.

Plaque is like money

In case anyone missed this in the June, 2007 Track Your Plaque Newsletter, I'm again posting how we calculate the annual rate of score increase, should it occur.

For instance, say your score in January, 2005, is 100. In November, 2006, you undergo another scan and the score is 140. Obviously, your score has increased an undesirable 40%. But what is the annual rate of score increase, the amount of increase per year?

In this example, the annual rate of score increase is 19%--not anywhere near as bad as the 40% that can scare the heck out of you.

Obviously, the best rate of heart scan score increase is a negative number, i.e., a drop in score from, say 100, to 60. You might even eliminate the need for this calculation altogether if you drop your score.

Nonetheless, whenever there is a score increase over an uneven period of time, a fraction of year(s), this is the method we use to annualize the calculation. The equation we use is a modified form of the annual compound interest equation using continuous compounding, since that’s how coronary atherosclerotic plaque grows--just like money. The difference is, of course, is that while you might want more money, you certainly don't want more plaque.

You will need a calculator for this calculation, one with an exponential “y to the power x” function. For ease, calculate "1/t first, then use it as the “x” exponent on your yx function and "(score 2 / score 1)" as the "y".


Annual rate of plaque growth (APG) = ( score 2 / score 1 ) 1/t - 1

Multiply the result by 100 to yield a percent.


“Score 1” is your 1st heart scan score, “score 2” is your 2nd (or any subsequent heart scan score); “t” is the amount of time between the two scans expressed in years in decimal form. Time between scans should be expressed in years or fractions of years. To obtain the time interval in fractions of years, simply divide the number of months between scans by 12 (e.g., 18 months / 12 = 1.5 years ; 22 months / 12 = 1.83 years).

It’s not as tricky as it looks. For example, if your first heart scan score is 300 and your next scan 16 months later (or 16/12 = 1.33 years) is 372, then:

Annual rate of plaque growth (APG) = ( 372 / 300 ) 1/1.33 - 1 = 0.175

Multiply 0.175 x 100 = 17.5% annual rate of plaque growth


Some scan centers will do the calculation for you as part of a repeat scan. However, the equation can be used if you're left on your own, or if you go to a different scan center. If this is too much effort, perhaps it's just another reason to add to the list of reasons to drop your heart scan score!

Triglycerides: What is normal?

In The Track Your Plaque program, we advocate decreasing triglycerides to 60 mg/dl or less.

That's the level of triglycerides that minimize the presence of triglyceride-containing undesirable lipoproteins causing plaque, such as small LDL, VLDL, and the after-eating persistence of IDL (intermediate-density lipoprotein, a bad player). (The enzyme, cholesteryl-ester transfer protein, or CETP, is responsible for exchanging one triglyceride molecule for one cholesterol molecule between HDL and other lipoprotein particles. Thus, an excess of triglyceride availability permits CETP to operate unrestrained, creating more undesirable lipoproteins. This was the basis for Pfizer's now defunct CETP inhibitor, torcetrapib.)

Of course, this triglyceride target is far below that of the conventional guidelines. The Adult Treatment Panel-III of the National Cholesterol Education Panel suggests a triglyceride level of 150 mg/dl is okay.

In my view, a level of 150 mg/dl is highly abnormal, permitting the persistence of multiple lipoprotein particles and virtually guarantees plaque growth. In short, triglycerides of 150 are awful.

Curious thing: Successful participants in our program, i.e., people who achieve desirable weight, reduce processed carbohydrate junk foods and saturated fat sources, and aim for the 60-60-60 targets for conventional lipids, commonly end up with triglyceride levels of 25-50 mg/dl.

We have seen many people drop their heart scan scores just by achieving a triglyceride level of 60 mg/dl or less. So achieving a lower level below 60 is not necessarily a requirement for coronary plaque regression.

But it makes me wonder if a triglycere level of 30s or 40s is the level for perfect health. These are levels ordinarily regarded as impossibly low. When colleagues see the numbers we readily and routinely achieve, they declare that the numbers are spurious, temporary, or just flukes. "No way you can do that all the time!"

This level also seems to, in virtually all cases, eliminate the triglyceride-containing undesirable lipoproteins small LDL, IDL, etc., and allow full conversion of HDL into the healthy, large fraction.

Should we move the Track Your Plaque triglyceride target to below 45 mg/dl or even lower? I don't think so, but it makes me wonder.

NY Times Jane Brody misses the mark



NY Times' health columnist, Jane Brody, recently wrote a bit of fluff for her paper:

"CT Scans of the Heart Come With Trade-Offs


In her report, she says:

Coronary CT scans are being sold directly to the public, and they have found a market in health-conscious people who can afford them. But screening exams can have downsides. They can cause needless worry, and they sometimes reveal other potential conditions that require invasive procedures like biopsies to diagnose.

I soon learned that among the strongest proponents of CT scans of coronary arteries were physicians with financial ties to drug companies that make statins and others connected to imaging centers that would profit directly from widespread CT screenings.



She then goes on to discuss how the Framingham scoring calculation can tell you whether or not you are at low-, intermediate-, or high-risk for heart disease. She therefore concludes that heart scans are therefore irrelevant for the majority of people. She then proceeds to take a statin agent.

This sort of nonsense continues to get published, despite the clear lack of real "digging" for the truth. She clearly fell for the conventional arguments that continue to mis-guide the majority of people, myths like:

--the Framingham scoring system is reliable--Reliable it is NOT; it is susceptible to substantial "misclassification" bias, meaning people who appear low risk can actually be high risk, and people at high risk can actually be low risk. Among the latest studies that question the scoring system is Family history of premature coronary heart disease and coronary artery calcification: Multi-Ethnic Study of Atherosclerosis (MESA). This study pointed out how the Framingham scoring system, which leaves out family history, can cause people classified as low risk to actually have substantial heart scan scores. This is crucial. A heart scan gets beyond the uncertainties and shows with >95% certainty whether or not hidden coronary atherosclerotic plaque is present.

--"Coronary risk" is a dynammic phenomenon, subject to changes in a person's life. What if, for instance, a person smoked for 20 years, quit 10 years ago, lost 30 lbs, dropped their blood pressure as a result of the weight loss, then relied on the Framingham Risk Calculator to determine risk. They would likely be classified as low- risk, since risk factors now appear favorable. This person could easily have a heart scan score of 500, or 700, or 1000, levels that carry a cardiovascular event risk of 5-25% per year, hardly low-risk, because much of their risk accumulated earlier in life and is no longer revealed by an assessment of risk factors.

--There are sources of risk that have nothing to do with Framingham, such as lipoprotein(a), which is often revealed by family history; the presence of small LDL, which co-varies with HDL and triglycerides, but can behave independently also; and, my favorite, deficiency of vitamin D. This would explain part of the 60-70% of people who are typically mis-classified by Framingham.


Where did Ms. Brody get the idea that proponents of heart scans had ties to drug companies? I think she's barking up the wrong tree on that one. Of course, she ends up on a statin drug. For my part, I am a critic of statin drugs. Yes, they play a role, but they are miserably misused and abused by practicing physicians, based on the endless onslaught of drug company-sponsored trials that have served to distort their usefulness.

If I were Ms. Brody, I would be quaking in my shoes, not knowing what my true risk for heart disease was, relying on the--at best--30% reduction in heart attack risk of Lipitor or other statin drug. Ms. Brody: You are not cured, you're simply wearing a superficial Band-Aid. If you want to know your true risk for heart attack, and you want a precise value that you can track over time, the answer is simple: Reject the conventional notion and get a heart scan.

"There must be a mistake"

Neal is our current male record holder for greatest reduction in heart scan score. (Yes, the ladies have the lead!)

You may remember that this 40-year old man reduced his heart scan score from 339 to 161--a 51% drop. If you haven't yet read his story, go to

http://www.cureality.com/library/fl_07-001nealt51.asp


Neal reminded me of the experience he had when he underwent his second heart scan. Both scans had been performed at the same scanning center. At this center, the radiologists provide the added service of sitting down with people and actually going over the images and results.

After the scan, the radiologist pulled up the result from Neal's first scan for comparison. "There must be a mistake! This score is lower. Scores never drop."

The radiologist was apparently stumped, unable to provide an explanation. However, Neal then proceeded to tell the radiologist that we had warned Neal that this could happen and that he might even be told that it was due to error of some sort. This yielded a puzzled look on the radiologist but no further comment.

Of course it's not a mistake. It's something we achieve on purpose. Curiously, I still get comments that this is impossible, heart scan scores never drop, etc. Of course, those of you following this conversation know this is completely untrue. Heart scan scores DO drop, and sometimes drop enormous amounts, as it did for Neal.

I would have liked the radiologist to have had the lightbulb of understanding go off in his head when he realized that a reduction in heart scan score is a cause for celebration. Unfortunately, this radiologist's reaction is all too common: disbelief, confusion, dismissal.

Heart disease reversal is simply not in the realm of understanding of most doctors, radiologists and cardiologists alike. By conventional thought, if you have it, it just gets worse. "Maybe some high-dose Lipitor might help."

Ironically, when they see it right in front of their eyes, plain as day on the computer screen, they don't understand what has happened. It's Greek to them.

Should this happen to you, don't be surprised. Just bite your tongue, because you know better.

Jimmy Moore Interview: Is saturated fat the villain we thought?

Enter "weight loss" or "low carb" in your web search and you can't help but stumble across the prolific and widely-connected Jimmy Moore.

On his Blog, Livin' la Vida Lo Carb , Jimmy conducts a wide-ranging and informative discussion of the benefits of a low carbohydrate diet, a la Atkins. Though his initial claim to fame was the 180 lbs he lost in his first year of dieting on this approach, Jimmy has extended the conversation and built a considerable community of like-minded individuals, all of whom are participating in this grand "experiment."

Anybody who looks at lipoproteins and associated factors in health will quickly come to the conclusion that processed carbohydrates are the culprits in much of heart disease, diabetes, and heart disease. But I have had a hard time dismissing the ill-effects of saturated fat. After all, we've all been taught--drilled--with the idea that saturated fats cause LDL cholesterol to go higher, cause arterial constriction, growth of atherosclerotic plaque, inflammation, even cancer.

But there does indeed seem to be a growing sentinment that this long-held dogma may not be true. So I went to the ever-entertaining and informative Jimmy Moore, an able spokesman for these concepts.




TYP: It's certainly impossible to argue with the success you had in weight loss and the health you've regained on your program.

I think that the approach we use in diet in the Track Your Plaque program and the nutrition approach you advocate overlap to a great extent. We both emphasize plenty of vegetables, fruits, healthy oils, nuts, etc. The major point of difference seems to lie in saturated fat: We say restrict it, you say don't restrict it. Could you elaborate?





JM: Thank you for inviting me to your blog today, Dr. Davis. I have nothing but deep respect and admiration for the work you are doing to help educate others about how to keep their heart health in tip-top shape. Keep fighting the good fight, my friend.

While we do agree on probably 99% of the basic tenets of what I describe as
"livin' la vida low-carb," the issue of saturated fat to me is one where we
indeed do not. It's not a deal breaker regarding my support for what you do
just as I'm sure you would say the same regarding your backing of what I do. If
we all agreed on everything, then what a boring world this would be!

My thinking on saturated fat has evolved since I started eating this way nearly
four years ago. Like most people, I was terrified to eat ANY fat at all because
of the abject fear that people like Dr. Dean Ornish and other so-called health
"experts" instilled in me about how dangerously unhealthy it is to consume it.
This fat phobia is arguably the single biggest contributor to the ongoing
obesity crisis our world faces today.

With that said, you and I both know fat consumption is a part of a healthy
lifestyle. There are just too many benefits to the body that come from the
consumption of fats and even saturated fats such as coconut oil, butter, lard,
nuts, seeds, and animal fat when it is combined with a restricted carbohydrate
intake.

An intriguing study was presented at a scientific conference in November 2006 by two highly-respected researchers--Dr. Stephen Phinney from the University of California at Davis and Dr. Jeff Volek from the University of Connecticut--who conducted a side-by-side comparison of the amount of saturated fat in the blood of people on a low-carb diet with those following those highly-touted low-fat diets. What they found was the low-carb study participants had "significantly less" saturated fat in their blood than the low-fatties did.

Here are the actual numbers from the study:

- LOW-FAT/HIGH-CARB DIETERS: lowered saturated fat by 24%
- LOW-CARB/HIGH-FAT DIETERS: lowered saturated fat by 57%
- Eating 3X the saturated fat cut the amount in the blood in half

In an interview I conducted at my blog with Dr. Volek last year (here's the
link: http://livinlavidalocarb.blogspot.com/2006/09/volek-high-carb-low-fat-diet-useless-to.html),
he said the conventional wisdom regarding fat, especially saturate fat, is dead
wrong while the significance of carbs is all but ignored by those who claim to
understand the metabolic response mechanism.

Here's what Dr. Volek said in my interview:

"Eating fat does not make you fat, storing fat makes you fat. And carbohydrates play a major role in storing fat. So the level of dietary carbohydrate is really the most important factor to control because it dictates what happens to fat. Carbs are dominant and fat is passive. When carbohydrates are low, fat tends to be burned, and when carbohydrates are high dietary fat tends to be stored. The same holds true for the atherogenic effects of saturated fat. The body handles saturated fat better when carbohydrates are low."

Long-time low-carb practitioner and current President of the American Society of Bariatric Physicians (ASBP) Dr. Mary C. Vernon from Lawrence, Kansas confirms the findings of Dr. Volek and Dr. Phinney in a succinct recap of what their research showed.

Here's what she said:

"Eating fat (whatever kind) does not make you fat. It does not increase blood
stream saturated fat. Eating carbs does make you fat. Eating carbs does put
saturated fat in your blood stream."

To me, as a simple layperson with no medical background, it's all a matter of who you believe. Do we continue to buy into the low-fat propaganda machine and assume that what they are telling us about saturated fat is true? Or do we instead start paying closer attention to the latest research that is coming out about saturated fat that doesn't exactly line up with the edicts of the last three decades? The choice for me is a simple one.

And if you haven't read the brand new Gary Taubes book entitled GOOD CALORIES, BAD CALORIES yet, then it is REQUIRED reading to arm yourself with the research studies about fat. After you read that book, it will be almost impossible for ANYONE to believe fat, including saturated fat, is unhealthy.



TYP: In our program, we advocate a wheat-free approach for many people, because of the addictive potential of wheat products, as well as the flagrant creation of the small LDL pattern that wheat products create, thereby adding to atherosclerotic plaque growth. However, many people express a concern over a lack of fiber in their diets if they eliminate whole wheat bread, pasta, Fiber One, Raisin Bran cereal, etc.

Have you encountered any phenomena of low-fiber on your approach?

JM: What an excellent question and I even wrote a humorous blog post about the importance of fiber intake called "Allow Your Bowel To Shake, Rattle, And Roll" (http://livinlavidalocarb.blogspot.com/2006/06/allow-your-bowel-to-shake-rattle-and.html).

Fiber consumption is another one of those issues that not everyone who advocates
a controlled-carb approach agrees is necessary. I'm on the side that it IS a healthy part of your diet and should be consumed in high enough quantities to keep you regular...something many people think is impossible on a low-carb diet.
Not true! I take a fiber supplement like FiberCon, eat plenty of high-fiber vegetables, drink lots of water, and even consume high-fiber, low-carb products that help me maintain high levels of fiber in my diet (see my favorite ones in this post: http://livinlavidalocarb.blogspot.com/2007/04/there-are-plenty-of-low-carb-fiber.html).

As for consuming the highly-touted "healthy whole grain" cereals that you
mentioned, what a travesty that would be for people trying to manage their
weight and health. While the cereal manufacturers have had a heyday in their
marketing efforts promoting their whole grain content, it's all just a big fat
ruse on the public trying to convince them that these cereals are somehow healthy for their bodies. Sure, they're better than the sugary cereals, but all those grains are metabolized as sugar inside the body, so you might as well be eating Lucky Charms and Fruit Loops!

Many of these "healthy" cereals contain as many carbohydrates in a single bowl
without the milk as I would eat in an entire day. Raisin Bran, for example, which used to be my favorite cereal before my low-carb lifestye, has a whopping 47 grams of carbohydrates. Needless to say, I don't touch that with a ten-foot pole nowadays because I would surely gain weight and get back on the blood sugar rollercoaster ride that I was on prior to beginning the Atkins diet on January 1, 2004. Plus, all those carbs just make you hungrier sooner, so it's better just to eat some delicious eggs cooked in butter, a couple of slices of sausage, and tomato slices to start your day off right. You'll get enough fiber in your body the rest of your day.



TYP: 180 lbs of weight loss in your first year is absolutely astounding.

I take it that you've continued this trend and have lost more weight since your early success. What role did exercise play during your first year and subsequently?
How are your food choices today different from that first year?

JM: Yes, that weight loss was indeed one of the greatest accomplishments I have ever experienced in my life. It was a hard-fought battle that even included a 10-week period where I was stalled with no weight loss. But I knew my chosen diet was the right one for me because I felt better than I ever had on a diet, was never hungry because I ate every 2-3 hours, and could see myself doing this for the rest of my life. So far, so good!

It has been close to four years since I began this journey and I am indeed continuing this pathway to better health. My low weight in 2004 was 230 pounds and I currently weigh 225 pounds. As long as I keep my carbs reduced, I am able to maintain my weight right where it is. I've had minor fluctuations in both directions where I got down to as low as 215 pounds at one point (but didn't feel good at that weight) and as high as 252 pounds (when I was allowing myself one too many high-carb foods here and there).

There's a balance that people need to find for themselves and it's different for
all of us. I am one of the unlucky people who has to keep his carbohydrate
intake below 50g daily or I gain. It's just a fact of life that I've come to
grips with and realize is a necessity in order to manage my weight for the rest
of my life. But I wouldn't have it any other way!

Exercise was indeed a part of my low-carb weight loss success in 2004 as I
forced myself to do cardio every single day as a commitment to this journey. In
hindsight, that was probably not the best thing for me to do since the body has
a rather peculiar way of telling you it needs to wiggle and move spontaneously
on its own rather than forcing the issue. But I consider the exercise I did to
be such an integral part of my success that I dedicated an entire chapter of my
book to the subject.

Today, my daily cardio routine is out the window and I choose instead to engage
in activities outside the gym that let me burn calories and have some fun in the
process. I regularly play volleyball, basketball, and referee flag football at
my church which all give me quite a workout. I'm very physically active and fit
on my 6'3" body and just enjoy burning off all this excess energy that I have
been given since losing nearly have my weight! I do want to get into a little
more organized resistance training routine soon to try to shape and tone some
areas of my body that still show signs of that 410-pound man I used to be
(although the loose, hanging skin in my abdomen and inner thighs isn't going to
get any better with exercise since the elasticity has been ruined from being
stretched out so far). Here is a link to some posts and pictures I have written
about this subject:
http://lowcarblinks.blogspot.com/2007/04/theme-based-low-carb-links-loose-skin.html

As for my food choices today compared to my weight loss year in 2004, they
haven't really changed a whole lot. This was a lifestyle change in every sense
of the phrase and I've learned to implement this way of eating into a permanent
and healthy diet that I can and will gladly live with forever and ever amen. I
probably eat more berries, melons, and nuts today than I did then, but otherwise
it's the identical diet.



TYP: I'm sure that you are as impressed as I am that much of the wisdom in healthy eating doesn't always come from doctors or clinical studies, but from the collective wisdom that emerges from this national experiment (inadvertent, for the most part) in eating. Your Livin' La Vida Low-Carb is, in my view, a perfect example of the sort of wisdom that is helping all of us understand what happened to our health over the last 20 years.

Does the approach you advocate today differ in any substantial way from the diet as originally articulated by Dr. Atkins?

JM: Actually, my personal diet is precisely based on the teaching of the late great Dr. Robert C. Atkins in his classic bestseller DR. ATKINS' NEW DIET REVOLUTION (DANDR) book. But most people are surprised when they learn I do not necessarily advocate the Atkins diet as the nutritional approach for everyone.

Nope, I sure don't!

Instead, my philosophy is simple: Find the diet plan that will work for YOU, read and research everything you can about that chosen plan, follow that plan exactly as prescribed by the author of that book, and then KEEP doing that plan for the rest of your life. If you do that, then there's no reason why you can't succeed just like I did.

Anyone interested in doing the low-carb lifestyle and needs help finding which
plan is right for them, let me HIGHLY encourage you to pick up a copy of Dr. Jonny Bowden's LIVING THE LOW-CARB LIFE (read my review: http://livinlavidalocarb.blogspot.com/2005/05/must-have-book-for-everybody-doing-low.html).
It's the perfect overview of low-carb living with a comparison and recap of the
major plans.

THANK YOU again for allowing me to share my story with you and your readers, Dr.
Davis!

TYP: And thanks to you, Jimmy!



For more on Jimmy Moore's lively and informative discussion of these issues, go to

Livin' la Vida Lo Carb

Also, watch "Livin' La Vida Low-Carb on YouTube"

Join the conversation at Jimmy's new low-carb forum called "Livin' La Vida
Low-Carb Discussion
" at LowCarbDiscussion.com


Also, Jimmy's 2005 book on his weight loss experience:
"Livin' La Vida Low-Carb: My Journey From Flabby Fat To
Sensationally Skinny In One Year"

Mammogram of the heart

Some people have called CT heart scans the "mammogram of the heart." The analogy contains a lot of wisdom.

First of all, both--mammograms and CT heart scans--are screening tests, one for cancer, of course, the other for coronary atherosclerotic plaque. Both are performed in specific age groups, mammograms in women 40 years and over (generally), heart scans in women 50 years and over (generally).


















Mammograms: Left, normal; right, a small mass. (Courtesy Nat'l Institutes of Health and Wikipedia.)



Both are also meant to be repeated periodically when normal as a surveillance process.

Both use low quantities of radiation of about 0.3-0.4 mSv (the most real-life measure of total body exposure), a modest quantity of radiation.

Both are good for their purposes, though not perfect. Can a mammogram performed properly miss a small cancerous mass? Sure it can, but it's still unusual. Can a CT heart scan miss the non-calcified plaque prone to rupture? Sure it can, but this is also unlikely (<5% probability).

Given the exorbitant costs of medical tests, both are quite inexpensive. On the flip side, they are both also quite unprofitable for the centers providing the tests. Unfortunately, this means that mammography centers and heart scan centers come and go because of the difficulties of the profit-side of these services.

Both tests initially struggled to gain acceptance among the medical community. In 1960, for instance, mammograms were performed on standard x-ray devices, the same as that used to perform chest x-rays--low precision, high radiation back then. In 1969, dedicated mammography devices made the scene. However, it took over 10 years for even these new dedicated devices to become widely used. Use of mammograms has gradually increased over the ensuing 20 years. In other words, 47 years have passed since the introduction of mammography.

CT heart scans, of course, have had a shorter history of approximately 20 years, since engineer, Dr. Douglas Boyd, first invented the "ultra-fast" EBT devices, the first devices with sufficient scanning speed to scan the heart and coronary arteries.

One interesting difference between the two: In a woman between the age of 50 and 60, the likelihood of detecting cancer is 1 in 237. The likelihood of detecting coronary atherosclerotic plaque? About 1 in 4. Coronary disease eventually kills 1 in 3 females, hugely overshadowing breast cancer in frequency.


Progress on both fronts, one in cancer detection, the other in atherosclerotic coronary plaque detection. But still lots more progress to go.

Dr. Susie Rockway on conjugated linoleic acid (CLA)

I’m fascinated by the perspectives that nutritionists (free-thinking ones, at least), food scientists, and biochemists bring on nutrition and nutritional supplements.

A few months ago, I met a fascinating nutritionist/biochemist named Susie Rockway, PhD. Dr. Rockway brings a world of experience in the world of nutritional supplements, clinical trials with supplements, and their development. She has special expertise in conjugated linoleic acid (CLA), having been among the scientists who initially developed CLA as a supplement. We are also exploring CLA as a possible addition to the Track Your Plaque program and wanted to get Dr. Rockway’s perspectives.

So I asked Dr. Rockway if she’d answer a few questions for us.






TYP: Dr. Rockway, we understand that you are particularly excited about the prospects of CLA for FAT loss and perhaps for regression of atherosclerosis. Can you tell us about the origins of your interest in CLA and why you're so enthusiastic?

Dr. Rockway: I have been fascinated with this unique fatty acid since the early 1990’s when CLA was first being discussed as nature’s most potent anti-carcinogen. I was then working in the granting/funding section of the National Dairy Council and saw this molecule as truly one of the future functional fats that would likely benefit people (next to omega-3’s!)

I think the benefits of CLA have just begun to be investigated—animal studies are extraordinary for showing fat reduction, lean mass (muscle) increases, immune enhancements, blood glucose normalization, anti-inflammatory properties and plaque reduction!

Human data to date is very encouraging for fat reduction. As a nutritionist seeing the massive increase in abdominal fat (stomach fat) in the world population and the direct relationship to cardiovascular disease, I see CLA as a great supplement to take to help this. Of course eating lots of vegetables, fruit, lean protein and whole grain products is also a must for maximizing good health.

I am studying the impact of CLA in reducing muscle loss in aging women—a condition known as sarcopenia. As we lose muscle with age, we lose strength, falls increase, we become frailer, and eventually many of us lose our independence. Along with the muscle atrophy, most people gain fat—never a good thing! So, if CLA can reduce fat and increase muscle, our bodies are more likely to withstand the hurdles that life throws at us much more efficiently.

So, how can you not be excited about this very bioactive molecule?




TYP: What are your specific areas of interest in nutrition and health?

Dr. Rockway: I strive to understand the role of bioactive molecules that can be taken to improve the aging process and enhance health.

As a trained nutritional biochemist, we tend to look at cell metabolism in a very ideal sense: what we learned in our biochemistry texts years ago where all substrates, proteins, enzymes, etc. are made exactly when we need them, where all cells behave as they should.

Unfortunately, little research has been devoted to understanding the changes in metabolism as we age. Do we still produce everything as efficiently as when we were 20? I suspect not. So, I think we need a little help, and supplements are a key to getting there.

Two nutrients that I think are emerging as “super nutrients” are the fatty acids found in fish oil (EPA and DHA) and vitamin D. Where we know these two nutrients are essential for life, we are seeing that they play a huge role in the QUALITY of life. Mood, depression, PMS, wound healing, bone growth, atherosclerosis, and arthritis are clinical areas where we see a direct benefit with doses of omega-3 and Vitamin D that are probably much greater than the RDA. Our current requirements for nutrients are really based on fixing deficiencies and not maximizing health, and maximizing health is where I’m at.

Thus, I am very interested molecules like CLA as mentioned above, and other bioactive ingredients such as plant derived ingredients (phytochemicals) called flavonoids that may well help explain why people who have diets high in fruits and vegetables are less likely to have certain cancers and heart disease. Reducing oxidative stress through foods that provide these active molecules (think colored fruits and veggies) is a new and exciting area of research.



TYP:The big "diet experiment" in America has clearly steered people in the wrong direction, usually by 50 or more pounds. As a scientist in nutrition, what are your thoughts?

Dr. Rockway: The American Heart Association was keen 20 years ago to promote the low-fat diet for all Americans as the key way to reduce cholesterol levels and decrease chance of heart disease, the number one killer of men and women. However, I must admit the nutritional community bought into this one, too. Unfortunately, the general public took this message to reduce percent fat in their diet (and they did a bit), but increased overall calories instead—and a large portion of the increased calories was from simple carbohydrates. I’m convinced that this in itself has been part of the huge rise in obesity…we simply eat more food and it’s not the healthy kind of food either.

When you increase sugar intake beyond what you burn off, you will store some of it as glycogen in the liver and muscles, but you will convert most of the excess into fat—and that we can store very efficiently! The fat that is made in the liver is sent to the blood as VLDL’s which are the precursor to the class of lipids called low density lipoproteins (LDL) that are the “lethal” type of cholesterol circulating in our blood.

So, Americans now have to listen to a new message that they need to eat more fruits and vegetables in hopes they will cut down on fast foods—tending to be high in fat (saturated particularly), low in fiber and low in nutrients and other high calorie dense foods. We nutritionists have our work cut out for us, that’s for sure.



TYP: We are especially excited that nutritionists are assuming a leading role in shining light on the confusion in diet and nutrition that has characterized the last 40 years. Do you have a sense for the emerging important issues for the next 10 years?

Dr. Rockway: Certainly, the scientists in the nutritional field are well aware of the problems facing this nation—it’s in fixing them that we fall short!

We aren’t very well coordinated to get a single message out, nor do we all agree on what that message should be. I feel that people need to eat healthy MOST OF THE TIME, exercise all of the time, and take supplements that have clear evidence of benefit. Lots of my colleagues would not concur with supplement use. Our bodies were designed to move a lot and eat a lot…we just do the latter now and are paying the price!

One emerging and very exciting area that we have to teach Americans is that all fat is not bad. The different types of fat—omega-6 vs. omega-3, are where we need to focus our education.

Decreasing the corn oil we pour on everything needs to go out the window! Consume olive oil and eat fish or take fish oil supplements—we simply have tons and tons of research showing the benefits of reducing the ratio of omega-6 to omega-3. Did you know that cattle that are grass fed actually have less omega-6 in their tissues and more CLA? But most cattle are fed corn-based diets, so we have perturbed their natural selection of food and their fat composition.

See, it all comes back to CLA!


TYP: Thanks, Susie!




Susie Rockway, Ph.D., C.N.S.

Dr. Susie Rockway is an experienced scientist with accomplishments in both the academic and food and supplement industry business directing science/technology research. Her background includes faculty appointments at the graduate level in teaching and research at Rush University Medical Center and industrial experience managing basic and applied research studies.

Dr. Rockway received her Ph.D. in Nutritional Sciences, Biochemistry from the University of Arizona. Dr. Rockway has authored several publications in journals such as the Physiological Genomics, Journal of Nutrition, the Journal of Food Science, International Archives of Occupational and Environmental Health and has published chapters on nutrition on inflammatory bowel diseases. She is a member of the American Society for Nutrition, American Oil Chemists Society, the Institute of Food Technology, American College of Nutrition and is a Certified Nutrition Specialist.

We're also proud to add Dr. Rockway to our panel of Track Your Plaque Experts.

Which is better?

If you have the common pattern of high LDL particle number (NMR) with small LDL--a pattern highly related to coronary plaque--which is better:




Lipitor or a combination of fish oil, vitamin D, and elimination of wheat?


Lipitor quite effectively reduces LDL particle number, usually on the order of 40% or so. Effect on LDL particle size: None. Side-effects: plenty, including muscle aches (inevitable in my experience, not the ridiculous 2% they claim) and occasionally mental effects such as impaired short-term memory.

Lipitor does seem to exert a modest effect on reduction of C-reactive protein, around 30%. It also reduces cardiovascular events by 30%.



A combination of fish oil, vitamin D, and elimination of wheat:

Reduces LDL particle number commonly by a similar 40% (though variable, depending on body weight). There is substantial improvement in LDL particle size, a large drop in C-reactive protein, often >50%, a 30% or more reduction in cardiovacular events.



On this combination, however, you also:

--Lose weight, often substantially.

--Improve bone health, esp. osteoporosis and arthritis.

--Reduce cancer risk from the vit D supplementation.

--Reduce risk of stroke.

--Reduce postprandial (after-eating) abnormalities like intermediate-density lipoprotein.

--Reduce winter blues.

--Experience more energy.

--Obtain increased clarity of thought (from elimination of wheat).

--Reduce blood pressure.


Oh, and there's no muscle aches.

Heart health for stupid people

I'm kidding.

What I'm referring to is the incredibly lame information I come across that passes as "heart health" on the internet, magazines, and other media. Just to keep abreast of what is being said, I subscribe to multiple newsletters and magazines and I witness the sorts of advice offered to the reading public.

A recent long-winded article on a popular website listed the "exciting" strategies available for a healthy heart:

Eat healthy--by eating a "balanced" diet low in saturated fat

Don't smoke

Exercise

Don't ignore chest pain symptoms or breathlessness

Know your numbers! meaning your cholesterol numbers. "If your cholesterol is high, you may need to speak to your doctor about medication to reduce it."


Surely they must all believe we're stupid. Otherwise, why would they repeat the same obvious information over and over again? Quit smoking? Gee, you think so?

How about some real heart healthy advice:

Get a heart scan--since we have to accept that cholesterol values are a miserable failure in detecting hidden heart disease. So is waiting for symptoms to appear.

If you have any measure of coronary plaque, ask your doctor to assess lipoproteins, not lipids (cholesterol).

Take fish oil for omega-3 fatty acids--At a dose of 1000 mg or more of EPA + DHA, heart attack risk is reduced by at least 28%.

Eliminate wheat and other processed carbohydrates --Small LDL has emerged as the number one cause of coronary plaque, not high cholesterol from saturated fat.

Get vitamin D assessed--The effects are huge--HUGE. There's already a study in a kidney disease population that showed a substantial reduction in mortality with vitamin D supplementation. More data are coming, including our own.


That's a start--truly effective, practical heart healthy strategies that go way beyond the conventional bland advice.


Copyright 2007 William Davis, MD

Money, money, money, money

I've been asked the question numerous times:

Why aren't heart scans more popular?

First, let me qualify by saying that heart scan have indeed grown in popularity over the past decade. I think the real question is:

Given the enormous usefulness of CT heart scanning to detect hidden, asymptomatic coronary atherosclerotic plaque, why haven't they more readily been incorporated into conventional medical practice?

That's easy: There's no money in it.


Say, for instance, your doctor orders a heart scan and somehow receives a $1000 for the test. Scan centers would be scanning 100 people a day, falling over themselves to do scans.

This would be similar to a heart catheterization. Order a catheterization, do 30 minutes of work, and get $1000. Or, order a nuclear stress test. Depending on how its done and where, $1800-4000 is paid by the insurer.

Order a CT heart scan and how much is paid to the doctor? Usually nothing. At most, a nominal fee might be paid if the doctor reads the scan.

With heart scans, there simply is no big payoff.

We learned the implications of this situation 10 years ago when I was trying to help my friend, Steve Burlingame, the owner of Milwaukee Heart Scan. (I am NOT and NEVER WAS an owner.) Steve was trying to let everybody know about this great new $2 million dollar heart scan device in the Milwaukee area.

The first few years were tough for Steve: Carrying the substantial expense of this device while doctors essentially gave the technology the cold shoulder. It simply did not fit into the financial equation. Why change the way things were, particularly when there was virtually no financial reason to do so? To counter this, Milwaukee Heart Scan followed the model many other scan centers have followed and marketed directly to the public.

I see this as yet another example of why people need to take control of health care away from doctors and hospitals, the current controllers of the system who are providing a disservice to the public they are supposed to be serving. These institutions, for the most part, serve their self-serving financial interests, not your health interests. It's the same equation that drives food manufacturers to make more and more processed carbohydrate foods that they sell for substantial markups, not green peppers and cucumbers that make little money.

I regard heart scans as among the greatest self-empowering tools in health ever conceived. It was that way in 1997; it remains that way in 2007.

The many faces of LDL

Ginnie came in for an opinion about her heart scan score of 393. At age 57, this put her in the 99th percentile, a high score.

As usual, we did a lipoprotein analysis by NMR (Liposcience). Some numbers:

LDL cholesterol: 96 mg/dl
This value puts Ginnie's LDL in the most favorable 25% in the country.


LDL particle number: 2140 nmol/l
This value is in the worst 25% of the country and is the equivalent of an LDL cholesterol of 214 mg/dl (take off the zero).

In addition, over 90% of Ginnie's LDL particles fell into the small class.

Had we run some other values, how would they have turned out? These are my estimates (since we didn't actually run them in Ginnie), but having run side-by-side numbers in past, reasonable estimates would have put:

Apoprotein B somewhere in the 120 to 140 mg/dl range

Direct LDL 100-130 mg/dl range.


In other words, conventional calculated LDL is the least reliable of all the ways of examining low-density lipoprotein.

It can also go the other way: High calculated LDL, low LDL particle number or ApoB or direct LDL. And, indeed, these other measures have proven superior in their ability to predict "events" like heart attack over conventional calculated LDL.

Unfortunately, relying on conventional LDL is like a broken speedometer on your car. You really can't gauge accurately how fast you're going; sometimes you could be way off. While insurance companies and many physicians still continue to balk at this argument, the data have already been generated that show that lipoprotein analysis (my bias is NMR) is not just superior, but enormously superior for accuracy and event prediction.

In addition, lipoprotein analysis has proven a crucial tool that accounts for our extraordinary success in reducing and controlling CT heart scan scores in the Track Your Plaque program. I doubt that we could have achieved the same level of success using conventional lipids.

I'm also aware of the logistical difficulties obtaining lipoprotein testing in a world enthusiastically supportive of hospital procedures and smugly ignorant of superior prevention tools like lipoprotein analysis. I've learned just how difficult it can be in our Track Your Plaque Member Forum; I've also learned about some strategies for obtaining these tests that I hadn't been aware of, thanks to the resourcefulness of our Members.

We will be working on some solutions in the coming months.


Copyright 2007 William Davis, MD

What does "Success" mean in the Track Your Plaque program?

Say you begin with a CT heart scan score of 400.

You correct your lipoprotein pattterns, take fish oil, correct 25-OH-vitamin D3 to 50 ng/ml, correct your other hidden patterns, follow a diet suited to your patterns.

One year later, you get another heart scan. What score would constitute "success"?

With all of our recent talk about record-setting reductions in heart scan scores, is it really necessary to drop your score that much to succeed?

For instance, is our latest record-setting 63% drop in score better than "only" a 10% drop in score? Both represent reversal of coronary plaque. Both signify huge reductions in risk for plaque rupture, or heart attack.

You can read about how we view the various forms of success in the program by reading our latest Track Your Plaque Special Report, Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.

We are making the Report available to everyone. Just go to the www.cureality.com homepage.