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White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.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

 

Almonds are the new wheat

Once you eliminate this genetically-altered Frankengrain called modern wheat, the diet should center around vegetables, nuts, healthy oils like olive and coconut, fish, meats, cheese, olives, avocados and other real whole foods. This is, in fact, the diet that I have advocated in my heart disease prevention practice, as well as my online program for prevention and reversal of heart disease.

But what if you'd like a piece of cheesecake or a nice slice of dessert bread---but you don't want to gain two pounds, spend 48 hours in the bathroom suffering with diarrhea and cramps, 3 weeks of joint pains and leg swelling, wade through mental "fog," anxiety, and rage just because you had that momentary indulgence---as you would with wheat?

That's why I've been focusing on recipes that allow you to have something familiar, e.g., chocolate coconut bread or biscotti, but using ingredients that will not generate the metabolic contortions triggered by wheat.

On perusing these recipes, you will notice that there are recurring ingredient themes. Many of the same ingredients pop up time and again. Among the most frequent, versatile, user-friendly, and tasty: Almonds.

You can use almonds as ground whole almonds, ground blanched almonds for a finer texture, ground roasted almonds, almond butter (though, for maximum health benefits, I prefer the ground whole almonds). Ground almonds allow you to recreate muffins, breads, scones, pizza crust, pie crust, biscotti, and cookies with health benefits that exceed that of whole wheat---but with none of the downside: no weight gain, no high blood sugar, no triggering of small LDL particles (#1 cause of heart disease in the U.S.), no accumulation of visceral fat, no appetite stimulation.

In short, you just have your chocolate almond biscotti or mocha cupcake and enjoy it, no health price to pay. So I call almonds the new wheat, except better.

Being regular is dangerous to your health

No, I'm not referring to your daily morning ritual in the bathroom. I'm talking about heart rate.

Counterintuitively, a perfectly regular heart rate is a marker of poor health. People with perfect regularity of heart rate have more heart attacks, for instance.

Regularity of heart rate occurs more commonly in people with hypertension and other metabolic derangements, and it signals increased risk for both heart attack and death. A perfectly regular heart rate, i.e., no variation in the time interval from beat to beat, suggests that the parasympathetic nervous system, the component of automatic ("autonomic") nervous system control that is associated with the relaxation response, feelings of well-being, quiet, and relaxation, is weak. It also means that the opposing sympathetic nervous sytem that regulates the "fight or flight," adrenaline-like response is allowed to be dominant. Dominance of the sympathetic over the parasympathetic system generates regularity of heart rate. Heart rate also tends to be faster, e.g., 85 beats per minutes rather than 55 or 60 beats per minute. So perfect regularity, as well as increased rate, is undesirable.

What we want is irregularity of heart rate. But not irregularity that occurs chaotically with no rhyme or reason. More precisely, we want variability in heart rate. And we want variability to occur in synchrony with breathing, i.e., the respiratory cycle.

The ideal response is:

1) increase in heart rate with inspiration

2) decrease in heart rate with expiration.

Heart rate in healthy people typically varies 15-20 beats per minute within the respiratory cycle, e.g., 60 bpm at end-exhalation, 80 bpm at end-inspiration.

Restoration of increased heart rate variability is associated with reduced blood pressure, reduced blood sugars (HbA1c), reduced inflammatory markers and cortisol (associated with stress), even an increase in DHEA levels. Feelings of well-being and calm also develop.

Among the strategies to consider to restore heightened heart rate variability and slowed heart rate include:

--Omega-3 fatty acid supplementation
--Exercise
--Weight loss
--Deep breathing exercises
--Meditation, prayer, and biofeedback

For our Track Your Plaque purposes, we are folding in the HeartMath strategies, i.e., use of a heart rate monitor that calculates heart rate variability in the context of respiratory cycle. If you've not already done so, take a look at the two Special Reports devoted to this topic on the Track Your Plaque website.

You mean weight loss is hazardous to your health?

In my last Heart Scan Blog post, What is this wacky thing called weight loss?, I discussed how weight loss is associated with distortions in cholesterol and blood sugar values that can be very confusing, often leading your doctor to wrongly and unnecessarily prescribe drugs--since he/she likely rarely sees weight loss.

Blog reader, Donald K., posted his enlightening story:

I experienced this very thing.

After losing serious weight from the eliminating wheat, processed, and sugary foods (1 year in total) I lost 130 pounds. When I was nearly finished I went to see my doctor. He wanted to put me on statins. I explained to him how the data does not support application to me (no evidence of heart disease) and I got the mantra about standards of practice, etc, etc. I held my ground and decided I am much happier eating dairy, eggs, grass fed beef, wild caught fish, and as much raw foods (nuts, veggies, fruits) as my body desires to treat my health parameters.

Maintaining weight, it is easy. My BMI (23 down from 40) has remained constant for a few months now. You are right: metabolic processes definitely change. I no longer have sensations of glucose fluctuations or an uncontrolled appetite. I can only imagine the improved hormone regulation and metabolic communication going on inside my body.

The symptoms from obesity, all gone. Goodbye sleep apnea, hypertension, hemorrhoids, arrhythmias, gastroinestinal disruptions, smelly body, chaffing thighs, and others not mentioned. The positive effects are just as dramatic, but I don’t want to ramble on.

Weight loss? What is it? Getting your life back!


Brace yourself: If you are following the nutrition advice posted here and in the Track Your Plaque program, or the discussion I've initiated in Wheat Belly, then you may find yourself in the very same health predicament as Donald. Arm yourself to protect yourself against the drug-wielding ways of doctors. No, weight loss to achieve ideal weight is definitely not bad for health. But your doctor's misinterpretation of its effects can be!

What is this wacky thing called "weight loss"?

I've discussed this before, but it has proven such an (encouragingly!) frequent issue that I thought it was worth discussing once again.

What happens when you lose weight?

The process of weight loss is characterized by multiple shifts in metabolic patterns that can be confusing. To the uninitiated eye, weight loss can look like a disastrous distortion in metabolism. The naive doctor on seeing your lab values, for instance, might insist you take a statin drug, a fibrate like Tricor (to reduce triglycerides or increase HDL), or simply berate you for your bad health habits--when it's actually a good thing you've accomplished.

So when you lose weight, say, 30 pounds in 3 months, what have you accomplished?

Energy stored as fat, especially from visceral fat stores, is mobilized into the bloodstream. It floods the bloodstream as fatty acids and triglycerides. These fatty acids and triglycerides don't occur in isolation, but interact with other particles and metabolic patterns. The resulting blood patterns include:

--Increased triglycerides--An increase in triglycerides, for instance, from 90 mg/dl to 200 mg/dl in the midst of weight loss is common.

--Reduced HDL--The flood of triglycerides leads to increased degradation of HDL, thus a drop. A drop in HDL from, say, 40 mg/dl to 27 mg/dl--very frightening to people--is exceptionally common.

--Increased blood sugar--The flood of fatty acids and triglycerides results in insulin resistance, leading to higher blood sugars. It is not uncommon for someone with pre-diabetes to develop diabetic-range blood sugars, or a non-diabetic to show pre-diabetic blood sugars.

--Increased small LDL particles--Though small LDL is highly variable during weight loss. When it does happen, it's probably from the interaction of VLDL (triglycerides) with LDL particles and the reaction that overloads LDL particles with triglycerides and conversion to small LDL particles.

So why don't doctors often recognize these patterns when a patient loses weight? Because they rarely see it. Most of my colleagues are accustomed to having patients come back with weight gain, getting heavier and heavier each time. Lose weight? Impossible! So they just don't recognize weight loss effects when they see it. As followers of The Heart Scan Blog know, a frequent conversation around here is "Am I too skinny?" or "How do I stop losing weight?"

The solution: Be patient. Be patient and wait about two months after a weight plateau has been achieved. That's when the numbers "settle down" and you see marked drops in triglycerides, increases in HDL, drops in blood sugar, reductions in small LDL.

As with many things, it's all about timing.

Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Even moore from Jimmy Moore

The ubiquitous and irrepressible Jimmy Moore posted even more commentary about the Wheat Belly phenomenon here, what he calls "The Wheat Belly Bonanza."

Is low-carb really, at its core, little more than elimination of wheat? Sure, corn, rice, and sugar exert deleterious effects. But the dominant effect--by far--is the elimination of wheat. So is the low-carb movement really, at its core, a wheat-elimination movement?

Food (non-wheat-containing, of course) for thought.

Heart Scans: An Interview with Jimmy Moore

My friend, Jimmy Moore, of The Livin' La Vida Low Carb Show, posted this video of an interview I did with him.

I provide some background on how heart scanning came about and how it led to the creation of the Track Your Plaque program.

It reminds me how far we've come over the 8 years since the program got started. From its modest start as just an information resource to help people understand their heart scan score, to a comprehensive program that helps followers gain incredible control over coronary plaque and coronary risk that has now expanded to over 30 countries. High-tech heart procedures still dominate public consciousness, but the tremendous power of real heart disease prevention efforts are gaining more and more attention as each day passes.

Wheat Belly #5 on New York Times Bestseller list!

The New York Times just released its bestseller list due for release September 18th, 2011 . . . .

Wheat Belly is #5!! (That darned Jane Fonda woman elbowed me out for the #4 spot!

[caption id="attachment_4452" align="alignright" width="574" caption="Wheat Belly hits #5 on New York Times Bestseller List--in 1st week!"][/caption]

Interview with Jimmy Moore of Livin' La Vida Low-Carb

Here's my podcast interview with Jimmy Moore, host of the Livin' La Vida Low-Carb Show. (If you want to fast forward to the interview, go to time marker 41:20 on the slidebar.)



In the podcast, I talk about how the Track Your Plaque program and its focus on lipoprotein testing, along with the need to reverse the incredible epidemic of diabetes and pre-diabetes, led to elimination of all wheat from the diet and the book, Wheat Belly.

An open letter to the Grain Foods Foundation

Readers: Please feel free to reproduce and disseminate this letter any way you see fit.


To:

Ms. Ashley Reynolds
490 Bear Cub Drive
Ridgway, CO 81432
Phone: 617.226.9927
ashley.reynolds@mullen.com


Ms. Reynolds:

I am writing in response to the press release from the Grain Foods Foundation that describes your effort to "discredit" the assertions made in my book, Wheat Belly: Lose the wheat, lose the weight and find your path back to health. I'd like to address several of the criticisms of the book made in the release:

" . . . the author relies on anecdotal observations rather than scientific studies."
While I do indeed have a large anecdotal experience removing wheat in thousands of people, witnessing incredible and unprecedented weight loss and health benefits, I also draw from the experiences already documented in clinical studies. Several hundred of these studies are cited in the book (of the thousands available) and listed in the Reference section over 16 pages. These are studies that document the neurologic impairment unique to wheat, including cerebellar ataxia and dementia; heart disease via provocation of the small LDL pattern; visceral fat accumulation and all its attendant health consequences; the process of glycation via amylopectin A of wheat that leads to cataracts, diabetes, and arthritis; among others. There are, in fact, a wealth of studies documenting the adverse, often crippling, effects of wheat consumption in humans and I draw from these published studies.


"Wheat elimination 'means missing out on a wealth of essential nutrients.'"
This is true--if the calories of wheat are replaced with candy, soft drinks, and fast food. But if lost wheat calories are replaced by healthy foods like vegetables, nuts, healthy oils, meats, eggs, cheese, avocados, and olives, then there is no nutrient deficiency that develops with elimination of wheat. There is no deficiency of any vitamin, including thiamine, folate, B12, iron, and B6; no mineral, including selenium, magnesium, and zinc; no polyphenol, flavonoid, or antioxidant; no lack of fiber. With regards to fiber, please note that the original studies documenting the health benefits of high fiber intake were fibers from vegetables, fruits, and nuts, not wheat or grains.

People with celiac disease do indeed experience deficiencies of multiple vitamins and minerals after they eliminate all wheat and gluten from the diet. But this is not due to a diet lacking valuable nutrients, but from the incomplete healing of the gastrointestinal tract (such as the lining of the duodenum and proximal jejunum). In these people, the destructive effects of wheat are so overpowering that, unfortunately, some people never heal completely. These people do indeed require vitamin and mineral supplementation, as well as probiotics and pancreatic enzyme supplementation.


I pose several questions to you and your organization:

Why is the high-glycemic index of wheat products ignored?
Due to the unique properties of amylopectin A, two slices of whole wheat bread increase blood sugar higher than many candy bars. High blood glucose leads to the process of glycation that, in turn, causes arthritis (cartilage glycation), cataracts (lens protein glycation), diabetes (glycotoxicity of pancreatic beta cells), hepatic de novo lipogenesis that increases triglycerides and, thereby, increases expression of atherogenic (heart disease-causing) small LDL particles, leading to heart attacks. Repetitive high blood sugars that develop from a grain-rich diet are, in my view, very destructive and lead to weight gain (specifically visceral fat), insulin resistance, leptin resistance (leading to obesity), and many of the health struggles Americans now experience.

How do you account for the psychologic and neurologic effects of the wheat protein, gliadin?
Wheat gliadin has been associated with cerebellar ataxia, peripheral neuropathy, gluten encephalopathy (dementia), behavioral outbursts in children with ADHD and autism, and paranoid delusions and auditory hallucinations in people with schizophrenia, severe and incapacitating effects for people suffering from these conditions.

How do you explain the quadrupling of celiac disease over the last 50 years and its doubling over the last 20 years?
I submit to you that, while this is indeed my speculation, it is the changes in genetic code and, thereby, antigenic profile, of the high-yield semi-dwarf wheat cultivars now on the market that account for the marked increase in celiac potential nationwide. As you know, "hybridization" techniques, including chemical mutagenesis to induce selective mutations, leads to development of unique strains that are not subject to animal or human safety testing--they are just brought to market and sold.

Why does the wheat industry continue to call chemical mutagenesis, gamma irradiation, and x-ray irradiation "traditional breeding techniques" that you distinguish from genetic engineering? Chemical mutagenesis using the toxic mutagen, sodium azide, of course, is the method used to generate BASF's Clearfield herbicide-resistant wheat strain. These methods are being used on a wide scale to generate unique genetic strains that are, without question from the FDA or USDA, assumed to be safe for human consumption.

In short, my view on the situation is that the U.S. government, with its repeated advice to "eat more healthy whole grains," transmitted via vehicles like the USDA Food Pyramid and Food Plate, coupled with the extensive genetic transformations of the wheat plant introduced by agricultural geneticists, underlie an incredible deterioration in American health. I propose that you and your organization, as well as the wheat industry and its supporters, are at risk for legal liability on a scale not seen since the tobacco industry was brought to task to pay for the countless millions who died at their product's hands.

I would be happy and willing to talk to you personally. I would also welcome the opportunity to debate you or any of your experts in a public forum.

Wiliam Davis, MD
Author, Wheat Belly: Lose the wheat, lose the weight and find your path back to health (Rodale, 2011)

Report from Washington II

Today's discussions at the Society for Cardiovascular Computed Tomography (SCCT) focused on atherosclerotic "plaque characterization".

As CT scanners get better and better at imaging the various components of plaque, some fascinating issues emerge:

--CT heart scans provide insights into what exactly is contained in an individual's atherosclerotic plaque that are not often provided even during heart catheterization. In other words, CT heart scanning is, in many instances, superior to heart catheterization, since it provides images of the artery wall, not just the internal contents.

--Progression (i.e., increase) in heart scan score is a powerful predicter of heart attack risk. Dr. Matthew Budoff of UCLA argued persuasively that the annual rate of increase in score is probably the most accurate measure of risk available, superior to cholesterol and calculated measures like the Framingham risk score.

--Coronary calcium scoring remains the best method to gauge total plaque throughout the entire coronary tree. In a person free of symptoms, the risk of a cardiac "event" (heart attack, death, procedures) is low and additional imaging (like CT angiography) is generally unnecessary.


Dr. Budoff, among the true thought leaders in CT heart scanning, also recounted his perspective on the history of heart scans. He noted that the questions asked through the years have evolved:




1995-2000 Should we do coronary calcium scans?

2000-2002 Do high or low risk patients benefit from coronary calcium scoring?

2003-2004 What is the better scanner, EBT or MDCT?

2006 How often should we perform coronary calcium imaging?


I believe that Dr. Budoff summarizes wonderfully where the Track Your Plaque programs fits into the overall scheme of things: Serial (repeated)CT heart scans to gauge progression or reversal is the wave of the future. We shouldn't just be interested in identifying persons at risk for heart attack. We should also be interested in showing the person at risk exactly how to reduce or eliminate that risk.

Report from Washington





I'm presently attending the Society for Cardiovascular Computed Tomography meetings in Washington, DC, along with 500 of my colleagues. It's exciting to see how interest in CT scanning for heart disease has balloonned in the past couple of years.

Several trends are noticeable today, based on the content and tone of the discussions:

--CT scanning of the heart, and imaging in general, is just getting started. In other words, the capabilities for CT scanners and other devices to detect heart disease (coronary and otherwise) are where the gasoline engine was in the 19th century. Scanning is getting faster, easier, safer, and more precise. Just as few people in 1905 could have predicted that automobiles would be computer-enhanced, high-speed, ubiquitous devices with several per household, the potential for CT imaging for heart disease is truly in its infancy.

--CT coronary angiography (so-called "64-slice CT scans") are not screening tests for hidden coronary disease in people without symptoms. I was grateful that this point has been made and reiterated by several speakers, as this is consistent with our views. Simple CT heart scans for coronary calcium scoring, in contrast, are screening tests. When the radiation exposure of CT angiograms are reduced to tolerable levels, then they may be used as screening tests. We are probably 3-4 years away from this point.

--Both stress testing and heart catheterizations will be partially replaced by CT scanning. In particular, over the next decade, you will see a dramatic drop in unnecessary catheterizations, i.e,, far less people saying "I had a heart cath but they told me that it was normal."


There has been heavy focus on applications of CT scanning for acute settings, particularly the emergency room and hospitals.

What has surprised me is that there is virtually no conversation whatsoever about the preventive uses of CT heart scanning. So far, only Dr. Daniel Berman of UCLA has shown that he has "seen the light": CT scans are a crucial tool for identification of early coronary plaque, and this tells us whether prevention is necessary and with what intensity.

There has been, however, no discussion at all about quantification of plaque in a program of reversal. Perhaps that should come as no surprise, given the imaging-technology focus of this convention. For most of my colleagues, prevention is also not terribly interesting. Identification and treatment of acute disease like impending heart attack is.

Of course, applying the information from your CT heart scan to empower you in a program and reversal is what the Track Your Plaque program is all about. I hope you see the light. I admit that it's not always easy to follow what we are advocating here. Perhaps not too different than telling someone in his horse-drawn buggy that one day he'll be driving a sleek car with onboard computerized mapping, air-conditioning, and micro-chips to modulate engine performance. He's probably tell us we're nuts.

I'll continue to update if any news relevant to our interests crops up in these meetings.

What about the Track Your Plaque failures?

I’d love to tell you that the Track Your Plaque program track record is of 100% success. It’s not.

It is very successful. But we’ve had some people who have failed and failed BIG. These are the people who've undergone bypass surgery, received one or more stents, or had heart attacks. Lesser failures are the people who’ve had large, undesirable increases in heart scan scores of >30% in one year. (The expected rate of increase in your heart scan score without preventive efforts is 30% per year, on average.)

What can we learn from those failures? There were several characteristics that stand out among this small group:

· Non-compliance--meaning they just didn’t stick with it. They started out right but then rapidly lost interest in maintaining all the pieces of the program and neglected their fish oil, niacin, gain weight, etc. Matthew did this and ended up with three stents to his left anterior descending. His slow start was due to skepticism that the program worked and just plain forgetfulness.

· Extreme stress--One of our earliest failures was a 38-year old man whose heart scan score doubled in one year, despite doing everything right. But three family members, all close to him, died within the space of six months, including his mother and a brother. I regard this as one of those instances in which we were powerless, unfortunately, though it is a graphic example of the power of unresolved stress and grief.

· Having a “better way”--These are the couple of people who were convinced that they had a better way to control their heart scan score. David firmly believed that his two dozen supplements and exercise program would drop his score. Instead, they permitted a 42% increase. Lee relied exclusively on chelation, along with several supplements of his own design. Lee had three-vessel bypass surgery.

· Starting too late--Gerome started with a score of 1179, but also was having chest pressure with emotional stress. His stress test was abnormal, with the entire upper half of his heart not receiving blood with exercise on a stress nuclear study (“anterior ischemia”). Gerome received four bypass grafts. Unfortunately, Gerome never really had a chance to engage in the Track Your Plaque program, since his health and safety were in jeopardy as soon as he started.

Have we had any big failures of people who did everything right, were compliant, were not subject to extreme stress (more than just job stress, or financial worries), didn’t neglect the basic requirements of the Track Your Plaque program, and had sufficient time (at least 6 months to 1 year)? No, thankfully, we have not.

No one who has stuck to the program has had a big failure.

Be smarter than your cardiologist

“Do you need a stent?”

Sad to say, but that sentence condenses the wisdom of over 90% of practicing cardiologists.

Prevention of heart disease means take Lipitor or some other statin and cutting the saturated fat in your diet. That’s it. Maybe throw in exercise.

Regression of coronary plaque? That phrase has only entered the conversation since the AstraZeneca-supported trial of Crestor succeeded in achieving 8% regression of plaque (Track Your Plaque Members: See News) as demonstrated by intracoronary ultrasound.



In other words, in the minds of my colleagues, it can’t be true until a drug company tells them it’s true. It’s beyond me why this brainwashing of otherwise intelligent people has occurred, but it is blatantly evident in practice.

Fish oil is another example. The spectacular benefits of fish oil have been known for 20 years. But only recently has it become a “mainstream” practice to recommend fish oil, largely because a drug manufacturer has put a preparation through the rigors of FDA approval (Omacor) and is now marketing directly to physicians. All of a sudden, fish oil is a good thing? No, it’s just achieved legitimacy in the eyes of practitioners because it graces marketing literature.

If you’re reading this, you’re likely interested in coronary plaque regression using the only tool available for you to measure, track, and regress coronary plaque: CT heart scans. Intracoronary ultrasound will achieve the same goal, but it is an invasive procedure performed at heart catheterization, involves threading a wire and imaging probe all the way down the artery, involves real risk of tearing the inner lining of the artery, and is costly (around $14,000-$20,000 for the entire package). Do it every year? That’d be nuts.

If you’re thinking about coronary plaque regression, using fish oil, concerned about patterns like low HDL and small LDL, aware of the vitamin D deficiency issue as a coronary risk factor, etc., you are far more aware than the vast majority of practicing cardiologists. They are interested in what new brand of anti-coagulant to use during their heart catheterization (because the product representative gushes about the new agent—only $1200 a dose!). Or, they are interested in gaining the procedural skills to put in a new device like a biventricular pacemaker. Regress/reverse coronary plaque? What for?

You already know that a conversation about coronary plaque reversal will not be obtained in your cardiologist’s office. Your family practice doctor or internist? Fat chance! Knee arthritis, pap smears, pneumovax inoculations, sore throats, gout, back pain—they’re spread far too thin to know anything more than the most superficial amount about coronary plaque control. Most know nothing.

That’s where we come in. That’s our mission: Educate people about the extraordinary tools that you have available to you, all in the cause of control or reversal of coronary plaque.

Why am I here?

Frank came to the office for an opinion, sent by his (proactive) family physician.

"I really don't know why I'm here, to be honest."

Two years earlier, Frank had a heart attack, survived and received two stents to his circumflex coronary artery. He now took Zocor and his LDL cholesterol was a reasonably favorable 89 mg, total cholesterol 183 mg.

"I walk with my wife every other day. I've been avoiding fish fries. You'll never see me eat fast food."

Frank was correct: If we were going to engage in the conventional approach to coronary disease, Frank was on the right track. We would have postponed his next heart attack or procedure by a couple of years. Stroke, aneurysm, and other atherosclerotic manifestations would be set back, likewise, a few years.

Would Frank have profound control over his disease? Absolutely not. In fact, his disease had probably advanced a huge amount just in the two years since his stents were placed and he was on his "prevention" program. Without his current effort, his coronary plaque would be expected to grow 30% per year. On Zocor and his modest lifestyle efforts, plaque growth was probably in the 14-28% per year range.

So I explained the unique Track Your Plaque approach to Frank. First, we start with a CT heart scan to establish where he was starting. Although he had two stents in his circumflex artery, we still had two other arteries (LAD, right coronary) to score and track.

We then attempt to identify all hidden causes of his heart disease and then correct them.

Of course, Frank had multiple hidden causes:

--HDL too low at 38 mg/dl
--Small LDL-severe, in fact, with 95% of all LDL particles in the small category
--Triglycerides too high
--Excesses of several triglyceride-containing particles (VLDL, IDL)
--Pre-diabetes--Frank had both a borderline high blood sugar and a high insulin level. This is a sure-fire stimulus to coronary plaque growth.
--A severe deficiency of vitamin D (<20 ng/ml)
--An excessivelyhigh blood pressure during exercise--With a blood pressure of 190/102 on the treadmill.

There were others(!), but that was the bulk of the causes behind Frank's coronary disease.

Once Frank recognized that there was indeed a huge panel of hidden causes for heart disease, not just too much fat in his diet and LDL cholesterol, he jumped into the program head first.

The message: The conventional approach is absurdly oversimplified, a certain path to failure for the majority of people. Even if you don't have known coronary disease like Frank, but just have a heart scan score >zero, the same principles apply to you.

Catheterization to “define coronary anatomy”

Gary is an avid jogger. On an average day, he runs 5-6 miles at a good clip. On two occasions recently, however, Gary experienced an ache in his left shoulder at mile 4. It was a toothache-like feeling, but he kept on going without difficulty.

Gary also had a heart scan score of 370.

Upon hearing of Gary’s score and his shoulder sensation, the cardiologist who saw him advised a heart catheterization “to define coronary anatomy”. (This is a real incident.)


What exactly does that mean? Why would Gary’s cardiologist need to define it?

In my view, this is an absurd notion. No one needs to “define coronary anatomy”. This catch-all phrase is commonly used to justify heart procedures. I believe what the cardiologist is saying is that it’s the easiest (for the cardiologist) and perhaps most generously reimbursed method to determine whether Gary’s symptoms are warning of an impending heart attack or not.

The problem is that the question can also be answered quite well by doing a stress test. Though not perfect diagnostic tests, stress tests are useful when symptoms are present that are doubtful in nature. Gary’s left shoulder ache could have been related to his heart, but the likelihood was that it was not. A stress test would have answered the diagnostic question quite adequately.

Instead, this man was subjected to an invasive test that was likely unnecessary. This happens dozens, if not hundreds, of times per day just around here. Nationwide, it is an epidemic of malpractice.

There are, indeed, times when a person should proceed directly to a heart catheterization. This is commonly and appropriately performed when a person develops unstable heart symptoms, such as chest discomfort or breathlessness at rest while not doing anything physical, or if the frequency is increasing, or if a stress test shows an important abnormality. There is no question that heart procedures can be lifesaving at times.

The problem is that thousands of people every year are scared into these procedures inappropriately. Beware!

It doesn't matter what I eat!

"How are your food choices?" I asked.

"What does it matter, doc? I take Lipitor. Doesn't that take care of it? I eat what I want!"

So declared Matthew. What he "wanted" was pretty much the diet of a teenager: pizza, cheeseburgers, soft drinks, snacks. His "beer belly" (visceral fat) gave it away. So did his blood work that showed flagrant lipoprotein abnormalities--small LDL, an HDL of 37 mg, and a severe after-eating flood of fat represented by increased "intermediate-density lipoprotein" (IDL).

Like many people, Matthew had been persuaded (or chose to believe) that LDL cholesterol was the sole cause for heart disease. Lipitor was therefore was all he needed. It must be great--how else could they afford all those slick TV commercials?

Well, it is definitely not true. In fact, with the persistence of Matthew's abnormal lipoprotein patterns, we should expect his heart scan score to continue to grow by 30%--the very same rate of increase as if he were taking nothing.

Specifically, Lipitor and drugs like it do not:

--Raise HDL.

--Correct or reduce the proportion of small LDL.

--Block after-eating flood of fat, nor do they accelerate clearance of unhealthy fats persisting in the bloodstream after eating.


Yes, what you eat does have real consequences, even if you take a statin drugs. In fact, the foods you ingest have a remarkably rapid and dramatic effect on what your blood contains. Any diabetic who checks his/her blood sugar knows this. They eat a slice of whole wheat toast and watch their blood sugar skyrocket.

Mind what you eat. Make it enjoyable, of course. But drugs do not provide impunity.

People with higher scores need to try harder

Sam is a 69-year retired physician. He was thoroughly enjoying retirement: golf, travelling, going out to dinner two or three times a week, spending weekends with his grandchildren. His lifestyle tended towards overindulgence, but he managed to stay fit and trim. At 6 ft 1 inch, he weighed 194 lbs and could still run 3 miles without too much difficulty. Not as good as his marathon-running days, but still not too bad for 69.

Sam's heart scan score in 2003 was a concerning 1983--extensive plaque. His doctor wasn't much help in interpreting the scan and so Sam simply chose to ignore it.

A chance conversation with a physician friend 18 months later made Sam think that perhaps this shouldn't be ignored. That's when he came to my office.




I find that sometimes the best way to motivate someone to take action is to demonstrate just how fast plaque grows if action isn't taken. So I advised Sam to get another scan first, since 18 months had passed. His score: 2441, or a 23% increase.




Sam was now starting to catch on. We made several changes in his prevention program (starting from virtually nothing). He did undergo a stress nuclear (thallium type) of test, which he passed without difficulty--normal blood flow in all heart territories despite the extensive plaque.

But, for some reason, Sam simply allowed himself to drift back to old habits: poor choices in food, overindulging in hard liquor, missing his fish oil and other supplements, and his medication, sometimes up to several days a week.

Sam started having unusual feelings in his chest. He described a sort of nervousness along with skipped heart beats. So we repeated a stress test. This time, a large area of reduced blood flow in the front of his heart ("anterior left ventricle") was detected. Sam ended up receiving three stents in a difficult procedure.

The moral: If you're starting out with a lower heart scan score of, say, 100 or 200, maybe you'll get by without trying too hard--maybe. But if your score is higher, say, several hundred or in the thousands, you got to try harder.

You're starting later in the process. Your disease will allow you very little slack. Let your guard down and it will get you. Control over your plaque is, indeed, very possible--we do it all the time. Score reduction is also possible. But your effort must be more serious and consistent.

Money can't buy health

Fallen Enron CEO, Kenneth Lay, was pronounced dead early this a.m. after suffering a heart attack.

Mr. Lay apparently had no history of heart disease and there's been no indication that symptoms provided any warning. His death was therefore classified as "sudden cardiac death".


Yet here's a man previously worth hundreds of millions of dollars with access to any test or medical system he desired--many times over. Even more recently, with his wealth reduced following his legal troubles, he and his wife managed to put away $4 million dollars to ensure an income from the interest through annuities, untouchable by the courts.

Detecting Mr. Lay's heart disease would have cost him around a few hundred dollars or whatever it costs for a CT heart scan in his city. This would have alerted his (hopefully knowledgeable) doctor that he was a time-bomb. Pile on all the stress he'd been suffering, whether deserved or no, and the diagnosis would have required little thought.

Instead, Mr. Lay has joined the thousands of Americans who will die this year because of failing to get a simple, 30-second test that costs one-tenth the cost of a stress test. Mr. Lay wasn't as lucky as former President Bill Clinton, whose doctors likewise blundered their way through and missed obvious levels of heart disease.

All Mr. Lay needed was better information: get a heart scan, then follow a program of prevention like the Track Your Plaque program. You may not have hundreds of millions of dollars, but you have the information on how to not follow in Ken Lay's footsteps. Track Your Plaque--and stay alive.

What's important, what's not in your plaque-control program

Sometimes it's hard to know what is really important in your plaque-control or plaque-reducing efforts.

There are, indeed, crucial make-it-or-break-it factors that are necessary to gain control over plaque. If you hope to stack the odds of reducing your heart scan score as much as possible in your favor, then fish oil, vitamin D, 60-60-60 in the way of standard lipids, elimination of small LDL, etc. -- all the elements of the Track Your Plaque program--are necessary.

But there's lots of things that sidetrack people. I spend much of my day fielding questions from patients about all the things that either provide very little benefit for plaque control, or provide none at all.

Among the things that we have found to be too weak or useless for plaque control, or are "non-issues", include:

--Caffeine--Go ahead and enjoy a couple cups a day (though not a pot). The effect is too trivial to make much difference.

--Hawthorne--Yes, it may dilate coronary arteries modestly, but not enough to make any difference.

--Garlic--with the possible exception of a specific preparation called Aged Garlic Extract (an acqueous, non-oil-based, extract from Kyolic), garlic's effects are too tiny to help, e.g., drop in blood pressure 1-2 points. Use it, but don't expect much. Aged Garlic Extract may be an exception, in that a single study from UCLA suggested specific effects on slowing coronary plaque growth. We await more info on this.

--Anti-oxidants--There is no shortage of extravagant claims about the benefits of anti-oxidants. Unfortunately, there's very little human exerience with pine bark extract, pycnogenol, grapeseed extract, and so on. Is the purported benefit from anti-oxidation or through some other means, e.g., enhancement of nitric oxide synthase? No data.

--Policosanol--If you've followed the Track Your Plaque Special Reports, you already know what a disappointment this agent has been, despite the too-good-to-be-true clinical data. It doesn't work.

--"No-flush niacin"--Unfortunately, no flush, no effect. This high-priced supplement is still sold widely in the U.S. despite its complete lack of efficacy. It does not work in humans. (It works great in rats!)

Track Your Plaque continues to try to be the arbiter of truth in what works, what doesn't in truly stopping or reversing your coronary plaque. The proof positive? Stopping or dropping your heart scan score.
All posts by william-davis

"I gained 30 lbs from one cracker"


Let me tell you a story, a tale of a woman who gained 30 lbs by eating one cracker.

At age 50, Claire's health was a disaster. Her initial lipoprotein patterns were a mess, including HDL 36 mg/dl, triglycerides 297 mg/dl, blood sugar 122 mg/dl (pre-diabetic range), blood pressure 155/99. Small LDL comprised over 90% of all LDL particles.

At 5 feet 3 inches, she weighed 210 lbs--90 lbs over her ideal weight. Her face was flushed and red, her eyes swollen and weighted down with bags, her eyes dull. While interested in hearing about how to improve her health, I would hardly call her enthusiastic.

We talked about how removing wheat products entirely from her diet could result in weight loss--enormous weight loss--yet with reduced appetite, increased energy, less daytime sleepiness and fogginess, improved sleep quality. Removing wheat would also allow substantial correction of her lipoprotein patterns with minimal medication.

At first, she seemed confused by this advice. After all, it ran directly opposite to what she'd been told by her family doctor, not to mention the advice from TV, food ads, and food packages.

To my surprise, Claire did it. She didn't return to the office for another 5 months. But she came in, a big beaming smile on her face.

Even at 167 lbs--still overweight--Claire looked great. She glowed. She'd already dropped nearly 2 1/2 inches from her waist. She felt lighter on her feet, discovered energy she thought she'd lost 10 years earlier. Her blood results matched, with dramatic shifts in each and every pattern.

I quizzed Claire on her diet, and she had indeed made substantial changes. In addition to eliminating all foods made of wheat flour, she also eliminated foods made with cornstarch, rice flour, snacks, and other sweets. She ate her fill of vegetables, fruits, raw nuts, lean meats, and healthy oils. She was less hungry while eating less. Even her husband, skeptical at first, joined Claire after the first two months and her initial 20 lbs of weight loss. He, too, was well on his way to dropping to ideal weight.

But a dinner party invitation came. In the few that Claire and her husband had gone to over the few months, she had religiously stuck to her program, choosing cheese, pickles, olives, vegetables that she dipped, but avoided the pretzels, breads, Doritos, potato chips, and others.

This time, a tray of whole wheat crackers was laid on the buffet table, covered with some sort of sweetened cheese. She had just one. She savored the taste that she'd missed. "Maybe one more. I'll be extra good this weekend,'" she told herself.

Now Claire was hungry. The bruschetta covered with tomatoes and mozzarella looked awfully good. "It's got some good things on it, too!" she thought. She had three.

The floodgates opened. I saw Claire three months later, weighing just shy of 200 lbs. "I almost cancelled this appointment," she whispered quietly, tears at the corner of her eyes. "I don't know what happened. I just lost control. After losing all that weight and feeling so good, I blew it!"

I've seen it before: Fabulous success eliminating the foods that created the situation--the insatiable appetite, the endless cycle of hunger, brief satiety, the rolling, rumbling hunger--followed by temptation, then disaster. The weight lost comes right back.

It's experiences like Claire's that have absolutely, positively convinced me: Wheat products are addictive. It's not true for everybody, but it's true for many people, certainly most people who have weight struggles. It triggers some sort of appetite button, a signal to eat more . . . and more, and more. Keep it up long enough, and you have drops in HDL, increases in triglycerides, upward jumps in blood sugar and blood pressure, diabetes, etc. It doesn't matter if it's whole grain, 7-grain, or 12-grain. Yes, the whole grains contain more fiber and more B vitamins. But they all share one characteristic: They trigger a desire for more.

So that's the story of how one whole wheat cracker caused one woman to gain 30 lbs.


Next week's story:

California woman claims: My children are aliens!


Just kidding.


Copyright 2008 William Davis, MD

Wheat-free is not gluten-free

Eliminate wheat from your diet and wonderful things happen:

--Lose 15-20 lbs, sometimes in the first 1-3 months. (More or less, depending on your prior dietary habits, weight, age, etc.)
--HDL cholesterol goes up, triglycerides go down
--Blood sugar drops
--Small LDL is reduced
--C-reactive protein is reduced
--Pre-diabetics often convert to non-diabetics
--Diabetics gain far better control over blood glucose. Some even become non-diabetic (as long as they maintain the wheat-free, low-glycemic index diet and weight control).
--You feel better: Less mental fogginess, more energy, better sleep.
--Appetite shrinks dramatically.


(Many diet programs makes lots of money promising similar results. Prescription medications like the pre-diabetes drugs, Actos and Avandia, and the fibrates, Tricor and Lopid, nearly--nearly--reproduce the effects of eliminating wheat. Of course, these medications do not lead to weight loss or make you feel better. In fact, Actos and Avandia usually trigger a weight gain of 8 lbs in the first year of use.)


All of these wonderful effects develop with elimination of wheat. . . unless you confuse wheat-free with gluten-free. There's a difference.

Remove wheat from your diet, but discover the world of gluten-free products made for people with celiac disease, or gluten enteropathy, and you can regain the weight and recreate many of the phenomena associated with wheat. I've talked about this in past, but it trips up so many people that it's worth talking about again.

The concept that I am advocating is really low-glycemic index (or low glycemic load, actually). Foods that trigger a substantial rise in blood sugar, whether immediate (like whole wheat crackers) or delayed (like whole wheat pasta) are the culprits. The same effects develop with candy, cookies, fruit drinks, pizza, chips, table sugar, and other junk foods.

However, I pick on wheat specifically because it so dominates the American diet. It has grown to fill so many processed food products. It is also a food ingredient that is falsely advertised as healthy. In reality, pretzels, whole wheat crackers, whole grain bread, high-fiber cereals, etc. exert the same effect on blood sugar as candy or white table sugar. They also generate all the "downstream" phenomena listed above.

But wheat is hardly the only food that makes us fat, diabetic, and unhealthy. This is true for foods made with cornstarch (taco shells, cornbread, tortillas, chips, breakfast cereals); rice flour, puffed rice, and polished rice; and potatoes, particularly pulverized potato starch (potato chips). There are others.

These are the gluten-free products that are marketed to the gluten enteropathy (celiac disease) market. Yes, you can make muffins with cornstarch and no wheat gluten, but is it good for you?

No. It is nearly as bad as wheat. It can still skyrocket blood sugar, drop HDL, raise triglycerides, create small LDL, heighten inflammation, etc.

Ground flaxseed, oat bran, barley, quinoa, are some of the alternatives that do not create these effects. But not the majority of gluten-free products on the market.




Ingredients: Potato starch, rice flour, modified corn starch, olive oil, yeast, vegetable protein(lupine), corn syrup, sugar, salt, hydroxypropyl methylcellulose, sodium bicarbonate, ammonium bicarbonate, diacetyltataric acid esters of mono- and diglycerides of edible fats, natural flavor.

". . . only naturally gluten-free and wheat-free ingredients and adhere to the strictest quality processes, testing every batch for gluten using the ELISA assay."

NUTRITION FACTS
Serving Size 7 bread sticks (31g)
Servings per container 5

Calories 120 Calories from fat 25
Amount per serving
Total Fat 2.5g
Saturated Fat 0.5g
Trans Fat 0g
Cholesterol 0mg
Sodium 310mg
Total Carb 24g
Dietary Fiber 1g
Sugars less than 1g
Protein less than 1g

Death to chelation?


Does chelation work?

It's a question I get asked fairly frequently. Although I have never performed chelation, IV or oral, and therefore have no direct experience, my concerns for this purported therapy have included:

1) The concept of extracting calcium from atherosclerotic plaque by removing it first from the blood is absurd. Early chelationists believed that this was the means by which EDTA might reverse coronary atherosclerosis. However, removing calcium from blood would more likely lead to osteoporosis or calcium extraction from bone, since bone is a more ready repository for calcium. Blood calcium levels are also tightly and narrowly controlled; any significant reduction in calcium ("hypocalcemia") can be life-threatening. And, indeed, there have been deaths from hypocalcemia in people receiving chelation.

More recently, chelationists have argued that removal of heavy metals like lead and mercury are responsible for the purported benefits of chelation. And, indeed, blood levels of these heavy metals can be reduced by chelation. That alone may be a benefit. But to then make the leap to say that it also regresses atherosclerotic plaque by the same mechanism has no basis in science.

2) Practitioners associated with chelation tend to be shady. I have seen homeopathic therapies (among THE most ridiculous of concepts), "energy balance" therapies, desiccated organ extracts ("applied kinesiology"), and a variety of other fringe treatments offered by practitioners offering chelation. This doesn't necessarily mean, of course, that chelation is also fringe or suspect, but it tends to be offered by practitioners who engage in generally unscientific, unfounded practices.


The few people I've seen go through multiple courses of chelation (usually 30 or so infusions) have shown no impact on heart scan scores or any other measure of heart disease.

In response to the many questions I receive on chelation, I had been answering that, if we would simply wait for the publication of the NIH-sponsored trial of IV chelation therapy, perhaps we'd know once and for all.

However, in a lengthy criticism, four expert authors argue that the TACT trial to assess chelation study is doomed to failure for an entire list of reasons and should therefore be abandoned. The discussion is available on Medscape Cardiology. (Free sign-in required.)



Why the NIH Trial to Assess Chelation Therapy (TACT) Should Be Abandoned
We investigated the social and the scientific histories of chelation therapy beginning in the 1950s. We examined TACT protocols and consent forms, which, in response to Freedom of Information Act (FOIA) requests, the NIH provided to us with curious redactions. We examined the existing RCTs and the numerous case series cited by the TACT protocols. We examined evidence for risks, including information that is not in the standard medical literature. We examined various hypotheses that advocates have offered to explain how chelation "works."

We present our findings in 4 parts. First, we provide a brief history of the use of disodium EDTA as a treatment for CAD. Next, we describe the origin and nature of the TACT. Next, we discuss the evidence for chelation as a treatment for CAD and for atherosclerosis in general, and place it in the context of other proposed treatments that have been ineffective after an initial period of enthusiasm. Finally, we discuss the risks. For each topic, we contrast our findings with relevant statements in the TACT literature, to the extent that such statements exist.



Among the highlights:

--Since the mid-1970s, court documents and newspapers have reported at least 30 deaths associated with IV disodium EDTA, most of it administered by ACAM members.

--Early chelation investigators had chosen the disodium salt of EDTA, reasoning that if it could remove calcium from atherosclerotic plaques, it might shrink them. That notion was soon demonstrated to be invalid. It has largely been replaced by a "toxic heavy metals" antioxidant hypothesis, which is based on the potential for metal ions to produce free radical damage. Chelationists now cite "removing heavy metals" as the basis for their claim that chelation is effective for approximately 70 conditions, ranging from schizophrenia and autism to cancer. This provides them with numerous reasons to ignore any trial that finds chelation ineffective for CAD.

--Biochemical literature, either not cited or misrepresented in the TACT protocols, has demonstrated that the heavy metals hypothesis is implausible. Antithetically, it also demonstrates that the chelation mixture used in the TACT has pro-oxidant effects in vitro.

--In our opinion, TACT literature -- including 2 versions of the protocol, the consent form, information posted on the NCCAM Web site, and 2 editorials co-authored by the PI -- has misrepresented chelation, its risks, and the facts of the study. It has exaggerated the value of supportive case series, not only by ignoring evidence of bias and incompetence, but by misrepresenting citations and reporting erroneous data. It has minimized the dangers, both by understatements and by omissions of specific, published complications. It has not acknowledged the deaths mentioned above. It has repeatedly conflated disodium EDTA and a different drug, calcium-sodium EDTA.

--The TACT includes nearly 100 "chelation site" co-investigators who, in our opinion, are unsuitable to care for human subjects or to report trial data. Most espouse implausible health claims while denigrating proven methods; several have been disciplined, for substandard practices, by state medical boards; several have been involved in insurance fraud; at least 3 are convicted felons. Several were members of the ACAM or GLACM IRBs mentioned above. Few appear to have real expertise, required by TACT literature, in treating patients with CAD or in conducting clinical trials. Most continue to promote chelation while the TACT is in progress, contrary to good science, to human studies ethics, and to US Federal Code.


While the criticism itself does not prove the point one way or another, as a clinical trial should, anyone contemplating chelation therapy would be well-advised to read the document first. Another reference: EDTA chelation therapy for cardiovascular disease: a systematic review.


The authors of the exhaustive discussion are:
Kimball C. Atwood IV, MD, Anesthesiologist, Newton-Wellesley Hospital, Newton, Massachusetts; Assistant Clinical Professor, Tufts University School of Medicine, Boston, Massachusetts; Associate Editor, Scientific Review of Alternative Medicine
Author's email: katwood@partners.org

Elizabeth Woeckner, AB, MA, President, CIRCARE (Citizens for Responsible Care and Research), Columbia, Maryland

Robert S. Baratz, MD, DDS, PhD, Medical Director, South Shore Health Center, Inc., Braintree, Massachusetts; Assistant Clinical Professor of Medicine, Boston University School of Medicine, Boston, Massachusetts; President, National Council Against Health Fraud, Inc.

Wallace I. Sampson, MD, Clinical Professor of Medicine (Emeritus), Stanford University, Stanford, California; Senior Attending Physician and formerly Chief of Medical Oncology, Santa Clara Valley Medical Center, San Jose, California; Editor-in-Chief, Scientific Review of Alternative Medicine



The authors provided the following disclosures:


Disclosure: Kimball C. Atwood IV, MD, has disclosed no relevant financial relationships in addition to his employment.

Disclosure: Elizabeth Woeckner, AB, MA, has disclosed that she has received compensation for consulting in civil litigation and professional disciplinary actions.

Disclosure: Robert S. Baratz, MD, DDS, PhD, has disclosed that he has been retained by state licensing boards, the Office of the US Attorney, and plaintiff counsel as an expert in disciplinary proceedings and litigation with regard to chelation therapy and associated matters. He is compensated only for his time and has no commercial interest in the outcome of the proceedings or litigation.

Disclosure: Wallace I. Sampson, MD, has disclosed no relevant financial relationships in addition to his employment.

American Diabetes Association


These are actual quotes from the American Diabetes Association website:


Myth #2 (from list of Diabetes Myths): People with diabetes can't eat sweets or chocolate.
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more “off limits” to people with diabetes, than they are to people without diabetes.



Myth #5: If you have diabetes, you should only eat small amounts of starchy foods, such as bread, potatoes and pasta.
Starchy foods are part of a healthy meal plan. What is important is the portion size. Whole grain breads, cereals, pasta, rice and starchy vegetables like potatoes, yams, peas and corn can be included in your meals and snacks. The key is portions. For most people with diabetes, having 3-4 servings of carbohydrate-containing foods is about right. Whole grain starchy foods are also a good source of fiber, which helps keep your gut healthy.





How can I have sweets and still keep my blood glucose on target?
The key to keeping your blood glucose on target is to substitute small portions of sweets for other carb-containing foods in your meals and snacks. Carb-containing foods include bread, tortillas, rice, crackers, cereal, fruit, juice, milk, yogurt, potatoes, corn, and peas. For many people, having about 45 to 60 grams at meals is about right. Serving sizes make a difference. To include sweets in your meal, you can cut back on the other carb foods at the same meal.

For example, you’d like to have cookies with your lunch. Your lunch is a turkey sandwich with two slices of bread. Your first step is to identify the carb foods in your meal. Bread is a carb. You decide to swap two slices of bread for two slices of low-calorie bread and have the cookies -- it’s an even trade. Your total amount of carbohydrate remains the same for the meal.



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


Or take a look at the recipes for breads, muffins, cakes, pies, cookies, and pizza.


My point? As I often say, while the "official" organizations like the American Diabetes Association, the American heart Association, and the USDA dominate the message provided to mainstream Americans, to those of us who know better, they have become irrelevant. You can see how obviously boneheaded their advice is. I'd go so far as to say that, if you want diabetes, follow the American Diabetes Association diet. If you have diabetes, and you'd like to accelerate complications like kidney disease, heart disease, and neuropathy, then follow the American Diabetes Association diet.

I'm going to bet that American Diabetes Association sponsors like Lilly, Novo Nordisk, Merck, Pfizer, Abbott ($1 million or more annual contributions) and Cadbury Schweppes (3-year, multi-million dollar support for Weight Loss Matters program) will continue to charge full-speed ahead to maintain the status quo. Cadbury Schweppes are the proud makers of Dr. Pepper, Hawaiian Punch, Snapple, Motts' Apple Juice, and Hires Root Beer--you know, the foods and drinks that you can have as long as you adjust your insulin dose or talk to your doctor about adjusting your diabetes medications. And if you gain, say, 30 or 40 lbs eating these foods. . . well, we've got a treatment for that. Merck's Januvia , for instance, can help you out for only about $200 a month!

Looking at the facts this way, and it seems like some cheap conspiracy theory: They're all out to get us. Dispense information that virtually guarantees propagation of the disease, and all your friends and cronies profit. I don't know if it is or it isn't, but it sure smells like it sometimes.

A tan does not equal vitamin D

The sun is getting stronger and the days are getting longer, even here in Wisconsin.

Some people are coming to the office with nice tans obtained by sunning themselves for several hours. Others have come back from winter getaways to Florida, Arizona, or the tropics, also sporting nice, dark tans.

Several people, in fact, were so confident that sunning themselves provided sufficient vitamin D that they reduced their usual dose. Some even stopped their vitamin D altogether.

But, when blood levels of 25(OH) vitamin D were checked, they were virtually all low, sometimes as low as <20 ng/ml. Yet all had nice tans.

Why does this happen? Why would people with dark tans remain deficient in vitamin D?

One big factor is age: Anyone over 40 years old is fooling themselves if they think that a tan ensures raising vitamin D levels to a desirable range. Also, the more you tan, the more melanin skin pigment accumulates, and the more vitamin D activation in the skin is blocked.

Weight is another factor: Heavier people need more vitamin D, sometimes three- or four-fold more than slender people.

Why does aging result in inefficient skin activation of vitamin D? It seems that, once we are beyond our reproductively useful years, this ticking clock of aging gets triggered. The older we get, the less activation of vitamin D occurs in our skin, the less of the youth-maintaining, disease-preventing benefits of vitamin D we obtain with sun exposure.

The message: Don't rely on a tan to gauge the adequacy of vitamin D. Maybe that works when you're 16 years old, but not at age 50 or 60. There's only one way to know your vitamin D status: a blood level of 25(OH) vitamin D.


Copyright 2008 William Davis, MD

Planned obsolence

In the 1960s, you’d purchase a new car. If you changed the oil, adhered to the maintenance schedule—and were lucky—you might expect to get 100,000 miles out of your automobile. Only an occasional car made it beyond that odometer hurdle. Even if the engine made it past the 100,000 mile milestone, the automobile body would inevitably start to develop rusting decay at the edges of the fenders, signaling body rot that threatened to open gaping holes of metal.



Then along came Toyota and Honda, whose cars easily reached 100,000 miles and well beyond, reliably and with bodies intact. As this realization sunk into the American consciousness, many asked, “Why can’t American automakers accomplish the same sort of trouble-free longevity?” “Buy American” emerged as a mantra to preserve American jobs and prop up an economy vulnerable to the superior automotive products from Detroit’s competitors.

Of course, American automakers have since responded to the challenge posed by the Japanese auto industry and produced automobiles that essentially matched the reliability and longevity of Japanese cars. But, the great unanswered question remains: For years before the onslaught of Japanese competition, did Detroit quietly plot to maintain a policy of planned obsolescence that ensured Americans would have to scrap the old and buy a new car every few years whenever the odometer tipped over 100,000 miles?

We will never know. At worst, it may represent the behind-closed-doors, back-slapping sort of plotting that, for many years, maximized revenues, ensured shareholder returns, and secured executive paychecks. Or, perhaps it wasn’t some evil conspiracy but just complacency, a profitable position of comfort at that. There’s little incentive for industry insiders to reveal such self-incriminating information.

But the example set by the American auto industry presents an unusual learning opportunity for us, a chance to make some useful comparisons to the heart healthcare industry.

Is the American healthcare industry also guilty of practicing a policy of “planned obsolescence,” just like Detroit? The product that helplessly crumbles is, of course, not your rust-riddled automobile, but you.

When someone sees a primary care physician year after year, yet appears one morning in the emergency room, clutching his or her chest in agony from the closed coronary artery responsible for a life-threatening heart attack—prompting the flurry of activity that results in $100,000 in hospital procedures . . .

Perhaps “planned obsolescence” is not the perfect phrase to describe the situation, but the principle still applies: A failure to inform the patient that such an outcome was possible—no, probable—makes you wonder whether such an outcome was predictable and thereby preventable in the first place.

What should we do when planned obsolescence leads us down a path engineered by someone who has something, often substantial, to gain? Even if it's just complacency, or adhering to a beaten, ineffective status quo (can you say "low-fat diet?), it all points in the same direction.

You have a choice: Refuse to buy a 1962 Impala of health care, otherwise known as conventional heart disease management.

Melatonin for high blood pressure?

Melatonin is fascinating stuff.

In addition to its use as a sleep aid, melatonin exerts possible effects on cardiovascular parameters, including anti-oxidative action on LDL, reduction in sympathetic (adrenaline-driven) tone, and reduction in blood pressure.

Several studies document the blood pressure-reducing effect of melatonin:

Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension.

Melatonin reduces night blood pressure in patients with nocturnal hypertension.

Prolonged melatonin administration decreases nocturnal blood pressure in women.

Blood pressure-lowering effect of melatonin in type 1 diabetes.


But blood pressure may be increased when melatonin is added to nifedipine, a calcium channel blocker:

Cardiovascular effects of melatonin in hypertensive patients well controlled by nifedipine: a 24-hour study.


Effects on BP tend to be modest, on the order of 5-8 mmHg reduction in systolic, half that in diastolic.

But don't pooh-pooh such small reductions, however, as small reductions exert mani-fold larger reductions in cardiovascular events like heart attack and stroke. NIH-sponsored NHANES data (see JNC VII), for example, document a doubling of risk for each increment of BP of 20/10. The Camelot Study demonstrated a reduction in cardiovascular events from 23% in placebo subjects to 16.7% in subjects taking amlodipine (Norvasc) with a 5 mm reduction in systolic pressure, 2 mmHg drop in diastolic pressure. Small changes, big benefits.

Many people take melatonin at bedtime and are disappointed with the effects. However, a much better way is to take melatonin several hours before bedtime, e.g., take at 7 pm to fall asleep at 10 pm. Don't think of melatonin as a sleeping pill; think of it as a sleep hormone, something that simply prepares your body for sleep by slowing heart rate, reducing body temperature, and reducing blood pressure. (You may need to modify the interval between taking melatonin and sleep, since individual responsiveness varies quite a bit.)

I also favor the sustained-release preparations, e.g., 5 mg sustained-release. Immediate-release, while it exerts a more rapid onset of sleep, allows you to wake up prematurely, The sustained-release preparations last longer and allow longer sleep.

The dose varies with age, with 1 mg effective in people younger than 40 years, higher doses of 3, 5, even 10 or 12 mg in older people. Sustained-release preparations also should be taken in slightly higher doses.

The only side-effect I've seen with melatonin is vivid, colorful dreams. Perhaps that's a plus!

The forces that shape heatlh care

Thinking about the programs for health care reform proposed by the three Presidential candidates highlights a distinct peculiarity of American style health care.

American health care is shaped to an unprecedented degree by five forces:

1) The drug industry

2) The health insurance industry

3) Hospitals

4) Fear of litigation

5) The uniquely American attitude of refusing compromise in access to health care services or products, regardless of the cost (for those who can afford health insurance)


All five of these unique forces have created this thing (monster?) we call health care. Remove or modify any one of these forces, and the health care landscape would look dramatically different.

The drug industry has recently been on the receiving end of plenty of negative press. This warms my bones. Decades of heavy-handed lobbying, sleazy marketing to physicians (all too willing to be wined and dined), and behind-the-scenes manipulation of clinical data are coming back to bite them. Sadly, the drug industry is so powerful that this bit of fuss is not likely to substantially change their ways.

I am thrilled that all three Presidential candidates agree that reimportation of drugs from outside the U.S. is a good idea. While the shrug of the shoulders federal and state attitude towards importation of drugs from Canada has not resulted in cost savings sufficient to impact on overall costs, it surely will lead to savings when practiced on a broad basis by pharmacies, distributors, and other bulk buyers of pharmaceuticals.

Senator Obama, in particular, has used strong language in his criticism of the health insurance industry, tough talk that is needed in an age in which insurance executives bring home salaries in the hundreds of millions of dollars and stock prices are climbing due to substantial profit gains within the industry, going against the grain of increasingly costly premiums. However, the Clinton experiment of federalizing health care during Bill Clinton's term that caused all the big boys to band together (most notably health insurance companies and drug industry) has tempered enthusiasm for attacking the insurance industry head-on. In both Democrats' health care reform proposals, the option of private insurance is preserved, as it is in the McCain proposal.

How about hospitals? Hospitals, though on a smaller scale than the nationwide reach of the drug and insurance industries, aim to maintain health service delivery in hospitals. For instance, the high-tech bypass service in the hospital gets plenty of local media coverage, as does the newest DaVinci robotic surgery, bariatric surgery, and other revenue-rich services. Many hospitals have forgotten that their mission is delivery of health, of which revenue creation and profiting from disease should only be part.

How big is fear of litigation? Estimates vary, but several have quoted numbers in the neighborhood of 20 to 30% of overall health care costs. At the street level from what I see, I'd say at least that much. Fear of litigation is rampant, often unrestrained, and sometimes leads to the craziest, illogical sequence of testing. Chest pain, for instance, no matter how trivial, will typically trigger around $5000 worth of testing (nuclear stress test, echocardiogram, laboratory work, etc.) Emergency room visit for a minor injury? CT scan of head, chest, abdomen. A formula to minimize this aspect of fear in health care delivery would generate enormous savings.

The last issue, the uncompromising nature of Americans in health--always wanting the latest new drug, new procedure, "best" surgeon--often simply causes the health care consumer to fall victim to marketing. If a hospital advertises the newest procedure, people want it regardless of whether it represents genuine improvement over the older procedure. The newest sleeping pill, antidepressant, antihypertensive, etc. replaces the old yet equivalent product, but at considerably greater cost.

I am optimistic that, regardless of which candidate gains the White House, that some reform is on the way. I do fear, however, that progress will be small and incremental, since major change of the sort that would slash hundreds of billions of dollars in costs would rouse the powers-that-be (drug industry, health insurers, etc.) to once again combine forces and combat the disruption of their franchise.

Until you and I see real change and cost savings coming through either legislation or free market advances, we need to continue to make full use of the self-empowering health information that we gain through venues like the web.



Copyright 2008 William Davis, MD

Lipoprotein(a): Surprising Poll Results

No doubt, our little informal poll asking readers whether they have lipoprotein(a), is skewed towards people inclined to respond because they have this genetic trait.

Nonetheless, the response is telling. Of 82 respondents:

--40 (48%) said they did have Lp(a)

--16 (19%) said that they did not have Lp(a)

--26 (31%) said that they did not know whether or not they had Lp(a)


Though admittedly an informal analysis, I'd draw several conclusions from this simple "experiment".

One, while the proportion of people responding that they have Lp(a) may not be accurate, it is a prevalent genetic risk factor that, according to formal studies, is present in 17% of people with coronary or vascular disease, 11% of the broader population. This number may be even higher if the newer particle number assays (measurements) are used (with results expressed in nmol/L), since an occasional person with a "normal" Lp(a) in mg/dl (weight-based) will prove to have increased Lp(a) by nmol/L (particle number-based). (The reason for this phenomenon is not clear. It may be consequent to variation in apo(a) size, with larger apo(a) varieties of Lp(a) occasionally escaping detection .) As our little poll shows, plenty of people have Lp(a).

Two, readers of this blog tend to be highly motivated, sophisticated, and knowledgeable about health and heart disease. Yet a substantial portion--31%--did not know whether they have this crucial risk factor. That shouldn't be. The unnecessary difficulty of getting this simple blood test performed has been driven home to me repeatedly when I identify this factor in someone and then suggest that their grown children and parents, each of whom have a 50% chance of having Lp(a), be tested. It's not uncommon for a 35-year old son, for instance, to say that his doctor refused, claiming it is an unproven risk marker, or to simply say that he/she doesn't know what it is.

No doubt, just knowing whether you have Lp(a) or not is not the end of the story. Reducing Lp(a) and its associated co-factors is no easy matter. With several hundred patients in my practice with Lp(a), it occupies much of my time and energy. Sometimes it leads to enormous successes , but it can also pose a real challenge.

There should no longer be any doubt that Lp(a) is associated with significantly increased risk of cardiovascular disease. This has been demonstrated conclusively across dozens of studies. Risk from Lp(a) is over and above that posed by other risk factors; it also amplifies the risk posed by other factors, e.g., small LDL, inflammatory phenemena, homocysteine, total LDL, low HDL.

In the world of Lp(a), our two most desperate needs for the future are:

1) Better education of physicians and the public, and

2) More effective treatment options.

Thus, our reasons to form The Lipoprotein(a) Research Foundation. Steps to gain tax-exempt status are being pursued as we speak.

I can't help but wonder whether, like vitamin D, a solution is right beneath our noses. An investment in research to fund the trials to better explore both basic science as well as practical treatment options might yield an answer more readily than we think. Wouldn't that be great?
All posts by william-davis

Fish oil makes you happy: Psychological distress and omega-3 index

For another perspective on omega-3 blood levels, here's an interesting study in northern Quebec Inuits.

Traditionally, Inuits consumed large quantities of omega-3-rich seal, fish, caribou, and whale, even eating the fat. However, like the rest of the world, modern Inuits have increased consumption of store-bought foods, largely processed carbohydrates. Along with this trend has emerged more heart disease, diabetes, and depression.

A group from Laval University and University of Guelph, both in Canada, examined the relationship of plasma EPA + DHA levels and measures of psychological distress. This group had previously shown that Inuits older than 50 years had twice the plasma omega-3 levels (11.5%) compared to those younger than 50 years (6.5%), reflecting the shift away from the traditional diet.

Psychological distress was measured with The Psychological Distress Index Santé-Québec Survey (PDISQS-14): the higher the score, the greater the psychological distress. (In the graphs, tertile 1 is least distressed; tertile 5 is most distressed. Sorry about the small chart graphic--click on the graphic to make it bigger.)


From Lucas M et al 2009 (http://www.nutrasource.ca/NDI/Assets/Articles/Plasma%20omega-3%20and%20psychological%20distress%20among%20Nunavik%20Inuit.pdf)

"Our main finding was that women in the second and third tertiles of EPA+DHA concentrations in plasma PLs [phospholipids] had a 3 times lower risk of having a high-level PD [psychological distress] score than women in the lowest tertile."

While the relationship is stronger for women, you can see that, the higher the EPA + DHA plasma level, the lower the likelihood of psychological distress. Interestingly, the tertile with the greatest distress and lowest EPA + DHA levels had a plasma level of 7.0-7.5%--far higher than average Americans.

(Plasma levels of EPA + DHA were used in this study, which tend to reflect more recent omega-3 intake than the more stable and slower-to-change RBC Omega-3 Index that we use. Plasma levels also tend to run about 10-20% lower than RBC levels.)

Of course, there's more to psychological distress than omega-3 blood levels. After all, eating fish or taking fish oil capsules won't make money worries go away or heal an unhappy marriage. But it is one variable that can be easily and safely remedied.

Hospitals are a hell of a place to get sick

I answered a page from a hospital nurse recently one evening while having dinner with the family.

RN: "This is Lonnie. I'm a nurse at _____ Hospital. I've got one of your patients here, Mrs. Carole Simpson. She's here for a knee replacement with Dr. Johnson. She says she's taking 12,000 units of vitamin D every day. That can't be right! So I'm calling to verify."

WD: "That's right. We gauge patients' vitamin D needs by blood levels of vitamin D. Carole has had perfect levels of vitamin D on that dose."

RN: "The pharmacist says he can replace it with a 50,000 unit tablet."

WD: "Well, go ahead while Carole's in the hospital. I'll just put her back on the real stuff when she leaves."

RN: "But the pharmacist says this is better and she won't have to take so many capsules. She takes six 2,000 unit capsules a day."

WD: "The 50,000 units you and the pharmacist are talking about is vitamin D2, or ergocalciferol, a non-human form. Carole is taking vitamin D3, or cholecalciferol, the human form. The last time I checked, Carole was human."

RN: (Long pause.) Can we just give her the 50,000 unit tablet?

WD: "Yes, you can. But you actually don't need to. In fact, it probably won't hurt anything to just hold the vitamin D altogether for the 3 days she's in the hospital, since the half-life of vitamin D is about 8 weeks. Her blood level will barely change by just holding it for 3 days, then resuming when she's discharged."

RN: (Another long pause.) Uh, okay. Can we just give her the 50,000 units?"

WD: "Yes, you can. No harm will be done. It's simply a less effective form. To be honest, once Carole leaves the hospital, I will just put her back on the vitamin D that she was taking."

RN: "Dr. Johnson was worried that it might make her bleed during surgery. Shouldn't we just stop it?"

WD: "No. Vitamin D has no effect on blood coagulation. So there's no concern about perioperative bleeding."

RN: "The pharmacist said the 50,000 unit tablet was better, also, because it's the prescription form, not an over-the-counter form."

WD: "I can only tell you that Carole has had perfect blood levels on the over-the-counter preparation she was taking. It works just fine."

RN: "Okay. I guess we''ll just give her the 50,000 unit tablet."


From the alarm it raises trying to administer nutritional supplements in a hospital, you'd think that Osama Bin Laden had been spotted on the premises.

I laugh about this every time it happens: A patient gets hospitalized for whatever reason and the hospital staff see the supplement list with vitamin D, fish oil at high doses, iodine, etc. and they panic. They tell the patient about bleeding, cancer, and death, issue stern warnings about how unreliable and dangerous nutritional supplements can be.

My view is the exact opposite: Nutritional supplements are a wonderful, incredibly varied, and effective array of substances that, when used properly, can provide all manner of benefits. While there are selected instances in which nutritional supplements do, indeed, have interactions with treatments provided in hospitals (e.g., Valerian root and general anesthesia), the vast majority of supplements have none.

Does fish oil cause blood thinning?

Omega-3 fatty acids from fish oil have the capacity to "thin the blood." In reality, omega-3s exert a mild platelet-blocking effect (platelet activation and "clumping" are part of clot formation), while also inhibiting arachidonic acid formation and thromboxane.

But can fish oil cause excessive bleeding?

This question comes up frequently in the office, particularly when my colleagues see the doses of fish oil we use for cardiovascular protection. "Why so much fish oil? That's too much blood thinning!"

The most recent addition to the conversation comes from a Philadelphia experience reported in the American Journal of Cardiology:

Comparison of bleeding complications with omega-3 fatty acids + aspirin + clopidogrel--versus--aspirin + clopidogrel in patients with cardiovascular disease.(Watson et al; Am J Cardiol 2009 Oct 15;104(8):1052-4).

All 364 subjects in the study took aspirin and Plavix (a platelet-inhibiting drug), mostly for coronary disease. Mean dose aspirin = 161 mg/day; mean dose Plavix = 75 mg/day. 182 of the subjects were also taking fish oil, mean dose 3000 mg with unspecified omega-3 content.

During nearly 3 years of observation, there was no excess of bleeding events in the group taking fish oil. (In fact, the group not taking fish oil had more bleeding events, though the difference fell short of achieving statistical significance.) Thus, 3000 mg per day of fish oil appeared to exert no observable increase in risk for bleeding. This is consistent with several other studies, including that including Coumadin (warfarin), with no increased bleeding risk when fish oil is added.

Rather than causing blood thinning, I prefer to think that omega-3 fatty acids from fish oil restore protection from abnormal clotting. Taking omega-3 fatty acids from fish oil simply restores a normal level of omega-3 fatty acids in the blood sufficient to strike a healthy balance between blood "thinning" and healthy blood clotting.

Heart Scan Blog readers take impressive doses of omega-3s

Here are the results from the latest Heart Scan Blog poll:

What is your dose of omega-3 fatty acids, EPA + DHA, from fish oil? (Add up the total content of EPA + DHA per capsules; multiply times number of capsules.)

The 479 respondents answered:

Less than 1000 mg per day
65 (13%)

1000-1999 mg per day
145 (30%)

2000-2999 mg per day
98 (20%)

3000-3999 mg per day
79 (16%)

4000-4999 mg per day
33 (6%)

5000-5999 mg per day
14 (2%)

6000 mg per day or more
45 (9%)


The poll did not discriminate between who has heart disease, who does not; who is taking omega-3 fatty acids for high triglycerides or for reduction of lipoprotein(a) (which requires high doses), or other indications. So variation is to be expected.

We can say that nearly all respondents are likely receiving sufficient omega-3s to impact cardiovascular risk, since the benefits begin just by consuming fish twice per month. I am especially impressed at the proportion of respondents (53%) who take at least 2000 mg per day of EPA + DHA. It's clear that people are really embracing the notion that omega-3 fatty acids pack a real wallop of health benefits.

Because different people in different situations and lipid/lipoprotein patterns have different omega-3 needs, there is really no "right" or "wrong" dose of omega-3 fatty acids.

However, there are several factors that enter into knowing your ideal omega-3 intake:

--Higher triglycerides require higher doses
--Lipoprotein(a) can respond to higher doses
--Having coronary or carotid plaque means you desire a "therapeutic" dose of omega-3s, not just a "preventive" dose

Time is a factor, also: The longer you take omega-3s, the higher your blood levels go. You can accelerate the replacement of non-omega-3s with higher doses of omega-3s.

But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL.

Much of the uncertainty about dosing will also be cleared up as we get more experience with the Omega-3 RBC Index, i.e, the proportion of fatty acids in red blood cells that are omega-3s. We are currently aiming for an Omega-3 Index of 10%, given the heart attack reductions observed at this level.

How old are you?

George walks into my office. I ask him his age.

"I'm 21 years old," he declares.

Yet I look at George. He's got gray thinning hair, his posture is slumped forward rather than erect, the flesh on his upper arms hangs loosely, he's got wrinkles on his hands and face, brown spots on the back of his hands and arms. He looks more like 70 years old to me. "I don't think you're 21 years old. I think you're 70."

"Prove it," he says.

Okay. What now? Minus any formal identification like a driver's license, how do I prove that George is really 70-something and not 20-something? Not an easy thing, when you think about it. If George were a tree, I'd cut him down and count his rings. Is there such a phenomenon in humans?

This is actually a fascinating area of research, looking for reliable biomarkers of aging.

Among the most quantitative markers of aging is telomere length. Telomeres were once dismissed as nonsense sequences in DNA. However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

What can slow or stall the shortening of telomere length? There are two I'm aware of:

1) Caloric deprivation--i.e., taking in fewer calories. This was among the theories explored by Dr. Roy Walford during his Biosphere2 experience, based on his work in mice that showed that caloric deprivation nearly doubled lifespan.

2) Vitamin D--Richards et al (2007) found that, the higher the vitamin D, the longer the telomere length. The highest vitamin D levels conferred a 5-year effective difference in telomere length.

So, if I could look inside George's cells and count his telomeres, I could judge with confidence whether he was 21 or 70. Or, he could take vitamin D sufficient to increase blood levels to a healthy range and be more like 65.

No high blood pressure

Primitive cultures that were, until recently, unexposed to the modern world, reveal some important insights into blood pressure.

The Yanomamo of South American, the Xingu Indians of Brazil, rural Kenyans, and the natives of Papua, New Guinea have average blood pressures of 103/63 mmHg. Even more incredibly, while 90% of modern Americans will develop high blood pressure as they age, the members of these primitive cultures do not develop age-related hypertension.

What's the secret? Perhaps the full "secret" of their remarkably low blood pressure has not been fully unraveled, but several observations have emerged:

--They are not exposed to modern processed foods like pretzels, crackers, and breakfast cereals.
--Low-carbohydrate foods. Carbohydrates are largely the product of the food industry, convenience foods bought in stores. No such thing in the jungle.
--Living outdoors, having to forage and hunt, walk to your destination, not drive or wait in line for food.
--Outdoor lives, wearing little more than a few strands of clothing, exposes you to plentiful vitamin D activation from sunlight exposure.
--Consuming wild game, rich in omega-3 fatty acids, enhances endothelial health and reduces blood pressure.
--Wild plants, roots, and berries, as well as wild game, along the coast, are richer in iodine.

The studies examining the habits of the Yanomamo and other primitive cultures focused principally on sodium intake. Indeed, the very low sodium intake of primitive cultures was associated with lower blood pressure--up to 6 mmHg reduction. But there's clearly more to learn than "cut your salt."

Name that food

What common food can:

• Cause destructive intestinal damage that, if unrecognized, can lead to disability and death?
• Increase blood sugar higher and faster than table sugar?
• Trigger an autoimmune inflammatory condition in the thyroid (Hashimoto’s thyroiditis)?
• Create intestinal bloating, cramps, and alternating diarrhea and constipation, often labeled irritable bowel syndrome?
• Trigger schizophrenia in susceptible individuals?
• Cause behavioral outbursts in children with autism?
• Cause various inflammatory diseases such as rheumatoid arthritis, ulcerative colitis, dermatitis herpetiformis, systemic lupus, pancreatic destruction, and increase measures of inflammation like c-reactive protein?
• Cause unexplained anemia, mood swings, fatigue, fibromyalgia, eczema, and osteoporosis?


The food is wheat. Yes, the ubiquitous grain we are urged to eat more and more of by the USDA (8-11 servings per day, according to the USDA food pyramid), American Heart Association, American Dietetic Association, and the American Diabetes Association. Wheat is among the most destructive ingredients in the modern diet, worse than sugar, worse than high-fructose corn syrup, worse than any fat.

What other common food can result in such an extensive list of diseases, even death?

Celiac disease alone, a severe intestinal inflammatory condition from wheat gluten, affects an estimated 3 million Americans (Celiac Disease Foundation). The medical literature is filled with case reports of deaths from this disease, often after many years of struggle with incapacitating intestinal dysfunction and the sufferer's last days plagued by encephalopathy (brain inflammation).

What happens when you remove wheat from the diet?

The majority of people quickly shed 20-30 lbs in the first few weeks, selectively lost from the abdomen (what I call “wheat belly”); blood sugar plummets; triglycerides drop up to several hundred milligrams, HDL increases, LDL drops (yes, wheat elimination is a means of achieving marked reduction in LDL cholesterol, especially the small, heart disease-causing variety); c-reactive protein plummets. In addition to this, intestinal complaints improve or disappear, rashes improve, inflammatory conditions like rheumatoid arthritis improve, diabetes can improve or be cured, and behavioral disorders and mood improve.

Along with the ill-fated low-fat dietary advice of the last 40 years, the advice to eat plenty of "healthy whole grains" is responsible for untold disease and suffering. Yes, if you start with a fast food and junk diet and replace some of the calories with whole grains, you will be better off. (That was the logic--the Nutritional Syllogism--of the studies that established the benefits of whole grains over processed, "white" grains.)

But eliminate wheat grains and health takes a huge leap forward. And, no, there is no such thing as wheat deficiency--B vitamins, insoluble fiber, some protein--can easily be replaced by other foods.

Heart Defects Simplified



For as long as I've known him, echocardiography technologist, Ken Heiden, has had a deep fascination with congenital heart disease. Ken has just written a wonderful book on congenital heart disease called Heart Defects Simplified.

While this is a bit off-topic for the Heart Scan Blog, I know that there is a serious lack of helpful information for people with congenital heart disease and parents of children with congenital heart defects. So I asked Ken to tell us something about his book.



WD: I've reviewed your book and have been thoroughly impressed with the clarity and detail with which you handle a complicated topic. You somehow manage to make it easy to grasp, far more than any other resource I've used in past. Do you feel that your book serves a previously unmet need?

KH: This book serves an unmet need in that it presents the complex subject of congenital heart defects in a simplified manner. Most books on this subject are anywhere from 300-1700 pages in length and tend to be written for doctors. Further, most of these books have very few diagrams, and they rely upon their explanations to describe these defects.

Heart Defects Simplified is 104 pages in length, describes the most common defects, including surgical repairs, in a two-page format with full-color diagrams on the left and complete descriptions on the right of each chapter. The book is particularly written for sonographers, nurses and parents, but it is valuable for anyone interested in this subject. It is particularly useful in clinical situations because it is convenient to lay out at your side with a coil-bound format and durable pages. Further, there are appendixes which include "Surgical Procedures in Alphabetical Order," "Prevalence of Congenital Heart Disease," "Scanning Protocols for Echocardiographers," "Imaging Tips," a glossary and a worksheet for echocardiographers.


WD: I know that many people with loved ones who have congenital heart defects, particularly parents of children with such conditions, are often kept in the dark about the details of the condition. Is your book suitable for the non-technical reader, such as parents?

KH: This book is an excellent resource for parents. It is written in language that is understandable by parents as well as technologists and nurses. The full-color diagrams provide invaluable insight into this very complex world. Most importantly, this book attempts to make the subject of congenital heart defects accessible to anyone who wishes to comprehend this subject.


WD: I understand that people with congenital heart defects and parents are active participants in online discussion groups. Will your book serve as a resource for people who participate in these groups?

KH: This book is not only a resource for sonographers and parents, but the book is accompanied by a blog (HeartDefectsforEveryone.blogspot.com) that attempts to address many of the concerns commonly encountered with congenital heart defects. This blog is a work in progress, but I hope to provide a forum for parents, healthcare personnel, and others to share their questions and concerns about congenital heart disease.

My experience with the omega-3 index

I just got back my own results from the Gene Smart laboratory reporting my omega-3 index and omega-6:omega-3 ratio.

My results:

Omega-3 index: 8.2%

Omega-6:omega-3 index: 3.2 to 1

Not too bad, but not as good as I'd expected. Hmmm.

Although the omega-3 index of 8.2% puts me in the lower risk category for sudden cardiac death, I was hoping for a level of 10% or slightly greater, the level that I believe is more likely to be related to plaque inactivation or reversal. I obtained this level of omega-3 averaging an intake of EPA and DHA of about 2500 mg per day.

I was somewhat disappointed by the omega-6:omega-3 index. Although it's clearly better than the American average range of 20:1, it is short of the ideal of 2:1 or even 1:1. Since I purposely avoid omega-6-rich sources like corn oil, vegetable oils, sunflower or safflower oils, I wonder if I've overdone the nuts. The two ways to improve the omega-6:omega-3 ratio are to 1) decrease omega-6, or 2) increase omega-3. I'm going to do both.

So I thought I was doing pretty well. But there's clearly room for improvement.

Remember: If just reduction of cardiovascular risk is your interest, then a lackadaisical attitude towards these issues might work. But if your interest is elimination of risk and reversal of atherosclerotic plaque, then it pays to go the extra mile. In this case, knowing your omega-3 index and omega-6:omega-3 ratio might tighten up your program.

The Omega-3 Index: The higher, the better?

So you take a few fish oil capsules every day and eat fish once or twice a week. What is the blood and tissue level of omega-3 fatty acids generated by your habits?

A number of variables enter into the equation. For instance, if you take fish oil capsules, what is the concentration of omega-3 fatty acids? How well are they absorbed? After absorption, how effectively are omega-3 fatty acids incorporated into cell membranes?

Even if you take fish oil supplements, it is hard to know just how much you’ve increased blood levels. It is now possible to measure the amount of omega-3 fatty acids in your bloodstream, a value called the omega-3 index. Too little and you might still be at high risk for cardiovascular events.


The Omega-3 index and sudden cardiac death

Two large studies have demonstrated that higher omega-3 blood (the level in red blood cells, or RBCs) levels were associated with reduced likelihood of sudden cardiac death. The risk for sudden cardiac death was 10-fold higher for the lowest omega-3 RBC levels compared to the highest.



Harris WS 2008; adapted from Siscovick DS et al 1995 and Albert CM et al 2002
(The omega-3 Index was derived from whole blood omega-3 levels, which correlate with RBC omega-3 levels, and are thus “estimated.”)



What’s the average omega-3 RBC level for Americans? Most Americans have omega-3 RBC levels in the 2.5-4.0% range, consistent with the tallest bars at the left and associated with greatest risk for sudden cardiac death. People with heart disease can have levels less than 1%. Some authorities propose that this new measure be called the omega-3 index.

Subsequent studies have shown that the omega-3 index has greater power to discriminate who will have a heart attack or die from sudden cardiac death better than any other common laboratory measure of coronary risk, including LDL cholesterol, HDL cholesterol, triglycerides, total cholesterol to HDL ratio, homocysteine, and c-reactive protein.

Just as hemoglobin A1c offers a 3-month look into blood glucose levels, the omega-3 index reflects your long-term omega-3 intake. The quantity of RBC omega-3s also closely parallels the quantity of omega-3s in heart tissues.


What is an ideal omega-3 index?


The above studies relating RBC omega-3 levels and sudden cardiac death suggest that a level of 6.3-7.3% is associated with far fewer fatal events?but events are not eliminated at this level. Is there even greater benefit with levels higher than 6.3-7.3%?

A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks. This suggests that even higher levels are necessary to prevent non-fatal events.

Should we target 10%? 12%? Maybe higher? Any higher and we are toeing the level achieved by the Inuits, the “Eskimoes” of Greenland, northern Canada and Alaska who have been observed to have a low rate of heart disease.


What’s your omega-3 index?

The appreciation of the importance of omega-3 fatty acids marks one of the greatest health revelations of the last 50 years. We can now measure it.

The ability to measure the proportion of omega-3 fatty acids in red blood cells may provide yet another means for all of us to further reduce risk for cardiovascular events.

If you are interested in knowing your omega-3 index, we are now making the fingerstick test kits available by going here.