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

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

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

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

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

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

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

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

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

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

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

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

Einkorn now in Whole Foods

I just saw this at Whole Foods: einkorn pasta.

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

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

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

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

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

Noodles without the headaches

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

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

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

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


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

You're fried

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

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

Let's take them one by one:

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

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

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

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

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

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

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

Bosom buddies

Male breast reduction surgery is a booming business. While most industries are in a downward tailspin, breast reduction surgery in men is growing at double-digit rates.

Other efforts, some legitimate, some not, are also cropping up, all intended to help men deal with this embarassing problem:

Exercise programs to reduce male breast size.

Liposuction--Not just for the belly!

Plastic surgery

Gynexin--a supplement that purportedly reduces male breast size.

Conventional medical treatment also includes estrogen blocking drugs, the same ones used to treat breast cancer, drugs like tamoxifen. There's even clothing intended to make breasts less obvious.


While male breast enlargement--"gynecomastia"--can occasionally occur due to rare endocrinologic problems, such as high prolactin hormone levels (hyperprolactinemia) or somewhat more commonly as failed testosterone production (hypogonadism), the vast majority of men who suffer with this problem simply have high estrogen levels.

Makes sense: Women develop larger breasts during development mostly due to increased levels of estrogen. A parallel situation in men likewise stimulates breast tissue.

So where does the excess estrogen come from?

Visceral fat converts testosterone to estrogen. Men with excess visceral fat therefore develop low levels of testosterone and high levels of estrogen. Estrogen levels can, in fact, be substantially higher compared to slender males.

So what foods cause the accumulation of visceral fat and, thereby, increased estrogen and decreased testosterone?

Foods that increase blood glucose and insulin to the greatest degree are the foods that begin this cascade. The common foods that increase blood sugar the most? Here's a list, starting with most blood glucose-insulin provoke at the top, least at the bottom:

Gluten-free foods (dried, pulverized cornstarch, rice starch, potato starch, tapioca starch)
Whole wheat bread
Sucrose
Milky Way bars
Snickers bars

So the whole wheat sandwiches you've been eating increase blood sugar and insulin, leading to visceral fat. (And, yes, whole wheat bread increases blood sugar higher than Milky Way bars and Snickers bars.) The more visceral fat grows, the more resistant to the effects of insulin you become, further escalating blood sugar. Estrogen increases, testosterone drops, mammary gland tissue grows, normal male breasts grow to B- or C-cup size.

Yet again, an entire industry is growing from the unintended consequence of conventional advice. In this instance, the advice to "eat more healthy whole grains" leads to this booming industry of male breast reduction efforts from surgery to medications to clothing. The REAL solution: Eliminate the foods that start the process in the first place.

Don't be a dipstick

If I want to know how much oil is in my car's engine, I check the dipstick.

The dipstick provides a gauge of the amount of oil in my engine. If the dipstick registers "full" because there an oil mark at one inch, I understand that there's more than one inch of oil in my engine. The dipstick provides an indirect gauge of the amount of oil in my engine.

That's what cholesterol was meant to provide: A gauge, a "dipstick," for the kind of lipoproteins (lipid-carrying proteins) in the bloodstream.

Lipoproteins are a collection of particles that are larger than a single cholesterol molecule but much smaller than a red blood cell. Lipoproteins consist of many components: various proteins, phospholipids, lots of triglycerides, as well as cholesterol. In the 1960s, methods to characterize lipoproteins were not widely available, so the cholesterol in lipoproteins were used as a "dipstick" to assess low-density lipoproteins ("LDL cholesterol") and high-density lipoproteins ("HDL cholesterol"). (Actually, even "LDL cholesterol" was not measured, but was derived from "total cholesterol," the quantity of cholesterol in all lipoprotein fractions.)

Some other component of lipoproteins could have been measured instead of cholesterol, such as apoprotein B, apoprotein C, or others, all meant to act as the "dipstick" for various lipoproteins.

Relying on cholesterol to characterize lipoproteins provides a misleading picture. Imagine watching cars go by at high speed while standing on the side of the highway. You want to count how many people--not cars, but people--go by in a given amount of time. Because you cannot make out the detail of each and every car whizzing by, you count the number of cars and assume that each car carries two people. Whether it's rush hour, Sunday morning, late evening, rainy, sunny, or snowing, you make the same assumption: two people per car.

That's what cholesterol does: It is assuming that each and every lipoprotein particle (car) carries the same amount of cholesterol (people).

But that may, obviously, not be true. A bus goes by carrying 25 people. Plenty of cars may carry just the driver. People carpooling may be in cars carrying 3 or 4 people. Assuming just 2 people per car can send your estimates way off course.

That is precisely what happens when your doctor tries to use conventional cholesterol values (total cholesterol, LDL cholesterol) to gauge the lipoproteins in your bloodstream. Measuring cholesterol can also provide the false impression that cholesterol is the cause of heart disease, even though it was originally meant to simply serve as a "dipstick."

What we need to do is to characterize lipoproteins themselves. We can distinguish them by size, number, density, charge, and the type and form of proteins contained within. It provides greater insight into the composition of lipoproteins in the blood. It provides greater insight into the causes underlying coronary atherosclerotic plaque. It can also tell us what dietary changes trigger different particle patterns and how to correct them.

Until you have a full lipoprotein analysis, you can never know for certain 1) if you will have heart disease in your future, or 2) how your heart disease was caused.

Unfortunately, the vast majority of doctors are perfectly content to just count cars going by and assume two people per car, i.e., confine assessment of your heart disease risk using cholesterol . . . just as drug industry marketing has instructed them.

It's not your job to educate your doctor. If he or she refuses to provide access to lipoprotein testing to better determine your heart disease risk, then consider going out on your own. Many of our Track Your Plaque program followers have obtained lipoprotein testing on their own through Direct Labs.

The ultimate insurance company cost savings

I had a very disturbing conversation with a physician who is employed by an insurance company last week.

I admitted a patient in the hospital for very clear-cut reasons. She is one of my few non-compliant patients, doing none of the strategies I advocate--no fish oil, no vitamin D, no correction of her substantial lipoprotein abnormalities, not even medication. Much of this was because of difficult finances, some of it is because she is from the generation (she is in her late 70s) that tends to ignore preventive health, some of it is because she is a kind of happy-go-lucky personality. So her disease has been progressive and, now, life-threatening, including an abdominal aneurysm near-bursting in size (well above the 5.5 cm cutoff). The patient is also a sweet, cuddly grandmother. I have a hard time bullying nice little old ladies.

While she was in the hospital, the social worker told me that her case was being reviewed by her insurer and would likely be denied. Their medical officer wanted to speak to me.

So the medical officer called me and started asking pointed questions. "Why did you do that test? You know that she's not been compliant. Are you sure you want to do that? I don't think that's a good idea." In other words, this was not just a review of the case. This was an opportunity for the insurance company to intervene in the actual care of the patient.

Then the kicker: "Have you considered not doing anything and . . . just letting nature take its course?"

At first, I was stunned. "You mean let the patient die?"

Expressed in such blatant terms, while he was trying to be diplomatic, made him back down. "Well, uh, no, but she is a high-risk patient."

Anyway, this was the first instance I've encountered in which the insurance company is not just in the business of reviewing a case, but actually trying to intervene during the hospital stay, to the point of making the ultimate healthcare cost savings: Letting the patient die.

Unfortunately, never having had an experience like this before, I did not think to record the conversation or take notes. I am wondering if this is an issue to be taken up by the Insurance Board . . . or is this a taste of things to come as the health insurers fall under increasing pressure with the legislative changes underway?

Salvation from halogenation

Iodine is a halogen.

On the periodic table of elements (remember the big chart of the elements in science class?), the ingenious table that lays out all known atomic elements, elements with similar characteristics are listed in the same column. The elegant genius of the periodic table has even allowed prediction of new, undiscovered elements that conform to the "laws" of atomic behavior.

Column 17 (also called "group VIIa") contains all the halogens, of which iodine is one member. Other halogens include fluorine, chlorine, and bromine.

Odd phenomenon in biologic systems: One halogen can often not be distinguished from another. Thus, a chlorinated compound can cleverly disguise itself as an iodinated compound, a brominated compound can mimic an iodinated compound, etc.

What this means in thyroid health is that, should sufficient iodine be lacking in the body, i.e., iodine deficiency, other halogens can gain entry into the thyroid gland.

While a polychlorinated biphenyl (PCB) molecule may be recognized as an iodinated compound, it certainly doesn't act like an iodinated compound once it's in the thyroid's cells and can disrupt thyroid function (Porterfield 1998). Another group of chlorine-containing compounds, perchlorates, that contaminate groundwater and are found as pesticide residues in produce, are extremely potent thyroid-blockers (Greer 2002). Likewise, bromine-containing compounds, such as polybrominated diphenyl ethers (PBDEs), widely used as flame retardants, also disrupt thyroid function (Zhou 2001). Perfluorooctanoic acid (PFOA), found in Teflon non-stick cookware and stain-resistant products,  has been associated with thyroid dysfunction (Melzer 2010). PFOA, incidentally, can disrupt thyroid dysfunction that will not show up in the TSH test used by primary care physicians and endocrinologists to screen for thyroid dysfunction. (In fact, the presumed champions of thyroid health, the endocrinology community, have proven a miserable failure in translating and implementing the findings from  toxicological science findings to that of preserving or restoring thyroid health. They have largely chosen to ignore it.)

We therefore navigate through a world teeming with halogenated thyroid blocking compounds. We should all therefore avoid such exposures as perchlorates in produce by rinsing thoroughly or purchasing organic, avoid non-stick cookware, avoid use or exposure to pesticides and herbicides.

Another crucial means to block the entry of various halogenated compounds into your vulnerable thyroid: Be sure you are getting sufficient iodine. While it doesn't make your thyroid impervious to injury, iodine circulating in the blood in sufficient quantities and residing in sufficient stores in the thyroid gland provides at least partial protection from the halogenated impostors in your life.

I make this point in the context of heart disease prevention, since even the most subtle degrees of thyroid dysfunction can easily double, triple, or quadruple heart disease risk. See related posts, Is normal TSH too high? and Thyroid perspective update.

Lipitor-ologist

One of the things I do in practice is consult in complex hyperlipidemias, the collection of lipoprotein disorders that usually, but not always, lead to atherosclerosis.

First order of business: Make the diagnosis--familial combined hyperlipidemia, hypoalphalipoproteinemia, lipoprotein(a), familial heterozygous hypercholesterolemia, familial hypertriglyceridemia, hyperapoprotein B with metabolic syndrome, etc. These are the disorders that start with a genetic variant, e.g., a missing or dysfunctional enzyme or signal protein, such as lipoprotein lipase or apo C3.

I then ask: What can be done that is easy and safe and preferably related to diet and lifestyle?

By following an effective diet, many of these abnormalities can be dramatically corrected, sometimes completely. Familial hypertriglyceridemia, for instance, an inherited disorder of lipoprotein lipase in which triglyceride levels can exceed 1000 mg/dl, high enough to cause pancreatic damage, responds incredibly well to carbohydrate restriction and over-the-counter fish oil. I have a number of these people who enjoy triglyceride levels below 100 mg/dl--unheard of in conventionally treated people with this disorder.

Then why is it that, time after time, I see these people in consult, often as second or third opinions from lipidologists (presumed lipid specialists) or cardiologists, when the only solutions offered are 1) Lipitor or other statin drug, and 2) a low-fat diet? Occasionally, an aggressive lipidologist might offer niacin, a fibrate drug (Tricor or fenofibrate), or Lovaza (prescription fish oil).

Sadly, the world of lipid disorders has been reduced to prescribing a statin drug and little else, 9 times out of 10.

I don't mean to rant, but I continue to be shocked at the incredible influence the drug industry has over not just prescribing patterns, but thinking patterns. Perhaps I should say non-thinking patterns. The drugs make it too easy to feel like the doctor is doing something when, in truth, they are doing the minimum (at best) and missing an opportunity to provide true health-empowering advice that is far more likely to yield maximum control over these patterns with little to no medication.

All in all, I am grateful that there is a growing discipline of "lipidology," a specialty devoted to diagnosing and treating hyperlipidemias. Unfortunately, much of the education of the lipidologist is too heavily influenced by the pharmaceutical industry. Not surprisingly, the drug people favor "education" that highlights their high-revenue products.

Seeing a lipidologist is still better than seeing most primary care physicians or cardiologists. Just beware that you might be walking into the hands of someone who is simply the unwitting puppet of the pharmaceutical industry.

Robb Wolf's new Paleo Solution

The Paleo Solution: The Original Human Diet


The Paleo Solution: The Original Human Diet

I have to say: I'm impressed. If you would like insight into why a "Paleo" nutritional approach works on a biochemical level--why you lose weight, burn fat, and gain overall better health--then Robb's book is worth devoting a few hours to, of not a reread or two.

Robb has a particular knack for organizing and presenting information in a way that makes it immediately accessible. You will gain an appreciation for how far American nutritional habits have veered off course.

Because Robb brings expertise from his academic biochemistry background, as well as personal trainer and educator running a successful gym in northern California, NorCal Strength and Conditioning, he delivers a book packed with information that is extremely easy to convert to immediate action in health and exercise. He seems to anticipate all the little problems and objections that people come up with along the way, dealing with them in his characteristic lighthearted way, providing practical, rational solutions.

Robb's book nicely complements what Dr. Loren Cordain has written in his The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat and The Paleo Diet for Athletes: A Nutritional Formula for Peak Athletic Performance. (My wife is now reading The Paleo Diet for Athletes and loves it. I'm going to add Robb's book to her reading list for her to read next.)

If nutrition has you stumped, if the USDA food pyramid still sounds like a reasonable path, or if you just would like to understand nutrition a little bitter, especially its biochemical ins and outs, Robb's book is a wonderful place to start.
All posts by william-davis,

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.

 

 

 

 

 

 

 

You've come a long way, baby

In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.

 
All posts by william-davis

Diet by LDL

Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

So, cut the saturated fat in the diet, cut the overall fat content, and replace them with polyunsaturated oils like safflower, corn, and vegetable oils and increase consumption of whole grains and total and LDL cholesterol show a modest downturn. Thus, diets like the American Heart Association Total Lifestyle Change approach advocate limiting total fat to no more 25 to 35% of calories and saturated fat to no more than 7% of calories.

Orange Cream Cookies

If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

Ingredients:
2 cups almond meal
2 tablespoons coconut flour
1 teaspoon baking soda
½ teaspoon sea salt
¼ cup golden raisins
½ cup chopped pecans
Sweetener equivalent to 1 cup sugar
2 tablespoons finely-grated orange rind
1 large egg
2 tablespoons coconut oil, melted
½ cup whipping cream (or coconut milk)
1 tablespoon vanilla extract

Preheat oven to 350º F.

Combine almond meal, coconut flour, baking soda, salt, raisins, pecans, sweetener and orange zest in bowl and mix.

In separate bowl, whisk egg, then add coconut oil, whipping cream, vanilla extract and mix together. Pour wet mix into dry and blend by hand thoroughly.

Spoon onto parchment paper-lined baking pan (or oiled pan) and flatten with spoon to ½-¾ inch thickness. Bake for 20-25 minutes or until toothpick withdraws dry.

Why are heart attacks still happening?

I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease.

But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.)

Two high-profile deaths from heart attacks occurred this week:

Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain.

Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking.

It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health.

The followers of the Track Your Plaque program who

1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes)
2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction
3) correct the causes

enjoy virtual elimination of risk.

My letter to the Wall Street Journal: It's NOT just about gluten

The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health

60-year old man dies of high cholesterol

Never saw a headline like this? Neither have I. That's because it doesn't happen.

Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.

Back to basics: Coronary calcium

After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.

Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.

If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.

Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)

But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.

Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.

There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.

So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.

But it's the best we've got.

If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.

Myocardial infraction

I've seen a few heart attacks this past year . . . but none in the people who follow this program.

I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day.

I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind.

A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive."

There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates.

In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.

Diet is superior to drugs

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.


(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Low-carb is heart healthy

Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.

First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension.

Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk.

In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:

Reduced fasting triglycerides and VLDL
Reduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnants
Increased HDL and shift towards large HDL particles (presumably more protective)
Reduced small LDL particles
Reduced glycation and oxidation of small LDL particles
Reduced hemoglobin A1c
Reduced c-reactive protein and other inflammatory markers
Reduced blood pressure

By slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis.

Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.

Mocha Walnut Brownies

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . .  . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.


Ingredients:
8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)


Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.
All posts by william-davis

Vitamin D increased my cholesterol

A friend told me this story.

Her friend, Linda, had added vitamin D to her daily supplements. Because she'd had a vitamin D blood level of 22 ng/ml, she was taking 6000 units per day.

However, Linda also had a high cholesterol value with a total cholesterol of 231 mg/dl. After several months on the vitamin D, she had another cholesterol panel. Total cholesterol: 256 mg/dl.

"It must have been the vitamin D! So I stopped it right away."

Is this true? Does vitamin D raise the level of blood cholesterol? Yes, it does. But it's a good thing. Let me explain.

Followers of The Heart Scan Blog know that total cholesterol is really a mix of 3 other factors:

Total cholesterol = LDL cholesterol + HDL cholesterol + triglycerides/5

This is the Friedewald equation, still used today in over 95% of cholesterol panels. So, by the Friedewald equation, anything that increases LDL, HDL, or triglycerides will increase total cholesterol.

One of the spectacular changes that develops over a year of taking vitamin D is that HDL cholesterol skyrockets. While sensitivity to this effect varies (probably on a genetic basis), HDL increases of 10, 20, even 30 mg/dl are common. A starting HDL, for instance, of 45 mg/dl can jump up to 65 or 70 mg/dl, though the effect requires up to a year, sometimes longer.

Vitamin D can also reduce triglycerides, though the effect is relatively small, usually no more than 20 mg/dl or so. Likewise, the effect on LDL is minor, with a modest reduction in the small type of LDL.

So the dominant effect of vitamin D from a cholesterol standpoint is a substantial increase in HDL. Looking at the equation, you can see that an increase in HDL is accompanied by a commensurate increase in total cholesterol. If HDL goes up 25 mg/dl, total cholesterol goes up 25 mg/dl.

So Linda is absolutely correct: Vitamin D increases cholesterol--but it's a good thing that reduces risk for heart disease and is an important part of a coronary plaque-reversal program.

This is yet another reason why I advocate elimination of total cholesterol on lipid panels. There is no useful information in the total cholersterol value, only the potential for misinformation.

Nutrtional ignorance is not unique to the U.S.

Heart Scan Blog reader from Australia, Michaela, also a mother of a son with a complex congenital heart defect, wrote this series of e-mails to me. (Published with Michaela's permission.)


I've been reading the article, Valve disease and Vitamin D from April '07, by Dr William Davis. I'm hoping you may have some information on the topic. I'm hoping someone will have time to help me.

I have been supplementing my 15 year old son with Vit D for 4 months but only 1000 (U) per day. I would like to increase the dosage but am not sure if I would do him more harm than good.

I have been researching vitamins and supplements on the net for a few months and have been amazed at what I have found. I only wish I had done it years ago. My son has been let down by the Australian Medical Profession and it's a race against time now to keep him well and avoid a heart transplant.

My son was born with aortic stenosis and had a valvotomy at 4 weeks of age. This damaged the aortic valve and he had a Ross Repair procedure at aged 3. This left him with a damaged heart muscle and leaking aortic & pulmonary valves. In May '08, his heart grew more enlarged, causing the mitral & tricuspid valves to also leak.

I took him to Bangkok in Feb this year where he had 70 million of his own Adult Stem Cells directly injected into his heart muscle with the hope of strengthening the muscle and eventually valve replacement.

My son has recovered from the surgery and is once again symptom-free, thanks to the wonderful advice followed by the Author & Cardiologist, Stephen T. Sinatra. I have followed his supplement regime and what a difference! Of course, this won't last while my son's valves continue to leak.

My son has also developed secondary hyperparathyroidism, bone thinning and hypothyrodism. Vit D & Calcium have something to do with this I believe.

My Australian Doctors have never made mention of any vitamins or supplements .... EVER! Transplant is all they will consider and we are not having it.

If you have any info or links to any sites which may be useful to me, could you email them to me? I would be grateful for any help I could get.

Sincerely
Michaela



I responded to Michaela's e-mail:

Hi, Michaela--

Vitamin D is extremely important. Sometimes, hyperparathyroidism and calcium derangements are caused by vitamin D deficiency. You might be able to get help with this from an endocrinologist, since they are the ones who deal with hyperparathyroidism. An endocrinologist might even be familiar with several recent studies that document this phenomenon:

Vitamin D therapy in patients with primary hyperparathyroidism and hypovitaminosis D

Vitamin D deficiency and primary hyperparathyroidism

Also, see the discussions at www.vitamindcouncil.org from Dr. John Cannell.

Because of the complexity of your son's health, it might be hazardous to stray too far away from conventional care though you and I know that there are limitations to that perspective. For that reason, I would urge you to press for answers from a knowledgeable endocrinologist.

I hope you find the answers you need.

William Davis, MD



Several months later, Michaela provided this update:

Hi Dr Davis,

I wrote to you back in July regarding my 15 year old son's need for a Heart Transplant through a failed Ross Repair and the possible Vitamin D connection. You sent me some valuable links and I thank you again for that.

I just wanted to let you know, I think you have given me the answers. I increased Lee's Vitamin D supplement to 6000U a day and, along with the recommended nutritional supplements of US Cardiologist Dr Stephen T Sinatra, there have been remarkable improvements! Lee also had 70 million of his own Adult Stem Cells injected into his heart in February. As we know, Stem Cell Therapy takes time and Lee was looking like time was quickly running out.

I have removed him from the transplant list. He is now reading normal Kidney function, the BNP (Brain Natriuretic Peptide, a measure of heart failure] has dropped by 7000 and his liver size has reduced to where it no longer causes him discomfort. The liver tests show it's still affected but it's function is improving each month. His last Echo was in early July and there had been a reduction in the size of his heart, which is so important.

To the Doc's, Lee can't get better, there is only transplant or death so you can imagine the surprise on their faces to see him looking and feeling so well with their tests to back it up. Still, even though it's staring them in the face, they don't want to know about it. They have no interest in what supplements he is on or Stem Cell therapy. God help their other patients. I view them in the waiting room and think of them as lambs to the slaughter.

We are not spoiled for choice with Doc's here in Western Australia. I have to take what I can get and there is not many who would take on Lee's case. He was number 1 on the transplant list and a most urgent case. Not many were willing to even look at him with his cardiac history and all I had to help was the arrogant Doc's at the Advanced Heart Failure Unit. They were not at all interested in his secondary hyperparathyroidism. I suppose it didn't matter what else he had compared to his heart problems.

Anyway, I'm writing to thank you. Lee would be transplanted or dead now if it wasn't for Dr's like you sharing their knowledge online. I wish I had researched things years ago, Lee might not have sunk so low if I had. I don't know if the transplant can be held off indefinitely, but like I tell Lee, "Stay well. There are amazing people out there doing amazing things, if you can just hang on. The miracle is around the corner." He's so well, you'd have to see him to believe it. But I have 7 kids and Lee is as physically active and as well as the other 6! For how long he can stay like this, I don't know but if his ejection fraction [a measure of left ventricular strength] can keep climbing and his body gets stronger, I have hope for another attempt at valve replacement.

I'm still shocked and angry that nutritional supplements have never been mentioned in the 15 years I've been dealing with cardiologists. Surely they know about them. I have read through dozens of reports online of the benefits of them--Why haven't they?! Thank God for the online Doc's such as yourself, the valuable info would never make it out of a Doctor's office in Western Australia! I've had to leave my country for Stem Cell therapy and then implore overseas Doc's for advice and information. What does that say for the Australian Medical Profession? Not a lot! They put him in the position he is in yet don't want to help get him out.

I'm so very grateful to you, thank you and God bless.

Michaela



Note: The above is not meant to be an implicit endorsement of stem cell therapy. This was just part of Michaela's story about her son.

Eat cranberries

Most people already know that cranberries are useful for preventing urinary tract infections. Cranberries can also be useful for preventing other sorts of infections, such as dental cavities and stomach ulcers because of cranberry's ability to block bacterial adhesion.

Cranberries can also be a useful component of a heart healthy program.

Several unique properties of cranberries contribute to various aspects of heart health:

• Cranberries are a rich source of pectin--Pectin is a soluble fiber, the sort that binds bile acids in the intestinal tract and naturally reduces LDL cholesterol.
• Cranberries are a rich source of polyphenols and flavonoids--Including the wonderfully fascinating anthocyanins, the flavonoids that confer the beautiful red color. Surprisingly, cranberries are richer in polyphenols and flavonoids than blueberries, strawberries, and grapes. Cranberry juice is also rich in these compounds. However, beware of cranberry juice "cocktail," which is diluted with other liquids such as high-fructose corn syrup. Like grapes, cranberries are a source of resveratrol, the polyphenol also found in red wines that some believe is responsible for reduced risk for heart disease and extending life.
• Cranberries have high antioxidant activity--Cranberries are among the highest in antioxidant capacity against superoxide radicals, hydrogen peroxide, and hydroxyl radicals, oxidizing factors believed to underlie heart disease, cancer, and aging. Cranberries also reduce the oxidation of LDL cholesterol particles.
• Cranberries block uric acid production--Cranberries have the unique ability to block the activity of an enzyme, xanthine oxidase, that converts xanthine to uric acid. Uric acid is believed to add to heart disease risk and is the factor responsible for gout.
• Cranberries increase HDL cholesterol--Cranberry juice increases HDL by 3-4 mg/dl.

Cranberries are only modest sources of sugars, with 7.19 grams “net” carbohydrates (total carbohydrates minus fiber content) per cup of whole raw cranberries.

The best way to eat cranberries is to consume the real thing: eat the whole berry, as in sugar-free cranberry sauce or added to baked dishes like chicken. Second best are dried cranberries. However, be careful of the overly-sweetened dried cranberries that contain added sugar (for a total of 78 grams sugar per cup--far too much). Unsweetened dried cranberries can be purchased, or you can dry them yourself.

Cranberry juice is another way to obtain the health benefits of cranberries; the unsweetened juice, while quite tart, is the best with 30.5 grams sugar per 8 oz--so don't drink more than 4 oz at a time. The more common cranberry juice “cocktails” are generally too sugary and/or too dilute for full health benefit.

The cranberry harvest season in Wisconsin, Michigan, Oregon, Massachusetts, and New Jersey is just getting underway, so we should be seeing fresh cranberries on store shelves or farmers' markets any day now.

Procedures 'R Us

Kay came to the office for an opinion.

Over the past 8 months, she'd received a stent to the left anterior descending coronary artery and, during a separate procedure, a stent to the left subclavian artery.

"My cardiologist was very capable doing procedures. But when I asked, 'What do I do now?' he barely said a word and handed me a presciption for Crestor."

This kind of incredible neglect is the norm: Write a prescription for statin drug, delegate dietary advice to the hospital dietitian who advocates a heart disease-causing low-fat diet, followed by hospital discharge. You are expected to report any recurrent symptoms (which are inevitable), at which point you might "qualify" for another procedure.

It would be malpractice if it were not the prevailing standard in the community. Yes, the prevailing standard is neglect--neglect to identify, quantify, and correct all the identifiable causes of heart disease; neglect to discuss the nutritional methods that actually correct the abnormal patterns that cause heart disease; neglect to discuss nutritional supplements or medications beyond statins that further reduce heart disease risk and "need" for more procedures. In other words, the prevailing community standard is to stent, bypass, prescribe statin. It is not to understand why the disease occurred in the first place, correct the causes and minimize or eliminate any future danger or need for procedures.

I see consultation after consultation involving stories just like Kay's. People are frightened and they sense intuitively that nobody raised the question of why they have a potentially fatal disease.

Don't allow yourself to fall victim to this incredibly neglectful mode of practice, the one that has enriched hospitals, the drug industry, many cardiologists, but does little to address the actual disease.

Unexpected effects of a wheat-free diet

Wheat elimination continues to yield explosive and unexpected health benefits.

I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies.

A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops.

People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:

--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours.

--Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat.

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings.

--Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops.

--Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.


It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people.

Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Do "Heart Healthy" sterols cause heart disease?

The sterol question continues to pop up.

Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia?

Below, I've reprinted a previous Heart Scan Blog post on sterols.


Sterols should be outlawed

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

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

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Why obese people can't fast

Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

Test your own thyroid

134 people responded to the latest Heart Scan Blog poll:


When I ask my doctor to test my thyroid, he/she:

Accommodates me without question 45 (33%)

Questions why, but orders the tests 49 (36%)

Refuses because you seem "healthy" 20 (14%)

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)



That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.

However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.

Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.

Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.

So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."

You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?

You could:

--Drink more coffee
--Exercise more in the hopes that it will snap you out of your lethargy
--Sleep more
--Take stimulants of various sorts

Or, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?

You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here.

This is yet another facet of the powerful revolution that is emerging: Self-directed health.

Trains, planes, and heart scans

A Heart Scan Blog reader posted the following question:

It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?

Good question. Think of it this way:

Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc.

A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.

It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300.

Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:

1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat.

2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk.


With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.
All posts by william-davis

The world according to the Wheat Foods Council and the Whole Grains Council


You might get a kick out of what the Wheat Foods Council and the Whole Grains Council recommend for a sample meal plan:

Breakfast: Whole grain raisin toast
Lunch: Sandwich on whole grain
Snack: Rye bread crackers
Dinner: Whole grain pasta with your favorite sauce

Breakfast: Whole grain waffles 
Lunch: Hamburger on whole grain bun
Snack: Graham crackers
Dinner: Whole grain homemade pizza on whole grain pita crust

Remember Morgon Spurlock's documentary movie, Super Size Me? (If you haven't already seen it, Super Size Me is viewable for free on Hulu.) Spurlock conducts a self-inflicted 30-day experiment of eating at McDonald's fast food restaurants every day. In short, the results on Spurlock's weight and health are disastrous. 

How about Wheat Belly: The Movie? We would chronicle our star through a 30-day course of meals served up by the Wheat Foods and Whole Grains Councils, all featuring wonderful wheat products in every meal. We could measure blood sugar, triglycerides, LDL, small LDL, weight, etc.


Any predictions?

Why bananas increase cholesterol

Anything that increases postprandial (after-eating) blood sugar will increase the number of LDL particles in the blood.

An increase in LDL particles is an important factor in causing heart disease: The greater the number of LDL particles, the more opportunity they have to interact with the walls of arteries, contributing to atherosclerosis.

Carbohydrates increase small LDL, especially if postprandial sugar is increased. Here's another way carbohydrates increase LDL particles: The duration of time LDL particles hang around in the blood stream is doubled.

When blood sugar increases, such as after the 30 grams carbohydrates in a medium-sized banana, glycation of LDL particles occurs. This means that a gglucose (sugar) molecule reacts with a lysine residue in the apoprotein B of the LDL particle. This induces a change in conformation that makes it less readily recognized by the LDL receptor. Thus, the glycated LDL particle persists for a longer period of time in the blood stream.

LDL particles are therefore cleared less efficiently, numbers of LDL particles increase.

Plant-based or animal-based?

The ideal diet for heart and overall health restricts carbohydrate intake. I say this because carbohydrates:

Make you fat--Carbohydrates increase visceral fat, in particular.
Increase triglycerides
Reduce HDL
Increase small LDL particles
Increase glycation of LDL
Increase blood pressure
Increase c-reactive protein


Reducing carbohydrates reverses all the above.

But here's a common mistake many people make when following a low-carbohydrate diet: Converting to a low-carb, high-animal product diet.

It accounts for a breakfast of a 3-egg omelette with cheese and butter, 4 strips of bacon, 2 sausages, cream in coffee. Low-carb? It certainly is. But it is a purely high-animal product, no-plant-based meal.

I believe a strong argument can be made that a low-carbohydrate but plant-based diet with animal products as the side dish is a better way to go.

Consider that:

1) Animal products have little to no fiber, while plant-based products like spinach, avocado, and walnuts and other raw nuts have substantial quantities.

2) Plant products are a source of polyphenols and flavonoids--This encompasses a large universe of nutrients, from epigallocatechins in tea, polymeric procyanidins from cocoa, to hydroxytyrosol from olives, and anthocyanins from red wine and eggplant. The inflow of these beneficial compounds needs to be frequent and generous, not piddly amounts taken infrequently.

3) Vitamin C--While it's easy to obtain, the fact that you and I need to obtain vitamin C from frequent ingestion of plant sources suggests that humans were meant to eat lots of plants. While it may require a few months of deficiency before your teeth fall out, imagine what low-grade deficiency can do over a long period.

4) Vitamin K1--Rich in green vegetables, vitamin K1 is virtually absent in animal products.

5) Tocotrienols--I've been watching the data on this fascinating family of powerful oil-soluble antioxidants unfold for 20 years. Tocotrienols come only from plants. (I recently had an extended conversation with the brilliant biochemist, Dr. Barrie Tan, who is incredibly knowledgeable about tocotrienols, having developed several methods of extraction from plants, including his discovery of the highly concentrated source, annatto. Be sure to watch for future conversations about tocotrienols.)

6) Meats and dairy yield a net acid load--While plant foods are net basic. At the very least, this yields risk for osteoporosis, since acids are ultimately buffered by basic calcium salts from the bones. Tissue and blood pH is a tightly regulated system; veering off just a teensy-weensy bit from the normal pH of 7.4 to an acidic pH of, say, 7.2, leads to . . . death. In short, pH control is very important. A net acid challenge from animal products is a lot like drinking carbonated soda, a huge acid challenge that leads to osteoporosis and other health issues.

Conversely, a pure plant-based diet has its own set of problems. Eating a pure plant-based diet can lead to deficiencies of vitamin B12, omega-3 fatty acids (no, linolenic acid from flaxseed will NOT cut it), vitamin K2, carnitine, and coenzyme Q10.

So, rather than a breakfast of 3-egg omelet with bacon, sausage, cream, and cheese, how about a handful of pecans, some blueberries, and a 2-egg omelet made with basil-olive oil pesto? Or a spinach salad with walnuts, feta cheese, and lots of olive oil?

Fat is not the demon

So my patient, Dane, generously volunteered to be on the Dr. Oz show, as I discussed previously.

What we didn't know, nor did the producer who contacted us mention, that Dane would be counseled by low-fat guru Dr. Dean Ornish on a strict low-fat diet. The teaser introduction essentially tells the entire story.

Ironically, that is the exact opposite of the dietary program that I advocate. I rejected the 10% fat diet long ago after I became a type II diabetic, gained 30 lbs, and suffered miserable deterioration of my cholesterol values on this diet. I also witnessed similar results in many hundreds of people, all following a strict low-fat diet. In fact, elimination of wheat--whole, white, or otherwise--along with limitation or elimination of all other grains has been among the most powerful health strategies I have ever witnessed.

I now regret having subjected my patient to this theatrical misinformation. Dane is a smart cookie--That's probably why he was not allowed more than a "yes" or "no" during Dr. Oz's monologue, else Dane might have pitched in about some ideas that would have tripped Oz and Ornish up.

In their defense, if we took 100 Americans all following a typical 21st century diet of fast food, white bread buns, Coca Cola and other soft drinks, chips, barbecue sauce, and French fries, converting to a plant-based, high-carbohydrate, grain-rich diet is indeed an improvement. People will, at first, lose weight and enjoy an initial response. (The occasional person with the Apo E4 genetic pattern, heterozygote or homozygote, may even enjoy long-term benefits, a topic for another day.)

But the majority of people, in my experience, after an initial positive response to an Ornish-like low-fat, high-carbohydrate diet will either plateau (stay overweight, have low HDL, high triglycerides, plenty of small LDL, and high blood sugars) or deteriorate, much as I did.

Thankfully, Dane has been a good sport about this, understanding that this is essentially show business. I believe he understands that the information was all well-intended and, after all, we are all working towards the same goal: reduction of heart disease risk.

By the way, regardless of which diet you follow, it is, in my view, absurd to believe that diet alone will do it. What about vitamin D normalization, thyroid normalization (thyroid disease is incredibly common), omega-3 fatty acids from fish oil, identification of hidden sources of risk (something that is unlikely in Ornish, since small LDL particles skyrocket on a low-fat diet), postprandial glucoses, etc., all the pieces we focus on to gain control over coronary plaque? Eating green peppers and barley soup alone is not going to do it.

Near-fatal brush with nattokinase

Here is precisely why I have spoken out against nattokinase: People may put faith in this "supplement" when there are virtually no data to support its use in such dangerous conditions as pulmonary embolism.

Pulmonary embolism occurs when a large volume of blood clots in the veins of the pelvis, abdomen, and into the legs. A clot breaks off and lodges in the pulmonary arteries of the lungs. This can be fatal within minutes to hours, the victim struggling to breathe, since oxygen is not transferred to the blood and it causes terrible pain in the chest.

The treatments are fairly obnoxious: intravenous anticoagulants (blood thinners), followed by oral blood thinners like warfarin. While they carry risk of bleeding and other long-term risks, it's better than dying.

Would you bet that a "nutritional supplement" manufacturer's vague claims and lack of data are sufficient proof to treat a life-threatening condition? You're a fool if you are.

Anyone reading these pages knows that I am a vigorous supporter of nutritional supplements. I even consult for the nutritonal supplement industry. But I am also an advocate of TRUTH, not BS.

Here is a woman from England who inquired whether she should stop her husband's warfarin in favor of nattokinase. This is precisely the sort of thing that can happen because of the campaign of misinformation behind nattokinase.


Dr. Davis,

Thank you for your very interesting blogs, which I came across searching for natural alternative treatments to warfarin.

My husband has been following the low carb, high fat, real food regime over the past few years. He got off all the blood pressure and cholesterol drugs and never felt better. He even got his blood sugar down from a recorded high that we are aware of 13 nmol/L (234 mg/dol) to 6.1 nmol/L 109.8 mg/dl).

We were on holiday in the Caribbean. Just before our return home, we did a trip to a neighbouring island that included non-alcoholic fruit punches. They tasted great, but were very sweet. I broke my normal refusal to drink these things, but only had a couple of glasses. (After all, we were on holiday!) My husband believes he consumed around 1.5 litres of the stuff and now realises he was feeding his body a very toxic product – fructose. That night, he had an incredible toxic response and we only got him onto the plane with a visit to the hospital and a pain killer injection.

The symptoms of pulmonary embolism only showed 2 weeks later . . . and warfarin treatment was started. We would both like to use an alternative therapy if we can find someone with experience to provide the support.Do you know of any studies that support alternative options?

Do you know of any practitioners in the England who support a non-drug approach with an understanding of nutrition who we may be able to receive advice and support?

FB
York, England

Glucophobia: The Novel

Just kidding: No novel here. However, there is indeed a story to tell that should scare the pants off you.

If you haven't yet gathered that carbohydrates are a macronutrient nightmare, let me recount the list:


Carbohydrates increase small LDL particles
Or, in the cholesterol-speak most people understand, "carbohydrates increase cholesterol." It's counterintuitive, but carbohydrates increase LDL substantially, far more than any fat.


Carbohydrates increase blood sugar
Eggs don't increase blood sugar, nor do chicken, raw almonds, onions or green peppers. But a bowl of oatmeal will send your blood sugar skywards.


Carbohydrates make you fat
Carbohydrates, whether in the form of wheat flour in your whole wheat bread, sucrose in your ice cream, fructose in your "organic Agave nectar," or high-fructose corn syrup in your dill pickles. They all provoke de novo lipogenesis, or fat formation. They also stimulate insulin, the hormone of fat storage.


Carbohydrates cause glycation
High blood sugar, like the kind that develops after a bowl of oatmeal, triggers glycation, or modification of proteins by glucose (blood sugar). This is how cataracts, kidney disease, and atherosclerotic plaque develop. Small LDL is 8-fold more glycation prone than large LDL, providing a carbohydrate double-whammy.


Your glucose meter remains the single best tool to gauge the quality of your diet. Many people have horror stories of the shocking experiences they've had when they finally get around to checking their postprandial glucose.

Drama with the Dr. Oz Show

A producer from the Dr. Oz show recently contacted my office. They asked whether we could supply them with a volunteer patient from either my practice or the Track Your Plaque program who would be willing to appear on the show and discuss heart disease prevention. They needed someone to commit within 24 hours.

Despite the short notice, we identified a volunteer. He flew to New York the following week where he was interviewed along with several other men and women, all of whom had heart disease (heart attacks, stents, etc.). However, as this young man is very slender and follows most of the Track Your Plaque principles (e.g., vitamin D and omega-3 fatty acid supplementation; no wheat, cornstarch, or sugars, no restriction of fat, etc.), he apparently received less attention than the overweight, I-know-nothing-about-diet interviewees.

Then there was an odd turn of events: Dr. Dean Ornish, apparently a friend of Dr. Oz, will be providing the dietary counseling. The producer had made no mention of Dr. Ornish.

Now that's an odd collision of philosophies: Our Track Your Plaque version of low-carb with the guru of low-fat, Dr. Ornish.

The following week, Dr. Ornish called me and graciously asked whether I was okay with this. I'm not sure just how much he knew about the philosophy I advocate, nor how much I have bashed his program as a destructive approach to diet, nor whether he knew that I gained 30 lbs on the Ornish diet, along with a drop in HDL to 27 mg/dl, increased triglycerides to 350 mg/dl, and type II diabetes that I've talked about on this blog and the Track Your Plaque book and website. I suspect he knew little to none of this.

Anyway, I tried to diplomatically explain that my patient's cause for coronary plaque was small LDL particles that he expressed despite his very slender build, likely from excessive carbohydrates, controlled with carbohydrate restriction. Dr. Ornish maintained his usual arguments: Grains are good, provided they are whole grains, heart disease is "reversed" with his diet program, etc. (I didn't want to challenge him in a phone call and tell him that he never actually reversed coronary plaque, but just reversed endothelial dysfunction. But, as Dr. Ornish is not a cardiologist, I wasn't sure how far his understanding of these issues went.)

We agreed to disagree. This leaves my poor patient in an odd position: Being asked by Dr. Ornish and the Dr. Oz show to follow a low-fat program for the sake of entertainment, or adhering to the advice we follow that has so far served him well, given his small LDL particle size tendencies.

We'll see where this little drama leads.

Response from Nature Made

Here's the response from Nature Made when I emailed them about my concern that there appears to be no vitamin D in their vitamin D gelcaps.

It is the usually CYA corporate-speak that says nothing. The grammatical errors make it clear that this was a "canned" response.



Date: April 9, 2010
From: Marissa Reyes, Consumer Affairs Department
Subject: Reference #346236

Dear William Davis, MD:

We recently received your e-mail regarding Nature Made products. We regret to
hear that the quality standards of our company. [?]

Our company is called Pharmavite, and we manufacture Nature Made nutritional
supplements. We have been in business since 1971. We are committed to quality
control, and have very high quality standards. Our Quality Control personnel
sample and test all raw materials as they enter our plant, and again assay the
finished product, before final packaging.

Dietary Supplements are regulated under the FDA through DSHEA (Dietary
Supplement Health & Education Act of 1994). The United States Pharmacopoeia
(USP) establishes standards for the composition of drugs and nutritional
supplements. This voluntary non governmental organization was set up in 1820
and has officially been recognized by federal law since 1906. Standards
established by USP for products are legally enforceable by the FDA. At
Pharmavite we participate in the USP Dietary Supplement Verification Program
(DSVP). Many of our products have earned the DSVP seal and additional products
are currently being evaluated. Our DSVP certified products will have the DSVP
seal on the product label.

Our Nature Made Vitamin D 400 IU tablets have been reviewed by the USP and bears
the DSVP symbol on the label. Although the USP has not reviewed all of the
Nature Made Vitamin D supplements, all of our products go through the same
rigorous quality testing at Pharmavite. The products which have earned the seal
help us to demonstrate the high quality of our products.

We would like to look into the product(s) your patients have been using. If you
could provide the UPC and lot numbers of the product(s), we will be happy to
review our records. In addition, if you would like us to test the product(s)
that you currently have, we will be pleased to send a prepaid postage mailer so
you may return the product(s) to us so that our Quality Control Department can
examine it. Please let us know if you would like us to send you the prepaid
postage mailer.

We thank you for contacting us and hope that you will continue to use and enjoy
Nature Made products with complete confidence.

Sincerely,
Marissa Reyes
Consumer Affairs Coordinator
Pharmavite, LLC
MR:346236-10



Patients who come to the office do not provide me with the bottles nor lot numbers. In past, when I've gone to the trouble of doing this (with other companies, not Nature Made), it has come to nothing helpful. The information gets passed on to the company and we hear nothing and never learn if there was a problem, or receive some more corporate-speak letter saying everything was fine. This is obviously a liability-avoidance tactic: Admitting that something was wrong would open them up to legal risk. So, frankly, I can't be bothered.

So we are left with the unsatisfying experience of relying on street-level experiences.

For now, my advice: Avoid Nature Made vitamin D. Too many people have had blood tests demonstrating that they are not obtaining any vitamin D.

By the way, the Nature Made brand of fish oil is among the very few problem brands of fish oil we've encountered. Fish oil should be only mildly fish in smell and generally should not cause stomach upset and excessive belching if properly purified. Nature Made is excessively fishy when you smell it, suggesting oxidation. We've had repeated (dozens) of patients who have experienced difficulties with this brand. Rather than dealing with the frustrating gobbledy-gook of this company, just avoid their products.

What to Eat: The diet is defined by small LDL

I approach diet from the perspective of small LDL particles.

Small LDL particles have exploded in frequency and severity in Americans. It is not at all uncommon to see 70% or more small LDL particles (i.e., 70% of total LDL particle number or Apo B) on lipoprotein testing. (I saw two people today who began with over 95% small LDL.)

Small LDL particles are:
--More likely to persist in the bloodstream longer than large LDL particles.
--More likely to adhere to components of atherosclerotic plaque.
--More likely to gain entry to plaque.
--More likely to be taken up by inflammatory white blood cells which, in turn, become the mast cells that fill coronary plaque.
--More likely to be oxidized.
--More likely to be glycated (8-fold more likely than large)

To add insult to injury, foods that trigger small LDL formation--i.e., carbohydrates--also cause high postprandial blood sugars. High postprandial blood sugars, in turn, glycate small LDL. That combination of events accelerates 1) plaque growth, 2) plaque instability, and 3) aging.

So carbohydrates trigger this sequence, carbohydrates of all stripes and colors. Not just "white" carbohydrates, but ALL carbohydrates. It's all a matter of degree and quantity. So, yes, even quinoa, bulghur, and sorghum trigger this process. I've only recently appreciated just how bad oats and oatmeal are in this regard--really bad.

Foods that trigger small LDL also trigger higher blood sugars; foods that trigger higher blood sugars also trigger small LDL. Small LDL and blood sugar are two different things, but they track each other very closely.

So, in the Track Your Plaque approach to diet, we craft diet based on these simple principles:

1) Eliminate wheat, cornstarch, and sugars--These are the most flagrant triggers of small LDL, blood sugar, and, therefore, LDL glycation.
2) The inclusion of other carbohydrates, such as oatmeal, quinoa, rye, etc. depends on individual sensitivity. Individual sensitivity is best gauged by assessing one-hour postprandial glucose.

Stay tuned for more in this series. Also, Track Your Plaque Members: We will be having an in-depth webinar detailing more on thees principles in the next couple of weeks.

Is it or isn't it vitamin D?

Jackie takes 10,000 units of vitamin D(3) per day as a gelcap.

Her starting 25-hydroxy vitamin D blood level was 18.1 ng/ml. Severe deficiency, no surprise.

On her 10,000 units per day, Vitamin Shoppe brand, her 25-hydroxy vitamin D level was 76.2 ng/ml--perfect. It stayed in this range for about two years.

She then changed to the Nature Made brand gelcaps she picked up at Walgreen's. Repeat 25-hydroxy vitamin D level: 23 ng/ml.

This has now happened with five different people, all taking the Nature Made brand.

If you are taking this brand of vitamin D, please be on the alert. You might consider a 25-hydroxy vitamin D blood level to be sure it actually has the vitamin D it's supposed to have.

Or, change brands.
All posts by william-davis

Increased blood calcium and vitamin D

Conventional advice tells us to supplement calcium, 1200 mg per day, to preserve bone health and reduce blood pressure.

Here's a curious observation I've now witnessed a number of times: Some people who supplement this dose of calcium while also supplementing vitamin D sufficient to increase 25-hydroxy vitamin D blood levels to 60-70 ng/ml develop abnormally high levels of blood calcium, hypercalcemia.

This makes sense when you realize that intestinal absorption of calcium doubles or quadruples when vitamin D approaches desirable levels. Full restoration of vitamin D therefore causes a large quantity of calcium to be absorbed, more than you may need. In addition, two studies from New Zealand suggest that 1200-1300 mg calcium with vitamin D per day doubles heart attack risk.

We have 20 years of clinical studies demonstrating the very small benefits of supplementing calcium to stop or slow the deterioration of bone density (osteopenia, osteoporosis). These studies were performed with no vitamin D or with trivial doses, too small to make a difference. I believe those data have been made irrelevant in the modern age in which we "normalize" vitamin D.

Should hypercalcemia develop, it is not good for you. Over long periods of time, abnormal calcium deposition can occur, leading to kidney stones, atherosclerosis, and arthritis.

Until we have clarification on this issue, I have been advising patients to take no more than 600 mg calcium supplements per day. I suspect, however, that the vast majority of us require no calcium at all, provided an overall healthy diet is followed, especially one that does not leach out bone calcium. This means no foods like those made with wheat or containing powerful acids, such as those in carbonated drinks.

Heart health consultation with Dr. Joe D. Goldstrich

Cardiologist, nutritionist, and lipidologist, Dr. Joe D. Goldstrich, is a frequent contributor to the Track Your Plaque Forum, where we discuss the full range of issues relevant to coronary health and coronary plaque reversal.

I have come to value Dr. Goldstrich's unique insights, especially in nutrition. Formerly National Director of Education and Community Programs for the American Heart Association and a physician at the Pritikin Center, his dietary philosophy has evolved away from low-fat and towards a low-carbohydrate focus, much as we use in Track Your Plaque. Like TYP, Dr. Goldstrich is always searching for better answers to gain control over coronary health. His unique blend of ideas and background has helped us craft new ideas and strategies. Dr. Goldstrich has proven especially adept at understanding how to incorporate new findings from clinical studies in our framework of coronary atherosclerotic plaque management strategies.

Dr. Goldstrich is offering to share his expertise with our online community. If you would like a one-on-one phone consultation with Dr. Goldstrich, you can arrange to speak with him at his HealthyHeartConsultant.com website.

Wheat aftermath

Following my 4 oz whole wheat misadventure that yielded the sky-high blood sugar of 167 mg/dl, compared to einkorn wheat's 110 mg/dl, I suffered through a 36-hour period of misery.

After I obtained the blood sugar of 167 mg/dl, I biked hard for one hour. This yielded a blood sugar back down in the 80s. I felt spacey in the ensuing few hours, as well as a little queasy. However, about 12 hours later, I awoke with overwhelming nausea along with that hypersalivating thing that happens just prior to vomiting. It did not come to that, but persisted all through the following day.

The next morning, I could barely concentrate. Trying to read a study (admittedly on the complex topic of agricultural genetics), I had to read each paragraph 4 or 5 times. Abdominal cramps and a bloated feeling also developed, though I was able to eat.

The 2nd night was filled with incredibly vivid dreams and intermittent sleeplessless. I awoke about 5 times through the night, but periods of sleep were filled with detailed, colorful dreams. I dreamt that a large corporation was secretly trying to gain control over the world's water supply, and I snuck onto a complex underwater vessel that was exploring and mapping the coastline of the Great Lakes in preparation. Weird.

I recognized these odd feelings as various facets of wheat intolerance, since they were all reminiscent of feelings I used to experience before I removed wheat from my diet. They were amplified and compressed, likely because I had been wheat-free for so long.

The odd thing is that, despite the modest blood sugar effect of my einkorn experience, none of the gastrointestinal or neurologic effects of wheat developed. So far, two other people with acute gastrointestinal wheat sensitivities have consumed our einkorn bread, also without reproduction of their usual symptoms.

Einkorn contains gluten, though the structure of the many gluten proteins of einkorn differs from that of the wheat bread I consumed, an example of modern Triticum aestivum. 14-chromosome einkorn carries what biologists call the "A" genome, while Triticum aestivum has the combines genomes of 3 plants, the combination of the A, B, and D genomes. It is the D genome that contains the genes coding for the most obnoxious, immunogenic forms of gluten.

So einkorn may not be entirely benign, but it is a good deal less obnoxious than modern Triticum aestivum.

I am awaiting the reports from a few other people on their experiences.

In search of wheat: Einkorn and blood sugar

There are three basic aspects of wheat's adverse health effects: immune activation (e.g., celiac disease), neurologic implications (e.g., schizophrenia and ADHD), and blood sugar effects.

Among the questions I'd like answered is whether ancient wheat, such as the einkorn grain I obtained from Eli Rogosa, triggers blood sugar like modern wheat.

So I conducted a simple experiment on myself. On an empty stomach, I ate 4 oz of einkorn bread. On another occasion I ate 4 oz of bread that dietitian, Margaret Pfeiffer, made with whole wheat flour bought at the grocery store. Both flours were finely ground and nothing was added beyond water, yeast, olive oil, and a touch of salt.

Here's what happened:

Einkorn wheat bread:

Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 110 mg/dl

Conventional wheat bread
Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 167 mg/dl

The difference shocked me. I expected a difference between the two, but not that much.

After the conventional wheat, I also felt weird: a little queasy, some acid in the back of my throat, a little spacey. I biked for an hour solid to reduce my blood sugar back to its starting level.

I'm awaiting the experiences of others, but I'm tantalized by the possibility that, while einkorn is still a source of carbohydrates, perhaps it is one of an entirely different variety than modern Triticum aestivum wheat. The striking difference in blood sugar effects make me wonder if einkorn eaten in small quantities can keep us below the Advanced Glycation End-Product threshold.
 

In search of wheat: We bake einkorn bread

With the assistance of dietitian and health educator, Margaret Pfeiffer,MS RD CD, author of Smart 4 Your Heart and very capable chef and breadmaker (previously, before she gave up wheat), we made a loaf of bread using Eli Rogosa's einkorn wheat. Recall that einkorn wheat is the primordial 14-chromosome wheat similar to the wild wheat harvested by Neolithic humans and eaten as porridge.

The essential question: Has wheat always been bad for humans or have the thousands of hybridization experiments of the last 50 years changed the structure of gluten and other proteins in Triticum aestivum and turned the "staff of life" into poison? I turn to einkorn wheat, the "original" wheat unaltered by human manipulations, to figure this out. While einkorn wheat is still a source of carbohydrates, is it something we might indulge in once in a while without triggering the adverse phenomena associated with modern wheat?   

Here's what we did:

This is the einkorn grain as we received it from Eli's farm. This was enough to make one loaf (approximately 3 cups).











The einkorn grain is a dark golden color. I tried chewing them. They taste slightly nutty. They soften as they sit in your mouth.





Here's Margaret putting the einkorn grain into the electric grinder.









We tried to grind the grain by hand with mortar and pestle, but this proved far more laborious than I anticipated. After about 15 minutes of grinding, this is what I got:



Barely 2 tablespoons. That's when Margaret fired up the electric grinder. (I can't imagine having to grind up enough flour by hand for an entire family. Perhaps that's why ancient cultures were thin despite eating wheat. They were just exhausted!)

We added water, salt, and yeast, then put the mix into an electric breadmaker to knead the dough and keep it warm.

We let the dough rise for 90 minutes, much longer than conventional dough. The einkorn dough "rose" very little. Margaret tells me that most dough made with conventional flour rises to double its size. The einkorn dough increased no more than 20-30%.

The einkorn dough also distinctly smelled like peanut butter.





After rising, we baked the dough at 350 degrees F for 30 minutes. This is the final product.

Because I want to gauge health effects, not taste, the bread we made had no added sugar or anything else to modify taste or physiologic effect.

On first tasting, the einkorn bread is mildly nutty and heavy. It had an unusual sour or astringent taste at the end, but overall tasted quite good.

Next: What happens when we eat it? I'm going to give the einkorn bread (I've got to make some more) to people who experience acute reactions to conventional wheat and see if the einkorn does the same. I will also assess blood sugar effects since, after all, hybridizations or no, it is still a carbohydrate.



Margaret Pfeiffer's book is available on Amazon:

Ezekiel said what?

Some people are reluctant to give up wheat because it is talked about in the Bible. But the wheat of the Bible is not the same as the wheat of today. (See In search of wheat and Emmer, einkorn and agribusiness.) Comparing einkorn to modern wheat, for example, means a difference of chromosome number (14 chromosomes in einkorn vs. 42 chromosomes in modern strains of Triticum aestivum), thousands of genes, and differing gluten content and structure.

How about Ezekiel bread, the sprouted wheat bread that is purported to be based on a "recipe" articulated in the Bible?

Despite the claims of lower glycemic index, we've had bad experiences with this product, with triggering of high blood sugars, small LDL, and triglycerides not much different from conventional bread.

David Rostollan of Health for Life sent me this interesting perspective on Ezekiel bread from an article he wrote about wheat and the Bible. David argues that the entire concept of Ezekiel bread is based on a flawed interpretation.

"I Want to Eat the Food in the Bible."


Are you sure about that?

Some people, still wanting to be faithful to the Bible, will discard the "no grain/wheat" message on the basis of biblical example. After all, God told Ezekiel to make bread, he gave the Israelites "bread from heaven," and then Jesus (who is called the "Bread of Life"!) multiplied bread, and even instituted the New Covenant with what? Bread and wine! If you're going to live the Bible, it seems that bread and/or wheat is going to play a part.

But this is unnecessary. Sure, the Bible can and does tell us how to live, but this doesn't mean that everything in the Bible is meant to be copied verbatim. Applying the Bible to our lives requires wisdom, not a Xerox machine.

The Bible was written in a historical context, and the setting happened to be an agricultural one. Because of this, the language used to describe blessing spoke of things like fields full of grain, or barns overflowing with wheat. Had the Bible been written in the context of a hunter-gatherer culture, the language describing blessing probably would have been about the abundance of wild game, or baskets full of vegetables. Whatever is most valuable in your time and in your culture is a blessing. God accommodated His message to the culture as it existed at the time. This is done throughout Scripture.

There is a danger, then, in merely copying what the Bible says, instead of extracting the principles by which to live. Take the above example of Ezekiel, for instance. There's a whole product line in health food stores called "Ezekiel Bread" that supposedly copies the recipe given in Ezekiel 4:9. This is from the website:

"Inspired by the Holy Scripture verse Ezekiel 4:9., 'Take also unto thee Wheat, and Barley, and beans, and lentils, and millet, and Spelt, and put them in one vessel, and make bread of it...'"

Believing that this "recipe" has some kind of special power just because it's in the Bible is ridiculous. How ridiculous is it? I'll tell you in a moment, but first let me say that this is why it's so important not to confuse descriptives with prescriptives. Is the Bible telling a story, or is it telling us to do something? We would be well-advised not to confuse the two.

In the case of the Ezekiel Bread, what is going on in the passage? There's a siege going on, with impending famine, and Ezekiel is consigned to eating what was considered back then to be some of the worst possible food. It was basically animal chow. But that's not the worst thing going on in this passage. Apparently, when the makers of Ezekiel Bread were gleaning their inspiration for the perfect recipe, they stopped short
of verse 12:

"And thou shalt eat it as barley cakes, and thou shalt bake it with dung that cometh out of man, in their sight."

Um...what? Well, there was a good reason for this. God was judging His people, and by polluting this really bad bread with dung (which was a violation of Mosaic law; Lev. 5:3), He was saying that they were no different from the unclean Gentiles.

So why would we take this story and extrapolate a bread recipe from it? Beats me. If you were going to be consistent, though, here's what you'd have to end up with:



Let that be a lesson to you. We don't just go and do everything that we see in the Bible.

Low-carb gynecologist

I met infertility specialist, Dr. Michael Fox, on Jimmy Moore's low-carb cruise just this past March.

Dr. Fox is quiet and unassuming, but had incredible things to say about his experience with carbohydrate restriction in female infertility and pregnancy. While readers of The Heart Scan Blog already know that I advocate a diet free of wheat, cornstarch, and sugar for heart health and correction of multiple lipoprotein abnormalities, it was fascinating to hear how a similar approach seems to yield extraordinary benefits in this entirely unrelated area of female health. Obviously, female infertility and pregnancy are unrelated to heart health, but the extraordinary benefits witnessed by Dr. Fox in this area suggest that some fundamental lessons in human physiology can be learned. The results are so incredible that we are all sure to hear more about this approach as experience grows.

So I tracked Dr. Fox down in his busy Jacksonville, Florida practice to fill us in on some details.

WD: Dr. Fox, could you tell us something about yourself and what led you to use carbohydrate restriction in your female patients?

MF: I have been in practice as a reproductive endocrinologist for 15 years. During that time, I have seen our specialty move from a broad based practice of reproductive endocrinology to a narrow IVF [in vitro fertilization] focus, with patients being pushed through IVF in a cookie-cutter fashion without any emphasis on non-medical therapy.

Our focus has been to remain as a broad practice where we individualize care and attempt in every case to achieve pregnancy short of IVF. Five years ago, this continued quest for better care led us into the insulin resistance, low-carbohydrate metabolic world that has transformed our practice, although our practice offers all aspects of reproductive endocrinology including sub-specialized minimally invasive surgery, and all available infertility options.


WD: I have been intrigued by your comments about improved fertility with the low-carb diet. Could you elaborate on this?

MF: Yes, five years ago, as more information regarding Polycystic Ovarian Disease or Syndrome (PCOD/S) and its relationship to insulin resistance (high insulin levels) was emerging, we had a simple realization. As we've known for some time, insulin stimulates excess male hormone levels in the ovary, which disrupts ovulation and fertility. Then our job was to lower or virtually eliminate high insulin levels. Again, in simple fashion, we looked at physiology and realized that insulin is released only in response to dietary carbohydrates. Thus, elimination of carbohydrates should resolve the problem. This, in fact, is the effect that we have seen.

In our previous approaches to PCOD, we utilized oral ovulation medicines generating pregnancy rates in the 40% range overall. Now, with the nutritional approach, for those patients that follow our recommendations, our pregnancy rates are over 90%! This has dramatically reduced the need for in vitro fertilization in these patients.

To extend this idea further, we first started with relative low-carbohydrate diets, such as the South Beach diet, but quickly realized this didn't produce a metabolic effect. Over time, it has borne out that only the very low-carbohydrate diet (VLCD) approach produces significant metabolic change. Our impression then was that the current U.S. nutritional exposure probably increases insulin levels and that this has a detrimental effect on fertility.

To counter this effect, we now recommend the VLCD to all fertility patients and their spouses. The pregnancy rates do seem much better overall, as well as seeing a reduction in miscarriage rates. For the first time at our national meeting last year, there were three articles that showed improved pregnancy rates in patients without PCOD or insulin resistance in IVF when Glucophage was used. This drug decreases insulin. This supports the idea that our entire population is subjected to fertility-reducing high-carbohydrate diet.

WD: Do you see any other changes in these patients on the diet?

MF: Yes. All metabolic parameters, as well as many common complaints, improve. Cholesterol and triglyceride levels improve, while "good" HDL cholesterol levels increase. Weight drops at a pace of 12 lbs per month very steadily and we have many many patients who have experienced 50lb wt loss. Blood pressure decreases steadily in these patients and we are often able to get them off of cholesterol and blood pressure medicines. Common symptoms such as anxiety, sleep disturbances, decreased energy, migraine headaches and depression all dramatically improve. Again we can often get patients off depression and migraine suppression medications. So this approach helps in a multitude of areas.



WD: I was also interested in hearing more about your experience with morning sickness and the effects of a low-carb diet. Could you tell us more about this? Also, any thoughts on why this happens?

MF: As we continued to expand our thoughts about VLCD and fertility/pregnancy, we began to extend the nutritional approach into pregnancy. We know that pregnancy hormones dramatically worsen insulin resistance that is responsible for the condition, gestational diabetes. If insulin resistance is worsened, then reactive hypoglycemia is worsened. One of the biggest symptoms of hypoglycemia is nausea. So, in response to this, we have counseled our patients on the diet in pregnancy and have found a dramatic reduction in nausea. We recommend snacking every two hours in pregnancy.

The other "traditional" issue in pregnancy are cravings. These also likely stem from hypoglycemia. I have had many husbands tell us later that their wives, in contrast to friends etc, were calm and not moody or anxious during their pregnancies. Hypoglycemia probably is a serious issue for the fetus as well and may be the "signal" that turns on the insulin-resistant gene. Many theorists feel this might be an activated gene during the pregnancy.


WD: Do you use any unique approaches to the low-carbohydrate approach, e.g., inclusion of dairy, meal frequency, "induction" strategies (i.e., induction to the diet, not of labor!), etc.?

MF: Yes. As I'm sure everyone who works in the VLCD world does, we also have some tricks to make this work better. My biggest push, although hard to get patients to agree, is to see a counselor along with our follow-up in order to deal with "addictive behaviors" and "stress eating" that so many of our patients relate to us. Good stress management and cognitive behavioral therapy go a long way in helping this become a permanent change.

We also really push frequent calorie intake or "snacking." I think again that hypoglycemia produces an inborn drive to "cure" or "fix" starvation and leads to dramatic overeating. We have a short list of snacks that we recommend. The concept of hunger is offered as a failure of the program. We aim to eliminate hunger, as it represents hypoglycemia. The analogy I use is, if you drove your car until you ran out of gas before you ever sought to find gas, your life would be miserable. So it is the same with your metabolic engine: If you let it run out, the measures your system takes to fix it are very detrimental to life and certainly to nutritional health.

Our other big push is fat. People can wrap themselves around protein and vegetables, but they totally miss the high-fat (animal fat) part of the conversation. We have to really push that aspect. In regards to dairy, we allow for non-processed cheeses and minimal milk. An alternative is to mix about 4 oz whole milk with 4 oz of heavy whipping and 4 oz of water to create a "milk" with less sugar. Similarly, shakes and smoothies can be made with heavy whipping cream with pure whey protein powder added to create a liquid meal for those who "don't have time" to cook.


WD: Thanks, Dr. Fox. We look forward to hearing more about your approach in future.

Contact information:

Michael D. Fox, MD
Jacksonville Center
Reproductive Medicine
www.JCRM.org
Phone 904-493-2229

Track Your Plaque reduces healthcare costs 35%

Allow me to wear my Track Your Plaque hat for this post.

Mr. Richard Rawle is CEO of Utah company, Tosh, Inc. Mr. Rawle has been an avid follower of the Track Your Plaque program and has introduced the program to company employees. Here's what he has to say about the experience:

“Our company has been utilizing the principles of TYP [Track Your Plaque] for over a year and has experienced great results that have positively impacted the lives of our employees and our health care costs.

Since we began our wellness program, we have presented the TYP diet and lifestyle guidelines to all of our employees and their families. Although the overwhelming majority of our employees do not have cardiovascular issues, the preventative nature of TYP is too important not to be utilized. The TYP principles along with our increased focus on healthy living have already changed our group’s blood chemistry. HDL levels in particular have increased significantly and resulted in a large percentage of our employees having HDL levels of 60 or higher. Vitamin D levels have substantially increased and LDL levels have significantly decreased in the majority of our employees. Subsequently, in the 12 months just ended, our health care costs are some 35% less than other groups of comparable size and age.

I believe the TYP program has been an integral part of the success of our company's vast improvement in employee health/wellness, resulting in significant health care cost reductions."

Richard Rawle
CEO Tosh Inc.


Track Your Plaque saves lives. Track Your Plaque also saves money . . . lots of it. Despite the upfront costs of some additional blood testing and a heart scan, the dramatic reduction in need for medications, reduced heart attack, diabetes, and many other chronic conditions add up to a huge cost savings, much as Tosh, Inc. employees have enjoyed.

The Federal government has been looking towards large hospital systems to lead the way in healthcare delivery, systems that employ their physicians and possess economies of scale. But I say the answer to reducing healthcare costs will NEVER be found in hospital systems. Healthcare cost savings will be realized by delivering truly effective health solutions directly to people themselves, much as we do in Track Your Plaque.

In search of wheat

Many people ask: "How can wheat be bad if it's in the Bible?"

Wheat is indeed mentioned many times in the Bible, sometimes literally as bread, sometimes metaphorically for times of plenty or freedom from starvation. Moses declared the Promised Land "a land of wheat, and barley, and vines, and fig trees, and pomegranates; a land of oil olive, and honey" (Deuteronomy 8:8).

Wheat is a fixture of religious ceremony: sacramental bread in the Eucharist of the Christian church, the host of the Holy Communion in the Catholic church, matzoh for Jewish Passover, barbari and sangak are often part of Muslim ritual. Wheat products have played such roles for millenia.

So how can wheat be bad?

What we call wheat today is quite different from the wheat of Biblical times. Emmer and einkorn wheat were the original grains harvested from wild growths, then cultivated. Triticum aestivum, the natural hybrid of emmer and goatgrass, also entered the picture, gradually replacing emmer and einkorn.

The 25,000+ wheat strains now populating the farmlands of the world are considerably different from the bread wheat of Egyptians, different in gluten content, different in gluten structure, different in dozens of other non-gluten proteins, different in carbohydrate content. Modern wheat has been hybridized, introgressed, and back-bred to increase yield, make a shorter stalk in order to hold up to greater seed yield, along with many other characteristics. Much of the genetic work to create modern wheat strains are well-intended to feed the world, as well as to provide patent-protected seeds for agribusiness.

What is not clear to me is whether original emmer, einkorn, and Triticum aestivum share the adverse health effects of modern wheat.

Make no mistake about it: Modern wheat underlies an incredible range of modern illnesses. But do these primitive wheats, especially the granddaddy of them all, einkorn, also share these effects or is it a safe alternative--if you can get it?

I've ordered 2 lb of einkorn grain, unground, from Massachusetts organic farmer, Eli Rogosa, who obtained einkorn seed from the Golan Heights in the Middle East. We will be hand-grinding the wheat and making einkorn bread. We will eat it and see what happens.

Super-carbohydrate

Wheat starches are composed of polymers (repeating chains) of the sugar, glucose. 75% of wheat carbohydrate is the chain of branching glucose units, amylopectin, and 25% is the linear chain of glucose units, amylose.

Both amylopectin and amylose are digested by the salivary and stomach enzyme, amylase, in the human gastrointestinal tract. Amylopectin is more efficiently digested to glucose, while amylose is less efficiently digested, some of it making its way to the colon undigested.

Amylopectin is therefore the “complex carbohydrate” in wheat that is most closely linked to its blood sugar-increasing effect. But not all amylopectin is created equal. The structure of amylopectin varies depending on its source, differing in its branching structure and thereby efficiency of amylase accessibility.

Legumes like kidney beans contain amylopectin C, the least digestible—hence the gas characteristic of beans, since undigested amylopectin fragments make their way to the colon, whereupon colonic bacteria feast on the undigested starches and generate gas, making the sugars unavailable for you to absorb.

Amylopectin B is the form found in bananas and potatoes and, while more digestible than bean amylopectin C, still resists digestion to some degree.

The most digestible is amylopectin A, the form found in wheat. Because it is the most readily digested by amylase, it is the form that most enthusiastically increases blood sugar. This explains why, gram for gram, wheat increases blood sugar to a much greater degree than, say, chickpeas.

The amylopectin A of wheat products, “complex” or no, might be regarded as a super-carbohydrate, a form of highly digestible carbohydrate that is more efficiently converted to blood sugar than nearly all other carbohydrate foods.
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.