In search of wheat: We bake einkorn bread

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

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

Here's what we did:

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











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





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









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



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

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

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

The einkorn dough also distinctly smelled like peanut butter.





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

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

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

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



Margaret Pfeiffer's book is available on Amazon:

Ezekiel said what?

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

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

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

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

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


Are you sure about that?

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

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

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

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

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

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

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

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

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

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



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

Low-carb gynecologist

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

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

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

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

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

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


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

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

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

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

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

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

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



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

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

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


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

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

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

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


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

Contact information:

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

Track Your Plaque reduces healthcare costs 35%

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

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

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

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

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

Richard Rawle
CEO Tosh Inc.


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

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

In search of wheat

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

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

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

So how can wheat be bad?

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

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

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

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

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

Super-carbohydrate

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

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

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

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

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

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

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

Emmer, einkorn, and agribusiness

10,000 years ago, Neolithic humans did not obtain wheat products from the bagel shop, grocery store, or Krispy Kreme. They obtained wheat by locating a nearby wild-growing field of wild emmer or einkorn wheat grass, then harvesting it with their stone sickles.

Neolithic humans, such as the Natufians of the Fertile Crescent, carried their freshly-cut wheat home, then ground it by hand using homemade mortar and pestle. As yeast-raised bread was still some 5000 years in the future, emmer and einkorn wheat was not used to bake bread, but was consumed as a porridge in bowls. Einkorn has the simplest genetic code of 14 chromosomes, while emmer has 28 chromosomes.

A third variety of wheat appeared on the scene around 9000 years ago, a natural hybridization between emmer and goat grass, yielding the 42-chromosome Triticum aestivum species. Egyptians learned how to cause wheat to rise around 3000 BC, yielding bread, rather than the unleavened flatbreads of their predecessors.

From the original three basic varieties of wheat available to Neolithic man, over the past 30 years wheat has exploded to over 25,000 varieties. Where did the other 24,997+ strains come from?

In the 1980s, thousands of new wheat strains arose from hybridization experiments, many of them conducted in Mexico. Then, in the late 1980s, genetic engineering quietly got underway in which geneticists inserted or deleted single genes, mostly designed to generate specific characteristics, such as height, yield per acre, drought resistance, but especially resistance to various pesticides and weed killers. The fruits of these efforts were introduced into the market in 1994. Most of the genetically modified foods were thought to be only minor modifications of the unmodified original and thus no safety testing in animals or humans was conducted.

We now have many thousands of wheat strains that are different in important ways from original emmer, einkorn, and Triticum aestivum wheat. Interestingly, it has been suggested that einkorn wheat fails to provoke the same immune response characteristic of celiac disease provoked by modern wheat gluten, suggesting a different amino acid structure in gluten proteins. Another difference: Emmer wheat is up to 40% protein, compared to around 12% protein for modern wheat.

In other words, the wheat of earlier agricultural humans, including the wheat of Biblical times, is NOT the wheat of 2010. Modern wheat is quite a different thing with differing numbers of chromosomes, different genes due to human manipulation, varying gluten protein composition, perhaps other differences.

Somewhere in the shuffle and genetic sleight-of-hand that has occurred over the last 30 years, wheat changed. What might have been the "staff of life" has now become the cause of an incredible array of diseases of "wheat" intolerance.

Near-death experience with nattokinase

This is a true story that I personally witnessed.

A 60-some year old man heard that nattokinase "thinned the blood." So he had been taking it for the past 6 months.

One week before he came to see me, he abruptly became quite breathless. He was unable to walk more than 20 feet or bend over to tie his shoes due to the breathlessness.

He came to see me in the office. I was alarmed by how breathless he was without signs of heart failure or other obvious explanation. I sent him for an immediate CT pulmonary angiogram. Within 30 minutes, we had the diagnosis: a large "saddle" pulmonary embolus, meaning a large blood clot that straddled the right and left main pulmonary arteries. One wrong move and . . . bang! He would have been dead within a couple of minutes, since a large clot can completely occlude the large arteries feeding the lung, essentially corking any blood circuiting through the lungs and back to the left side of the heart. (Causing, incidentally, electromechanical dissociation, in which the heart keeps beating for a few minutes but no blood is being pumped. CPR can keep you alive for a few minutes, then it's over.)

When I advised the patient of the diagnosis (after initiating the REAL anticoagulants), he said, "But I was taking nattokinase!"

Exactly. Blood clots are no laughing matter. They are potentially fatal events. Betting your life on some company's advertisement is nothing short of foolish.

Anyone who reads The Heart Scan Blog knows that I am an avid supporter of nutritional supplements. I even write articles and consult for the supplement industry. But I truly despise hearing unfounded marketing claims that some supplement companies will make in the pursuit of a fast buck.

There is no doubt that we need better, safer methods to deal with dangerous blood clots, whether in the lung, pelvis, or other areas. But, before anyone takes a leap based on the extravagant marketing claims made by a supplement manufacturer, you want to be damn sure there are real data--not marketing claims, REAL data--before you use something like nattokinase in place of a proven therapy.

Don't confuse the very interesting, though unpalatable, natto with nattokinase. Natto contains vitamin K2 and some other interesting compounds, including nattokinase.

Blame the gluten?

Wheat is among the most destructive components of the human diet, a food that is responsible for inflammatory disease, diabetes, heart disease, several forms of intestinal diseases, schizophrenia, bipolar illness, ADHD, behavioral outbursts in autistic children . . . just to name a few.

But why?

Wheat is mostly carbohydrate. That explains its capacity to cause blood sugar to increase after eating, say, a turkey sandwich on whole wheat bread. The rapid release of sugars likely underlies its capacity to create visceral fat, what I call "wheat belly."

But neither the carbohydrate nor the other components, like bran and B vitamins, can explain all the other adverse health phenomena of wheat. So what is it in wheat that, for instance, worsens auditory hallucinations in paranoid schizophrenics? Is it the gluten?

First of all, what is gluten?

Gluten protein is the focus of most wheat research conducted by food manufacturers and food scientists, since it is the component of wheat that confers the unique properties of dough, allowing a pizza maker to roll and toss pizza crust in the air and mold it into shape. The distinctive “doughy” quality of the simple mix of wheat flour and water, unlike cornstarch or rice starch, for instance, properties that food scientists call “viscoelasticity” and “cohesiveness,” are due to the gluten. Wheat is mostly carbohydrate, but the 10-15% protein content is approximately 80% gluten. Wheat without gluten would lose its unique qualities that make it desirable to bakers and pizza makers. Gluten is also the component of wheat most confidently linked to immune diseases like celiac.

The structure of gluten proteins has proven frustratingly elusive to characterize, as it changes over time and varies from strain to strain. But an understanding of gluten structure may be part, perhaps most, of the answer to the question of why wheat provokes negative effects in humans.

The term “gluten” encompasses two primary families of proteins, the gliadins and the glutenens. The gliadins, one of the protein groups that trigger the immune response in celiac disease, has three subtypes: a/ß-gliadins, ?-gliadins, and ?-gliadins. The glutenins are repeating structures, or polymers, of more basic protein structures.

Beyond gluten, the other 20% or so of non-gluten proteins in wheat include albumins, prolamins, and globulins, each of which can also vary from strain to strain. In total, there are over 1000 other proteins that serve functions from protection of the grain from pathogens, to water resistance, to reproductive functions. There are agglutinins, peroxidases, a-amylases, serpins, and acyl CoA oxidases, not to mention five forms of glycerinaldehyde-3-phosphate dehydrogenases. I shouldn’t neglect to mention the globulins, ß-purothionin, puroindolines a and b, tritin, and starch synthases.

As if this protein/enzyme smorgasbord weren’t enough, food processors have also turned to fungal enzymes, such as cellulases, glucoamylases, xylanases, and ß-xylosidases to enhance leavening and texture. Many bakers also add soy flour to enhance mixing and whiteness, which introduces yet another collection of proteins and enzymes.

In short, wheat is not just a simple gluten protein with some starch and bran. It is a complex collection of biological material that varies according to its genetic code.

While wheat is primarily carbohydrate, it is also a mix of gluten protein which can vary in structure from strain to strain, as well as a highly variable mix of non-gluten proteins. Wheat has evolved naturally to only a modest degree, but it has changed dramatically under the influence of agricultural scientists. With human intervention, wheat strains are bred and genetically manipulated to obtain desirable characteristics, such as height (ranging from 18 inches to over 4 feet tall), “clinginess” of the seeds, yield per acre, and baking or viscoelastic properties of the dough. Various chemicals are also administered to fight off potential pathogens, such as fungi, and to activate the expression of protective enzymes within the wheat itself to “inoculate” itself against invading organisms.

From the original two strains of wheat consumed by Neolithic humans in the Fertile Crescent 9000 years ago (Emmer and Einkorn), we now have over 200,000 strains of wheat virtually all of which are the product of genetic manipulations that have modified the protein structure of wheat. The extraordinary complexity of wheat proteins have therefore created a huge black box of uncertainty in pinpointing which protein causes what.

But there's an easy cure for the uncertainty: Don't eat it.

Glycemic gobbledygook

The concept of glycemic index is meant to help determine what foods raise blood sugar a lot vs. what foods raise blood sugar a little. Dr. Jennie Brand-Miller's searchable database can be found here.

I have to admit that glycemic index provided me with a sense of false assurance for some years. It screwed up my health until I came to understand the issues a lot better.

For those of you just starting out in nutritional conversations, glycemic index (GI) represents a comparison of the blood glucose area-under-the-curve (AUC) over 2 hours after consuming 50 grams of the food in question compared to the AUC of glucose or white bread. Volunteers involved in developing these values are healthy people who are generally of normal weight.

Glucose, by definition, has a GI of 100. An equal quantity of sucrose (50% glucose, 50% fructose) has a GI of 60, lower than glucose. An equal quantity of whole wheat bread has a GI of 68-77 (Yes: The GI of whole wheat is higher than sucrose). Non-carbohydrate foods, such as eggs or avocado, have no GI since they do not impact on blood glucose.

Because the GI is also sensitive to how much carbohydrate is contained, the concept of Glycemic Load (GL) was introduced:

GL = (GI x amount of carbohydrate) / 100

GL is therefore the GI that incorporates the glycemic potential of the food of interest. GI does not vary with portion size; GL varies with portion size.

Let's take whole wheat pasta, a food regarded by most people as a healthy choice. Whole wheat pasta has a GI of 55--fairly low--and a GL of 29. A serving of 180 g (approximately 6 oz cooked) provides 50 g carbohydrates.

People who advocate that low-glycemic index foods would say that this is a desirable profile and should therefore replace high-glycemic index foods.

I say WRONG. First of all, most of us are not slender 20-somethings. We will therefore not show the same response as a young, slender person (like the GI volunteers), but will show exagerrated blood sugar responses. So this much low-glyemic index whole wheat pasta will typically yield a blood sugar of 120-200 mg/dl in non-diabetic people, high enough to trigger glycation. Sure, a high-glycemic index food, such as white flour birthday cake with plenty of sugary icing, might trigger a blood sugar of 140-250 mg/dl, much worse. But that doesn't make the lower blood sugar following pasta any less bad--it's still terrible.

Another issue: GI is assessed over a 2-hour timeline. What if blood sugar remains high in a sustained way, say, over 6 hours? That's precisely what whole wheat pasta will do: Keep blood sugar high for an extended period.

So not only does a low-glycemic index food like pasta increase blood sugar in most of us extravagantly, it does so in a sustained way.

Lastly, low-glycemic index pasta still triggers small LDL particles to an extreme degree, as I discussed in the previous Heart Scan Blog post, Small LDL: Complex vs. simple carbohydrates.

Don't be false reassured by the notion of low GI or GL. In fact, I'd go so far as to say that NO glycemic index is a GOOD glycemic index (or load). The foods we want to dominate our diet are the foods that aren't even listed in the GI database.

Bosom buddies

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

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

Exercise programs to reduce male breast size.

Liposuction--Not just for the belly!

Plastic surgery

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

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


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

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

So where does the excess estrogen come from?

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

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

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

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

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

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

Don't be a dipstick

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

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

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

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

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

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

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

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

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

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

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

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

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

The ultimate insurance company cost savings

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

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

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

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

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

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

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

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

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

Salvation from halogenation

Iodine is a halogen.

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

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

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

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

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

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

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

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

Lipitor-ologist

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

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

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

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

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

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

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

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

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

Robb Wolf's new Paleo Solution

The Paleo Solution: The Original Human Diet


The Paleo Solution: The Original Human Diet

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

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

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

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

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

Human foie gras

If you want to make foie gras, you feed ducks and geese copious quantities of grains, such as corn and wheat.

The carbohydrate-rich diet causes fat deposition in the liver via processes such as de novo lipogenesis, the conversion of carbohydrates to triglycerides. Ducks and geese are particularly good at this, since they store plentiful fats in the liver to draw from during sustained periods of not eating during annual migration.

Modern humans are trying awfully hard to create their own version of foie gras-yielding livers. While nobody is shoving a tube down our gullets, the modern lifestyle of grotesque carbohydrate overconsumption, like soft drinks, chips, pretzels, crackers, and--yes--"healthy whole grains" causes fat accumulation in the human liver.

Over the past few years, there has been an explosion of non-alcoholic fatty liver disease and non-alcoholic steatosis, two forms of liver disease that result from excess fat deposition. The situation gets so bad in some people that it progresses to cirrhosis, i.e., a hard, poorly-functioning liver that paints a very ugly health picture. The end-result is identical to that experienced by longstanding alcoholics.



While Hannibal Lecter might celebrate the proliferation of human fatty livers with a glass of claret, fatty liver disease is an entirely preventable condition. All it requires is not eating the foods that create it in the first place.

Let go of my love handles

When is fat not just fat?

When it's visceral fat. Visceral fat is the fat that infiltrates the intestinal lining, the liver, kidneys, even your heart. It's the stuff of love handles, the flabby fat that hangs over your belt, or what I call "wheat belly."

Unlike visceral fat, the fat in your thighs or bottom is metabolically quiescent. Thigh and bottom fat may prevent you from fitting into your "skinny jeans," but its mainly a passive repository for excess calories.

Visceral fat, on the other hand, is metabolically active. It produces large quantities of inflammatory signals ("cytokines"), such as various interleukins, leptin, and tumor necrosis factor, that can trigger inflammatory responses in other parts of the body. Visceral fat also oddly fails to produce the protective cytokine, adiponectin, that protects us from diabetes, cancer, and heart disease.

Visceral fat also allows free fatty acids to leave and enter fat cells, resulting in a flood of fatty acids and triglycerides (= 3 fatty acids on a glycerol "backbone") in the bloodstream. This worsens insulin responses ("insulin resistance") and contributes to fatty liver. The situation is worsened when the very powerful process of de novo lipogenesis is triggered, the liver's conversion of sugar to triglycerides.

Visceral fat is also itself inflamed. Biopsies of visceral fat show plenty of inflammatory white blood cells (macrophages) infiltrating its structure.

So what causes visceral fat? Anything that triggers abnormal increases in blood glucose, followed by insulin, will cause visceral fat to grow.

It follows logically that foods that increase blood glucose the most will thereby trigger the greatest increase in visceral fat. Eggs don't lead to visceral fat, nor do salmon, olive oil, beef, broccoli, or almonds. But wheat, cornstarch, potato starch, rice starch, tapioca starch, and sugars will all trigger glucose-insulin that leads to visceral fat accumulation.

Fructose is also an extravagant trigger of visceral fat. Fructose is found in sucrose (50% fructose), high-fructose corn syrup, agave syrup, maple syrup, and honey.

Increased visceral fat can be suggested by increased waist circumference. The inflammatory hotbed created by excess visceral fat has therefore been associated with increased likelihood of heart attack, cardiovascular mortality, diabetes, cancer, and total mortality.

So I'm not so worried that you can't squeeze your bottom into your size 8 jeans. I am worried, however, when you need to let your belt out a notch . . . or two or three.

Surviving a widow maker

Gwen came to me 5 years ago. In her late 60s, she'd been having feelings of chest pressure for the past 4 weeks with small physical efforts, such as climbing a flight of stairs or lifting her grandchildren.

She sat in my office, heaving small sobs, accompanied by her daughter.

Gwen had already undergone a heart catheterization at a hospital near home by a cardiologist who I knew to be honest and competent. She'd been told that she had a 90% stenosis ("blockage") of her proximal left anterior descending (LAD) coronary artery. He called it a "widow maker," since closure of the artery at this point can be fatal within minutes. He advised bypass surgery as soon as possible. Though a stent could be placed at this location, he felt that its proximity to the left main stem (i.e., the "trunk" that divides into the LAD and circumflex arteries) might be jeopardized by expanding a stent in this bulky plaque, what I felt was a reasonable concern.

I reviewed the images that she brought with her. Yes, indeed: a widow maker. The portion of the left ventricle (heart muscle) fed by the LAD was also impaired ("hypokinetic"), reflecting reduced flow through the artery.

I advised Gwen that her first cardiologist's advice was sound: This was a potentially dangerous and severe condition. Either a bypass or stent should be performed near-future, the less delay the better.

But Gwen and her daughter would have no talk of any more procedures. She'd come to me because she heard about the (then rudimentary) effort I'd been making at reversing coronary plaque. "I admire your commitment, Gwen, but I am concerned that there may not be sufficient time to implement a program of prevention or reversal. Prevention is very powerful, but very slow. When symptoms like yours are active, also, it can mean that we won't have full control over the plaque causing the symptoms. This risks closure of the vessel, since flow characteristics in the plaque are abnormal. I think that you should go through a stent or bypass. We can then start your prevention/reversal program once we know you're safe."

Gwen would still have none of it. I asked her to return in a few days after thinking it over. In the meantime, we drew her lipoprotein blood samples while she added fish oil, l-arginine (back then I used a lot of l-arginine for its endothelial health effects), and began the Track Your Plaque diet a la 2004. This was in addition to the aspirin, beta blocker, and statin prescribed by the first cardiologist.

Several days later, Gwen and her daughter returned, as committed as ever to not having a procedure and proceeding with our prevention/reversal efforts.

So off we went. I was nervous about Gwen's safety, but she had clearly made her mind made up. Gwen's lipoprotein analysis revealed a severe small LDL pattern along with markers for prediabetes (high insulin, high blood glucose, hypertension, along with the loose tummy of visceral fat). So I counseled her intensively in diet and added niacin.

Within 2 weeks, Gwen no longer had chest pain. Whether this was due to her efforts or to some resolution of an intraplaque phenomenon (e.g., resorption of internal plaque hemorrhage), I don't know. But her symptoms did not return.

As the program evolved, we added the new strategies along the way--vitamin D supplementation; elimination of all wheat along with other changes in diet; iodine and thyroid normalization; as well as discontinuing l-arginine after the initial two years. She also got rid of the statin drug after losing around 20 lbs on the diet.

It's now been six years with her "widow maker" and Gwen has been fine: no recurrence of her symptoms, all stress tests performed have been normal, reflecting normal blood flow in her coronary arteries.

Should ALL people with symptomatic widow makers undergo such an effort and avoid procedures? No, not yet. Prevention and reversal efforts are indeed powerful, but slow. Some people just may not have sufficient time to accomplish what Gwen did. The fact that Gwen showed evidence for reduced flow in the LAD worried me in particular. There is no question that mortality benefits for stenting or bypass of this location are not as large as previously thought (see here, for instance), but each case needs to be viewed individually, factoring in flow characteristics in the artery, appearance of "stability" or "instability" of the plaque itself, not to mention commitment of the person.

But it can be done.

Fred Hahn's Slow Burn

I just had a workout with personal trainer and fitness expert, Fred Hahn. After a workout that quickly taught me that I had a lot to learn about exercise and strength training, Fred and I had a nice low-carbohydrate dinner at a Manhattan restaurant and shared ideas.

Fred is coauthor of Slow Burn Fitness Revolution: The slow motion exercise that will change your body in 30 minutes a week, written in collaboration with the Drs. Eades, Michael and Mary Dan. Fred also blogs here.

I had heard about Fred's "slow-burn" concept in past, but made little of it. I then met Fred on Jimmy Moore's low-carb cruise this past year, where I gave a talk on how carbohydrate-reduced diets reduce small LDL particles. Fred provided a group demonstration on his slow-burn techniques. I watched the demonstration, even tried it a few times back home in the gym, but never really applied them, losing patience most of the time and just going back to my usual routine.

Well, Fred showed me today how to do his slow-burn. In a nutshell, it is the slow, methodical use of weight resistance until the muscle is exhausted. It involves slow movement--e.g., 5 seconds for a lat pulldown from top to bottom--repeated until exhaustion using a weight that allows, perhaps, 6 repetitions over a 60-second effort.

I've been strength training since I was a teenager. I've seen lots of bad training techniques, injuries, and hocum when it comes to how to use resistance training techniques. But I believe that Fred Hahn's slow-burn technique really provides something unique that I hadn't experienced before.

For one, the burn is nothing like I've felt before. Two, there appears to be nearly zero risk for injury, since the usual momentum-driven, herky-jerky motion often employed with weight machines is entirely gone. Three, if what Fred is seeing is true--enhanced visceral (abdominal) fat loss, reduced blood glucose, increased HDL, decreased LDL/total cholesterol--then there's something really interesting going on here.

I also discovered that Fred is no ordinary personal trainer. He has insights into metabolism that I found truly impressive. After all, he's been hanging around with Mike Eades, who's a pretty sharp guy. What Mike Eades is to metabolic insights is what Fred Hahn is to exercise physiology.

I'm going to take Fred's slow burn training insights home with me. I'll let you know how it goes. Some aspects I'd like to explore: Will strength, muscle mass, and blood sugar responses change?



Fred Hahn's latest book, adapting slow burn techniques for kids.