Calling all super-duper weight losers!






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

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

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

Lp(a): Be patient with fish oil

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

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

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

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

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

Baby your pancreas

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

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

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

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

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

Bread equals sugar

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

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








 

 

 

 

 

 

 

 

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

Gluten-free carbohydrate mania

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



 

 

 

 

 

 

 

 

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

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

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

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

Gluten-free is going DOWN

The majority of gluten-free foods are junk foods.

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

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

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

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

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

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

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

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

Medicine ain't what it used to be

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

For instance:

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

Normal cholesterol panel . . . no heart disease?

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

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

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

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

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

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

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

 

Idiot farm

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

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

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

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

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

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

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

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

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

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

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

Eat triglycerides

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

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

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

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

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

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

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

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

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

 

 

 

 

 

 

 
All posts by william-davis

Disease Engineering

Imagine you contract pneumonia.

You have a fever of 103, you’re coughing up thick, yellow sputum, breathing is getting difficult. You hobble to the doctor, who then fails to prescribe you antibiotics. You get some kind of explanation about unnecessary exposure to antibiotics to avoid creating resistant organisms, yadda yadda. So you make do with some Tylenol®, cough syrup, and resign yourself to a few lousy days of suffering.

Five days into your illness, you’ve not shown up for work, you’re having trouble breathing, and you’re getting delirious. An emergency trip to the hospital follows, where a bronchoscopy is performed (an imaging scope threaded down your airway) and organisms recovered for diagnosis. You’re put on a ventilator through a tube in your throat to support your breathing and treated with intravenous antibiotics. Delayed treatment permits infection to escape into the fluid around your lungs, creating an “empyema,” an extension of the infection that requires insertion of a tube into your chest through an incision to drain the infection. You require feeding through a tube in your nose, since the ventilator prevents you from eating through your mouth. After 10 days, several healing incisions, and a hospital bill totaling $75,000, you’re discharged only to be face eights weeks of rehabilitation because of the extreme toll your illness extracted. Your doctor also advises you that, given the damage incurred to your lungs and airways, you will be prone to more lung infections in the future, and similar situations could recur whenever a cold or virus comes long.

A disease treatable by taking a two week, $20 course of oral antibiotics at home has been converted into a lengthy hospital stay that generated extravagant professional fees, testing, and costly supportive care. You’ve lost several weeks of income. You’re weak and demoralized, frightened that the next flu or virus could mean another trip to the hospital.

Such a scenario would be unimaginable with a common infection like pneumonia, or it would be grounds for filing a malpractice lawsuit. But, as horrific as it sounds in another sphere of healthcare, it is, in effect, analogous to how heart disease is managed in current medical practice.

First, you’re permitted to develop the condition. It may require years of ignoring the telltale signs, it may require your unwitting participation in unhealthy lifestyle choices. Palliative treatments that slow, but don't stop, the progression of disease are prescribed like cholesterol drugs. The process then eventuates in some catastrophe like heart attack or similar unstable heart situation, at which point you no longer have a choice but to submit to major heart procedures. That’s when you receive your heart catheterization, coronary stents, bypass, defibrillators, etc. and you're proudly declared a "success" of medical technology.

Of course, none of these procedural treatments cures the disease, no more than a Band Aid® heals the gash in your leg. The conditions that were present that created your heart disease continue, allowing a progressive disease to worsen. At some point, you will need to return to the hospital for yet more procedures when trouble recurs, which it inevitably does.

A coronary bypass operation costs, on average $85, 653 (AHA 2008 Update; based on 2004 data). That doesn't include the $25,433 cost for the heart catheterization performed by a cardiologist to provide the surgical roadmap of your coronary arteries. If there are any complications of your procedure, then your hospital bill may total a substantially higher figure.

$85, 653 is just the upfront financial pay-off. Over the long run, your life is actually worth far more to the cardiovascular healthcare system because no heart procedure yields a permanent fix. In fact, repeated reliance on the system is the rule.

In fact, over 90% of people who enter the American cardiovascular healthcare system do so through a revolving door of multiple procedures over several years. It is truly a rare person, for instance, who undergoes a coronary bypass operation, never to be seen again the wards of the hospital because he remains healthy and free of catastrophe. A much more familiar scenario is the man or woman who undergoes two or three heart catheterizations, receives 3,4, or 6 stents, followed a few years later by a heart bypass, pacemaker, defibrillator, as well as the tests performed for catastrophe management, such as nuclear stress test, echocardiogram, laboratory blood analysis, and consultation with several specialists. Re-do bypass surgeries--a 2nd, 3rd, or 4th bypass--now comprise 25% of all bypass procedures.

The total revenue opportunity is many-fold higher than the initial 80-some thousand dollars, but instead totals hundreds of thousands of dollars per person.

What motivation can there possibly be to 1) identify coronary disease early, when in its asymptomatic stage, then 2) identify its causes, then 3) correct the causes, and finally 4) shut off the disease? You and I can accomplish this with a few hundred dollars of cost, perhaps a few thousand over many years (to cover costs of fish oil, vitamin D, niacin, and whatever else it takes to stop the expression of the disease). Nobody therefore profits substantially from your prevention effort--except you.

Then what if nobody told you that heart disease could be managed this way? That's what I mean by "disease engineering."

Dr. Steven Gundry on The Livin' La Vida Low-Carb Show

I stumbled on a great interview with cardiothoracic surgeon, Dr. Steven Gundry, on Jimmy Moore's Livin' La Vida Low-Carb Show. (Or, cut and paste: http://www.thelivinlowcarbshow.com/dr-steven-gundry-part-1-episode-179/)

Dr. Gundry has some fun ways of looking at eating and health. I found his comments on the activation of genes (discussed at a very light, non-scientific level) useful. He argues that when humans consume sugar-containing foods, the signal received by the body is that winter is approaching and it's time to build up fat stores in anticipation of the food shortages of cold weather. He finds parallels for this phenomenon in other species. Of course, for humans, winter (in the form of extended calorie deprivation) never comes. In fact, you might argue that, given our excessive reliance on grains, corn, and sugars, that we are, in effect, always in anticipation of a winter that never comes.

I've not read Dr. Gundry's books, but I found this light interview a lot of fun.

Does fish oil ADD to statin therapy?

Yet another patient came to my office today saying, "My primary doctor said that I should stop taking fish oil. He say's that I don't need it because I take Crestor."

The woman was in tears, confused and frightened over a potential disagreement between her doctors.

Is this true? If someone takes a statin drug, like Crestor, Lipitor, Zocor (simvastatin), pravachol, or lovastatin, they don't need to take anything else because the statin drug is so powerful that it eliminates risk?

No. Not even close to the truth.

First of all, let's accept that virtually the entire body of statin drug literature--hundreds of studies, billions of dollars spent--was paid for by the drug industry. It's no news that studies paid for by the sponsor are likely to favor the sponsor. Imagine Ford sponsored a study of Ford vs. GM cars vs. Toyota, paying $10 million to fund the effort. Guess who is likely to come out on top? "Studies show that Ford makes the best car in America." (Sorry, I don't mean to pick specifically on Ford. It's just a widely-recognized brand.)

So that means that the statin literature likely overestimates the benefit of statin drugs. Even so, it's clear from the hundreds of studies performed that the best we can hope for by taking statin drugs is a reduction of heart attack and death from heart attack of 30-35%--best case. That doesn't sound like elimination of risk to me.

What are the incremental benefits of adding omega-3 fatty acids from fish oil added to statins? The best data originate with the JELIS Trial (Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis), in which 19,000 Japanese participants (who already have a high omega-3 intake from diet, usually ranging from 1800-3000 mg per day) experienced a 19% reduction (relative reduction) in cardiovascular events.

GISSI Prevenzione demonstrated a 28% reduction in heart attack, 45% reduction in death from heart attack with fish oil.

Omega-3 fatty acids from fish oil also:

--Reduce triglycerides dramatically
--Accelerate after-eating clearance of digestive by-products, i.e., they correct post-prandial abnormalities
--Modify the character (fragmentation potential, structural strength) of plaque
--Raise HDL modestly

If you buy your fish oil from Sam's Club, Costco, or other discounter, a healthy dose of fish oil might cost you $3 per month. Compare that to the $120 per month average cost of a statin agent. Why is there even a discussion over this?

Sadly, the doctor on Main Street, U.S.A, is the unwitting puppet of the pharmaceutical industry. The pretty drug company representative with nice legs and a cute smile promises lunch, dinner and . . who knows what else? Wink. The fifty-something, hairline-receding doctor can't resist. "Of course I'll prescribe your drug!"

Don't kid yourself: The drug industry knows precisely how to manipulate the behaviors of the deliverers of their products.

So, do statin drugs make omega-3 fatty acids from fish oil irrelevant? Absolutely not.

It's all about trying to inch closer and closer--not to reduction--but to elimination of risk for heart disease.

HDL: “H” is for “happy”

What role do emotions play in HDL cholesterol?

I’ve often observed a peculiar phenomenon: People who come to the office or hospital in the midst of a difficult emotional situation-e.g., stress at home, financial struggles, hospitalization (usually an unhappy occasion)- can show dramatic drops in HDL cholesterol. Not uncommonly, HDL drops 20 or more mg/dl.

Take Agnes’s case. Agnes had to go to the hospital for an elective procedure, one she’d been dreading for months. Previously, Agnes had been proud of the fact that she’d incrased HDL from 42 mg/dl range all the way up to 71 mg/dl. She accomplished this dramatic increase by eliminating wheat and cornstarch from her diet (which helped her lose 24 lbs), taking vitamin D and omega-3 fatty acids from fish oil, exercise, 2 oz of dark chocolate per day, and a glass of red wine with dinner.

Although I wouldn’t have bothered checking a cholesterol panel for such a procedure, the hospital had a checklist that included a cholesterol panel regardless of necessity. (Such checklists are common in hospitals, meant to ensure that certain basic issues are not overlooked.)

Agnes’ HDL: 29 mg/dl-a 42 mg drop.

Agnes will recover and her HDL will rebound, but the same effect can occur with other stressful situations, such as death in the family, financial worries, marital stress, etc., as well as physical illness.

Interestingly, the opposite may also hold true: Low HDL may increase risk for depression and stress. A study from Finland of 124 depressed persons, for instance, showed a 240% increased likelihood of depression in those with lower HDL cholesterols.

In other words, there seems to be a curious interdependence between HDL and emotions.

Why? Does it represent the indirect effect of adrenaline, cortisol, or other “stress hormones”? Do factors that relate to low HDL, such as unhealthy diet full of carbohydrates and physical inactivity, also tend to cultivate depression?

It certainly seems to be a chicken-egg situation, with one often leading to the other.

Moral of the story: Maintaining a sense of optimism and engaging in activities that bring you satisfaction and enjoyment can help raise HDL, as can strategies such as those followed by Agnes. Avoiding unnecessarily stressful situations can help. HDL is important, since higher levels are associated with much reduced risk for heart disease . . . and perhaps depression.

Plaquology

Plaquology: A new term.

Plaquology: def: (plaque-: atherosclerotic plaque; -ology: study of.) The study of atherosclerotic plaque, originating in the early 21st century during the time period when the material underlying atherosclerosis gained recognition as a measure superior to "risk factors" for cardiovascular disease. Previous to the plaque concept, blood measures of cholesterol and adverse lifestyle habits, such as smoking and sedentary lifestyle, alone had been used to predict potential for cardiovascular events. With acceptance of the concept of plaque measurement, the concept of risk factors was abandoned.


Look it up in the current Oxford Dictionary of the English Language, or Webster's Dictionary, and I'm afraid that you still won't find plaquology . . . but you should.

I'm currently rewriting many parts of the Track Your Plaque book. The rewriting process has caused me to review just how much we've learned these past few years. One of the phenomena that fascinates me is that we now have non-medical people--teachers, software people, engineers, bankers, bed and breakfast owners, retired businesspeople, etc.--all discussing the finer points of coronary atherosclerotic plaque--plaquology--what constitutes plaque, what triggers plaque inflammation, how to quantify potential for plaque rupture or plaque quiescence, what effect various treatments have on plaque composition and behavior, etc.

We now have a legion of Plaquologists!

I'm very proud of our Plaquologists. Having devoted themselves to the study of plaque, their level of knowledge now exceeds that of 99% of practicing physicians, including my colleagues, the cardiologists. While cardiologists spend their day squashing/cutting/vaporizing plaque, they are no more experts in plaquology than a carpenter is an expert in trees. More often than not, cardiologists view plaque as just something that gets in their way, rather than the quantifiable, modifiable, reversible material that we can exert control over.

One of the software tools currently in the works for the Track Your Plaque website is a certification process. Members will be able to gain a "certification" in various topics relevant to plaquology, such as plaque quantification, lipoprotein testing, and nutritional supplements.

How about a Doctor of Plaquology?

Thyroid perspective update

Since the publication of the extraordinary HUNT Study relating the entire spectrum of thyroid function and heart issues, I have been vigorously and systematically examining thyroid function in numerous patients.

While there's no news in relating flagrant low thyroid function with triggering heart disease in several forms, the cut-off between low thyroid and normal thyroid has been a matter of dispute for decades.

In the early 20th century, low thyroid function wasn't diagnosed until someone gained 40 lbs, displayed extravagant amounts of edema (water retention) in the legs and huge bags under the eyes, hair fell out in clumps, and often eventually proved fatal. At autopsy, these unfortunates also showed advanced and extensive quantities of coronary atherosclerotic plaque.

Low thyroid is usually diagnosed on the basis of the blood test, thyroid stimulating hormone, or TSH. TSH is a pituitary gland hormone responsible for stimulation of thyroid function. When thyroid function flags, the pituitary increases TSH release. Thus, a high TSH signals lower thyroid hormone levels.

The difficulty is in distinguishing normal thyroid function from low thyroid function judged by TSH levels. As the years have passed, in fact, the cut-off for "normal" TSH has drifted lower and lower.

The HUNT Study, I believe, clinches the argument: A TSH of 1.5 or lower, perhaps even 1.0 or lower, is desirable to eliminate the excess cardiovascular risk provided by an underactive thyroid, not to mention feel better: more energetic, clearer thinking, greater well-being.

Having now applied this renewed appreciation for thyroid, I have come to believe that:

--Low thyroid function, even subtle levels, are rampant and far more common than ever previously thought. In my office practice, the case could be made that several people per day are marginally or mildly hypothyroid (low in thyroid).
--Restoration of optimal thyroid levels facilitates correction of lipid measures, especially LDL cholesterol and, to a lesser degree, lipoprotein patterns dependent on the insulin axis such as triglycerides and small LDL. It's a lot happier way to correct lipids than statins.

I don't discount the value of feeling better. People who feel better--more energetic, more upbeat, clearer thinking--tend to do better in health overall. If thyroid restoration is a part of that equation, then greater attention should be paid to this facet of health on our way to optimal heart health.

Though I sometimes feel like an endocrinologist dispensing desiccated thyroid (rarely the synthetic T4), I believe that this has been a previously neglected and important part of our effort to achieve coronary plaque stabilization and reversal.

Accidental Health


"I shall never have smallpox for I have had cowpox; I shall never
have an ugly pockmarked face."

Such was the idle comment made by a milkmaid to Edward Jenner in 1768 when Jenner was 19, a remark that later prompted his investigations into using isolates of cowpox injected into humans as the first vaccination against the devastations of the European epidemic of smallpox.

(A caricature of Jenner administering cowpox vaccine to people, causing them to sprout bovine appendages. Image courtesy Wikipedia and the Library of Congress.)

When I look back, something similar has happened here.

Although the Track Your Plaque program is intended to stop and reverse coronary plaque using the only available means of tracking coronary plaque, i.e., heart scans, an unintended panel of benefits follow:

--People lose weight, often dramatically
--People gain greater energy
--Thinking is clearer, emotions more stable
--Sleep is deeper
--Bone density increases
--Physical strength and coordination improve
--Winter blues dissipate
--Blood sugar drops dramatically
--Blood pressure drops

Cholesterol (lipid) panels also settle to values that most physicians deem impossible or impractical, given our target of 60:60:60, i.e., LDL 60 mg/dl or less, HDL 60 mg/dl or higher, triglycerides 60 mg/dl or less. And medications are not always necessary to achieve these values. (When I show these values to my colleagues, they declare them flukes, unobtainable only in select people with high doses of medications.)

I didn’t set out to find the next weight loss solution, nor the key to boundless energy. My goal was "simpler": create a program of heart health. I am, after all, a cardiologist.

I was so intently focused on achieving incremental improvements over the steps leading to heart disease prevention that I failed to recognize the profound phenomena that accompanied it: people were quicker, smarter, thinner, and healthier.

In other words, I believe that we have inadvertently created a program of super health and performance.

Ironically, most people don't want to talk about heart disease, let alone reversal of heart disease. They do want to talk about getting thinner, feeling more energetic, living longer, better cholesterol values, etc.

Perhaps there's a lesson in this.

Livin' La Vida Low Carb interview


I recently provided an interview for Livin' La Vida Low Carb's irrepressible Jimmy Moore.

Jimmy runs a fun set of blogs, webcasts, and the like to broadcast this message of reducing carbohydrates in the diet. He credits his 210 lb weight loss to a strict low-carbohydrate and exercise program.

For the interview, just go to The Livin' the Vida Low Carb Show, Episode 185, or click here.

And click here for Part 2


For more of Jimmy Moore's spin on the entire low-carbohydrate diet experience, he maintains several popular blogs, including Carb Wire and The Livin' La Vida Low-Carb Blog.

Wheat withdrawal: How common?

In response to the recent Heart Scan Blog poll,

Have you experienced fatigue and mental fogginess with stopping wheat, i.e., "wheat withdrawal"?

the 104 respondents said:


Yes, I have experienced it: 26 (25%)

No, I stopped wheat and did not experience it: 65 (62%)

I'm not sure: 3 (2%)

I haven't tried it but plan to: 7 (6%)

I haven't tried it and don't plan to: 3 (2%)



So 25% of respondents reported experiencing the fatigue and mental fogginess of wheat withdrawal. This is similar to what I observe in my practice.

I counsel many patients to consider the elimination of wheat, as well as cornstarch products, in an effort to regain control over:

--Weight
--Appetite
--Low HDL
--High triglycerides
--Small LDL
--High blood sugar
--High blood pressure

All of these issues respond--often dramatically--to elimination of wheat and cornstarch.

Why would there be undesirable effects of eliminating wheat?

One clear issue is that elimination of wheat and other sugar-equivalents deprives your body of glucose. Your body then needs to resort to fatty acid metabolism to generate energy. Apparently, some people are inefficient at this conversion, having subsisted on carbohydrates for the last few decades of their lives. However, as fatty acid metabolism kicks in, energy generation improves. That is my (over-)simplified way of reasoning it through.

However, are there other explanations behind the mental fogginess, drop in energy, and overwhelming sleepiness? Some readers of this blog have suggested that, since opioid-like sequences (i.e., amino acide sequences that activate opiate receptors) are present in wheat, perhaps withdrawal from wheat represents a lesser form of opiate withdrawal. I find this a fascinating possibility, though I know of no literature devoted to establishing a cause-effect relationship.

Whatever the mechanism, I find it very peculiar that this food widely touted by the USDA, American Heart Association, and other agencies actually triggers a withdrawal syndrome in approximately 25% of people. Spinach does not trigger withdrawal. Nor does flaxseed, olive oil, almonds, and countless other healthy foods.

Then why would whole wheat grains be lumped with other healthy foods?

Treat the patient, not the test

"Treat the patient, not the test."

That is a common "pearl" of medical wisdom often passed on during medical training.

It refers to the fact that we should always view any laboratory or imaging test in the context of the live, human patient and not just treat any unexpected value that doesn't seem to make sense.

I raise this issue because it recently came up on a discussion on the Track Your Plaque Forum. A Member with a high heart scan score of around 1100 was advised by his doctor that it should be ignored, because he'd prefer to treat the patient, not the test. The patient is apparently slender, physically active, and entirely without symptoms, with favorable cholesterol values as well. The high heart scan score didn't seem to jive with the appearance of the patient, as viewed by this doctor.

This common phrase is meant to impart wisdom. It is a reminder that we treat real people, not just a jumble of laboratory values.

But the unspoken part of the equation is that judgment needs to be applied. A well looking person who shows an unexpected rise in white blood cell count could just have a screwy result, or could have leukemia. Liver tests (AST, ALT) that top 400 could represent a fluke, or dehydration incurred during a long workout, or hepatitis from a long ago blood transfusion.

Yes, treat the patient. But don't be an idiot and entirely dismiss the signficance of an unexpected laboratory or imaging test. A heart scan score of 1100 should be as readily dismissed as discovering a white blood cell count of 90,000 (normal is less than 12,000), or a 5 cm mass in the lung. The absence of symptoms or the failure of conventional risk factors to suggest causation is insufficient reason to dismiss the concrete findings of a test.

In this particular person, dismissing the significance of the heart scan finding by suggesting that the doctor should treat the patient, not the test, is tantamount to:

--Colossal ignorance
--Malpractice
--A certain sentencing of the hapless patient to future major heart procedures, heart attack or death (20-25% likelihood every year, or a virtual certainty over the next 5 years).

There is an ounce of wisdom in this old medical pearl. But there's also plenty of room for a knuckleheaded doctor to misconstrue and abuse its meaning for the sake of covering up his/her ignorance, laziness, or lack of caring.