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.

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

Go the distance!

How long should it take to stop or reverse coronary plaque growth? How long will it require to stop your heart scan score of, say, 350, from increasing at the expected rate of 30% per year, slow it down (we say "decelerate") to less than 30%, or stop it altogether? Or, actually reduce your score?

It can vary widely. Several simple patterns do seem to emerge, however. Our experience is that lower scores, particularly less than 100 at the start, are easier to gain control over. Scores of 50 or less, in fact, commonly can return to zero.

Higher scores, particularly those >1000, are more difficult to slow or reduce, though we've done it many times. You'll generally have to try harder and it may take longer. It's not uncommon to not stop plaque growth with a starting score this high until your 2nd or 3rd year of effort.

Sometimes it may take even longer. An occasional person requires four or five years to gain control. And there are, unfortunately, some people who never really gain complete control. They slow plaque growth compared to what it would have been with conventional efforts, but never completely halt growth. Why? Sometimes it's a matter of less than full commitment. Other times, we just don't know. Thankfully, these especially difficult cases are few and the majority enjoy substantial slowing or reversal.

Since, in some people, success may take time, you've got to stick it out. Have you ever gotten lost in a strange city only to find out later that the place you were looking for was right around the corner? It can be the same way with stopping coronary plaque growth. If you start with a score of 1000 and, after two years of effort, you've only slowed growth to 11% per year and then give up in frustration, you may have missed the opportunity to have stopped growth entirely in your third year.

All we can do is tip the scales heavily in your favor. We provide you with the best tools known. You've got to provide the commitment, the consistent effort of taking your supplements or medication, making the lifestyle changes, choosing the right foods and avoiding the wrong ones. But you've got to go the distance and not give up too easily.

What you need is an expert in health!

Where can you find an expert in health?

In my experience, they're hard--very hard--to find.

Your hospital? Certainly not the hospitals I know. The hospitals I know are experts in disease, but not in health. Hospitals are helpful when you're sick. But if you're well and would like to stay that way, there's no reason to hang around a hospital. Prevent cancer, prevent heart disease, stay well? There's no place for this conversation in a hospital.

In fact, hospital staff are among the most unhealthy people I come across. Obesity is a nationwide problem affecting millions of Americans. But it's especially a problem among people who work in hospitals. I shudder in horror when I go to a hospital cafeteria and witness the sorts of food they serve in hospitals and see what the staff eat. Should they be regarded as experts in health?

How about doctors? If you associate with physicians like the ones I know, most have lots of knowledge about disease, but little understanding of health. A rare one has insight and interest in health.

I went to a recent meeting with my cardiology colleagues. Food served: pizza, Coca-Cola, spaghetti, fried onion rings, white bread with butter. They all dug in without hesitation. Over half were miserably overweight. Several were, in fact, diabetic; several more, pre-diabetic. I know that at least several are smokers. Experts in health?

Drug companies? Well, they're interested in health only as far as it provides profits. But health for its own sake? Ask anybody from a drug manufacturer about their views on the nutritional supplement movement and watch them sneer.

Food manufacturers? You mean like Coca-Cola, Pepsi-Cola, Nabisco, and General Mills? How about fast-food operations like McDonald's, Pizza Hut, and KFC?

The message: Know where to look for genuine information on health. You won't get it from hospitals. You won't get it from drug company marketing. For the most part, you can't even get it from your physician.

Instead, you're going to witness a broad movement towards self-empowerment in health, fueled by the internet and services like ours (Track Your Plaque). These are information resources that are not driven by profit, intent on providing truth, and not afraid to reject prevailing views.

It does not mean that hospitals are unnecessary, or that food manufacturers are evil, or that fast food should be legislated out of existence. We live in a capitalistic society, driven by supply and demand. Hopefully, demand is borne from educated choices from informed consumers. That's where information that's reliable, credible, and not profit driven come in.

Lipoprotein(a) and small LDL

It's been my suspicion for some time that the combination of lipoprotein(a), or Lp(a), in combination with small LDL particles is a really bad risk for heart disease. People with this combination seem to have much higher heart scan scores for age than others. This seems to be a pattern that we'll see in the occasional woman less than 50 years old who already has a high heaert scan score. (It's unusual for women to have detectable coronary plaque before age 50.)

Very little data exists to support this idea and we are in the process of performing a small study to see whether it's true or not. My gut sense: it's among the most potent causes of coronary plaque around.

Case in point: Even though I spend a great deal of my time and energy advocating heart disease prevention, I still maintain my hospital privileges and skills. I had to cover one of the emergency rooms in town this past weekend (a requirement to maintain my hospital privileges).

One of the patients I saw was a 40-year old man--we'll call him Roland-- suffering a very large heart attack, a so-called "anterior myocardial infarction", or a heart attack involving the most important front portion of the heart. Thankfully, he came to the ER within 45 minutes after his chest pain started. The situation was immediately obvious and I was called to the ER. We quickly took him to the cardiac catheterization laboratory and put a stent in the left anterior descending artery and flow was restored. His chest pain dissipated over the next few minutes.

Nonetheless, Roland was left with a large area of reduced contraction of his heart muscle. Only time will tell how much recovery he'll have.

Roland was extremely lucky. The majority of people with closure of the artery that he'd experienced die within minutes. He did, in fact, "arrest" briefly, i.e., his heart became electrically unstable, though he recovered promptly.

Along with the multiple tubes of blood we required to run tests for his heart attack management, we had Roland's lipids and other measures sent off, as well. Wouldn't you know: Lp(a) and small LDL. This may have accounted for a heart attack at age 40.

Keep a lookout for this when you have lipoprotein testing. Conveniently, niacin can be used to treat both patterns, though higher doses are generally required for the Lp(a) part of the pattern. It's also my belief that the sort of Lp(a) measurement performed by the Liposcience laboratory (www.liposcience.com) is superior. They use a particle number based measure, not a weight-based measure. It is therefore independent of particle size, which can vary. Further work will, I believe, reveal some very important insights into the dreaded Lp(a).

"Please don't tell my doctor I had a heart scan!"

I overheard this recent conversation between a CT technologist and a 53-year old woman (who I'll call Joan) who just had a scan at a heart scan center:


CT Tech: It appears to me that you have a moderate quantity of coronary plaque. But you should know that this is a lot of plaque for a woman in your age group. A cardiologist will review your scan after it's been put through a software program that allows us to score your images.

Joan: (Sighing) I guess now I know. I've always suspected that I would have some plaque because of my mother. I just don't want to go through what she had to.

CT Tech: Then it's really important that you discuss these results with your doctor. If you wrote your doctor's name on the information sheet, we'll send him the results.

Joan: Oh, no! Don't send my doctor the results! I already asked him if I should get a scan and he said there was no reason to. He said he already knew that my cholesterol was kind of high and that was everything he needed to know. He actually got kind of irritated when I asked. So I think it's best that he doesn't get involved.


This is a conversation that I've overheard many times. (I'm not intentionally an eavesdropper; the physician reading station at the scan center where I interpret scans--Milwaukee Heart Scan--is situated so that I easily overhear conversations between the technologists and patients as they review images immediately after undergoing a scan.)

If Joan feels uncomfortable discussing her heart scan results with her doctor, where can she turn? Get another opinion? Rely on family and friends? Keep it a secret? Read up about heart disease on the internet? Ignore her heart scan?

I've seen people do all of these things. Ideally, people like Joan would simply tell their doctor about their scan and review the results. He/she would then 1) Discuss the implications of the scan, 2) Identify all concealed causes of plaque, and then 3) Help construct an effective program to gain control of plaque to halt or reverse its growth. Well, in my experience, fat chance. 98% of the time it won't happen.

I think it will happen in 10-20 years as public dissatisfaction with the limited answers provided through conventional routes grows and compels physicians to sit up and take notice that people are dying around them every day because of ignorance, misinformation, and greed.

But in 2006, if you're in a situation like Joan--your doctor is giving you lame answers to your questions or dismissing your concerns as neurotic--then PLEASE, PLEASE, PLEASE take advantage of the universe of tools in the Track Your Plaque program.

People tell me sometimes that our program is not that easy--it requires reading, thinking, follow-through, and often asking (persuading?) your doctor that some extra steps (like blood work) need to be performed. The alternative? Take Lipitor and keep your mouth shut? Just accept your fate, grin and bear it, hoping luck will hold out? To me, there's no rational choice here.

Doctor, why do I have heart disease?

I see a great many people in my practice who come for a 2nd opinion regarding their coronary disease.

When I ask patients whether they ever asked their primary doctor or cardiologist why they have heart disease in the first place, I get one of several responses:

1) My doctor said it from high cholesterol.

2) My doctor said it was "genetic" or "part of your family history" and so unidentifiable and uncorrectable. Tough luck.

3) I didn't ask and they didn't tell me.


Let's talk about each of these.

Can heart disease be only from high cholesterol and, if so, can taking a statin cholesterol drug be a "cure"? In the vast majority of cases, in my experience, cholesterol by itself is rarely the only identifiable cause of coronary disease.

Most people have a multitude of causes (e.g., small LDL, low HDL, vitamin D deficiency, concealed pre-diabetic patterns, etc.). This explains why many people with high LDL don't have heart disease and why others with low HDL do have heart disease. High LDL cholesterol is only part of the cause.

Does "genetic" or being part of your family's history also mean unidentifiable and uncorrectable? Absolutely not.

What your doctor is really saying is "I don't know enough to diagnose the causes because I haven't kept up with the scientific literature", or "I don't want to be bothered with this because it takes a lot of time and pays me very little money; I'd rather wait until you need a stent ", or "The drug representatives haven't told me about any new drugs". This is ignorance and laziness at best, greed and profiteering at worst. Don't fall for it. I hope that by now you recognize that the great majority of causes of heart disease are identifiable and correctable.

If you didn't think to ask, now you know that you should. If you and your doctor don't think about why you have coronary plaque in the first place, how can you develop a program to control it?

You need to ask. And you need to get confident answers. "I don't know" or "It's genetic" and the like are unacceptable.

Pill pushers

Have you read the latest cover story from Forbes magazine? It's entitled "Pill Pushers: How the drug industry abandoned science for salesmanship".

It's great reading. (A condensed version is available at the www.forbes.com website: http://www.forbes.com/business/forbes/2006/0508/094a.html. They require you to provide your e-mail address though it's free.)

Drug industry advertising has raised consciousness of all the prescription therapies available for us--that's good. However, they've gone so far overboard trying to squeeze more and more revenues out of drugs that they've cost this country a huge amount in increased health care costs and even lost lives. (Forbes does a great job of summarizing some of these instances.)

Drugs like Lipitor, Crestor, Zocor; diabetes agents; anti-hypertensive agents, etc., that is, medications taken chronically, a huge financial bonanzas for drug companies. Not only do they get $100-200 per month, but they get it month after month after month. That's per drug.

Now not all medications are bad or unnecessary. There are times when they can be truly necessary and beneficial. But don't rely on drug company advertising to tell us when.

Heart disease reversal is getting easier and easier

I've recently observed that more and more of our patients on the Track Your Plaque program seem to be stopping or reducing their heart scan scores. And they're doing it faster, in less time, and with larger drops in score.

I'm not entirely sure why the sudden surge in success. However, I do wonder if adding therapeutic levels of vitamin D--at least in our generally sun-deprived Wisconsin participants--is responsible. However, we've also gotten a lot smarter on how to correct the parameters that seems to have outsized effects on plaque growth, especially small LDL.

Yesterday alone, we had two people we added to our list of successes. One, an attorney, stopped his score in one year, with no change (compared to the expected increase of 30%). Another, a woman from the northeast, dropped her score 10% in one year. Her story is remarkable for beginning at a score >1000. In general, the higher your starting score, the longer it takes to stop or reduce it.

These are just two examples. It seems to be happening at an accelerating pace.

I can only hope that our surge in success (not 100%--yet!) will continue. But, every week, we're adding more and more people to our list of success stories.

A used car lot on every street corner

Imagine that, every day, a parade of used-car salesmen knock on your front door to sell you a special "deal". Day in, day out they knock, expecting you to hear about their offers openly.

Is there any doubt about their intentions or motives? Of course not. They're just trying to profit from selling you a car.

That's how it is in a medical office nowadays. Drug representatives, 5, 6, or more each and every day, promoting drugs. Except that the profits from drugs are far greater than a used automobile, and there's a third party involved in the transaction: you.

Today, a pushy representative came to my office. My staff and I tried to tell him that I was not interested in speaking to him. But he proved such a nuisance that I finally came out to tell him that I objected to the idea of drug reps just hanging around trying to hawk their wares.

He blurted, "Doctor, do you have patients with angina? Our new drug, ranolazine, is perfect. Forget about nitroglycerin, beta blockers, and all that. Here's the latest study proving it's better." He tried to shove a reprint of the study at me.

Getting to the bottom line, I asked, "What does it cost the patient?"

"Well, the co-pay is between $40 and $60. We're not yet well covered by insurance, so it'll cost patients around $200 a month."

Need I say more? Here's a drug that does little more than help relieve anginal chest pains. It doesn't reverse coronary plaque. It won't avoid heart attack, death, or procedures. It just modestly cuts back on the frequency of chest pain. And all for the cost of a single heart scan--a heart scan that could have prevented the entire cascade of symptoms/procedures/medication/hospitalization etc.

Hospitals, drug companies, medical device manufacturers. They're all businesses that thrive on your doctor's failure to detect and control your coronary plaque. Sometimes, even your doctor is part of this conspiracy to squeeze dollars out of human disease. Don't fall for it.

Heart disease reversal at age 77

I met Agnes 18 months ago after she underwent a heart scan that revealed a scary score of over 1100. Although in her mid-70s, this was still a very high score. (Recall that a score this high carries a risk for heart attack and death of 25% per year.) Poor Agnes was a wreck over this unexpected result. "I can't sleep, I can't stop thinking about it!"

She'd undergone the scan because her 44-year old son had a heart scan score of 2200! Unfortunately, he ended up with a bypass operation for very severe disease.

Despite having been seeing a cardiologist in Boston for the last 8 years for a murmur, we uncovered multiple hidden lipoprotein patterns, many of which she shared with her son. Her most notable abnormalities were a low HDL and small LDL. Nearly 100% of all LDL particles were, in fact, small. This pattern also caused her LDL cholesterol to be underestimated by over 40%.

18 months on the Track Your Plaque program and Agnes came into town to get a repeat scan. Her score was 10.2% lower. She'd learned to live with the idea that she had hidden heart disease missed by her doctor and cardiologist for many years. But knowledge of the substantial reversal she'd achieved in the 18 months on the program gave Agnes tremendous peace of mind.

Agnes left the office with a big smile.

If you need a reason to quit smoking...

If you've read Track Your Plaque, you already know my feelings about smoking and coronary plaque. Smoke, and you will lose the battle for control over coronary plaque growth--it will grow and grow until catastrophe strikes.

Nonetheless, this is not sufficiently motivating for some people.

If you need more motivation to quit smoking, just take a look at your heart scan sometime, accompanied by either one of the doctors or technicians at the scan center you choose. After you've had an opportunity to look at your coronary arteries, take a look at the lungs. The heart is in the middle and the lungs are the two large black areas on either side of the heart. (They're not really black; that's just the way the images are color-coded.)

Smokers will see large cavities in their lungs--literally, half-inch to one-inch wide holes that contain only air. Many of them. These represent remnants of lung tissue, digested away and now useless from the damage incurred through smoking.

Non-smokers should see uniform lung tissue without such cavities.

What surprised me early on in my heart scan experience was how little smoking exposure was required to generate these cavities. A 40-year old, for instance, who smoked a half-pack per day for 10 years would have them. Heavier smokers, of course, showed far more extensive cavities.

Officially, these cavities are called "emphysematous blebs", meaning the scars of the lung disease, emphysema.

When I've pointed out these cavities or emphysematous blebs to patients, 9 out of 10 times they immediately become non-smokers. Commonly, they'd exclaim, "I had no idea I was really damaging my lungs!" Most admitted that they were awaiting some bona fide evidence that they were truly doing some harm to their bodies. Well, that's it.

Give it a try if you're struggling.
All posts by william-davis

High blood pressure vanquished

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado


Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl


I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.


1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.

Restaurant eating: A fructose landmine

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.