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.
/blog/2009/01/a-tale-of-two-ldls.html">calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.


All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Cranberry Sauce

Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque!

Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.

There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.

1 cup water
12 ounces fresh whole cranberries
Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía)
1 tablespoon orange zest + juice of half an orange
½ cup chopped walnuts
1 teaspoon ground cinnamon
½ teaspoon ground nutmeg
¼ teaspoon ground cloves

In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.

Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.

Transfer mixture to bowl, cool, and serve.


Apple Cranberry Crumble

Apple, cranberry, and cinnamon: the perfect combination of tastes and scents for winter holidays!

I took a bit of carbohydrate liberties with this recipe. The entire recipe yields a delicious cheesecake-like crumble with 59 “net” grams carbohydrates (total carbs – fiber); divided among 10 slices, that’s 5.9 grams net carbs per serving, a quantity most tolerate just fine. (To reduce carbohydrates, the molasses in the crumble is optional, reducing total carbohydrate by 11 grams.)

Other good choices for sweeteners include liquid stevia, stevia glycerite, powdered stevia (pure or inulin-based, not maltodextrin-based), Truvía, Swerve, and erythritol. And always taste your batter to test sweetness, since sweeteners vary in sweetness from brand to brand and your individual sensitivity to sweetness depends on how long you’ve been wheat-free. (The longer you’ve been wheat-free, the less sweetness you desire.)


Crust and crumble topping
3 cups almond meal
1 stick (8 tablespoons) butter, softened
1 cup xylitol (or other sweetener equivalent to 1 cup sugar)
1½ teaspoons ground cinnamon
1 tablespoon molasses
1½ teaspoons vanilla extract
Dash sea salt

Filling
16 ounces cream cheese, softened
2 large eggs
½ cup xylitol (or other sweetener equivalent to ½ cup sugar)
1 Granny Smith apple (or other variety)
1 teaspoon ground cinnamon
1 cup fresh cranberries

Preheat oven to 350° F.

In large bowl, combine almond meal, butter, sweetener, cinnamon, molasses, vanilla, and salt and mix.

Grease a 9½-inch tart or pie pan. Using approximately 1 cup of the almond meal mixture, form a thin bottom crust with your hands or spoon.

In another bowl, combine cream cheese, eggs, and sweetener and mix with spoon or mixer at low-speed. Pour into tart or pie pan.

Core apple and slice into very thin sections. Arrange in circles around the edge of the cream cheese mixture, working inwards. Distribute cranberries over top, then sprinkle cinnamon over entire mixture.

Gently layer remaining almond meal crumble evenly over top. Bake for 30 minutes or until topping lightly browned.

Biscuits and Gravy



Biscuits and gravy: the ultimate comfort food . . . one you thought you’d never have again!

The familiar dish of breakfast and holiday meals is recreated here with a delicious gravy that you can pour over piping hot biscuits. Because it contains no wheat or other unhealthy thickeners like cornstarch made with “junk” carbohydrates, there should be no blood sugar or insulin problems with this dish, nor joint pain, edema, acid reflux, mind “fog,” or dandruff—life is good without wheat!

While the gravy is also dairy-free for those with dairy intolerances, the biscuits are not, as there are cheese and butter in the biscuits, both of which are optional, e.g., leave out the cheese and replace butter with coconut or other oil.

Makes 10 biscuits

Gravy:
2 tablespoons extra-virgin olive oil
1 pound loose sausage meat
2½ cups beef broth
¼ cup coconut flour
½ cup coconut milk (canned variety)
1 tablespoon onion powder
1 teaspoon garlic powder
½ teaspoon sea salt
Dash ground black pepper

Biscuits:
1 cup shredded cheddar (or other) cheese
2 cups almond meal/flour
¼ cup coconut flour
¾ teaspoon baking soda
½ teaspoon sea salt
2 large eggs
4 ounces butter, melted (or other oil, e.g., extra-light olive, coconut, walnut)

To make gravy:
In large skillet, heat oil over medium heat. Sauté sausage, breaking up as it browns. Cook until thoroughly cooked and no longer pink.

Turn heat up to medium to high and pour in beef broth. Heat just short of boiling, then turn down to low heat. Stir in coconut flour, little by little, over 3-5 minutes; stop adding when gravy obtains desired thickness. Pour in coconut milk and stir in well. Add onion powder, garlic powder, salt, and pepper and simmer over low heat for 5 minutes. Add additional salt and pepper to taste. Remove from heat and set aside.

To make biscuits:
Preheat oven to 325° F.

In food chopper or processor, pulse shredded cheese to finer, granular consistency.

Pour cheese into large bowl, then add almond meal, coconut flour, baking soda, and salt and mix thoroughly. Add the eggs and butter or oil and mix thoroughly to yield thick dough.

Spoon out dough into 10 or so ¾-inch thick mounds onto a parchment paper-lined baking pan. Bake for 20 minutes or until lightly browned and toothpick withdraws dry.

Ladle gravy onto biscuits just before serving.

The Perfect Carnivore

People who carry the gene for lipoprotein(a), Lp(a), tend to be:

--Intelligent--The bell curve of IQ is shifted rightward by a substantial margin.
--Athletic--With unusual capacity for long-endurance effort, thus the many marathoners, triathletes, and long-distance bikers with Lp(a).
--Tolerant to dehydration
--Tolerant to starvation
--Resistant to tropical infections

In other words, people with Lp(a) have an evolutionary survival advantage. More than other people, they make clever, capable hunters who can run for hours to chase down prey, not requiring food or water, and less likely to succumb to the infections of the wild. In a primitive setting, people with Lp(a) are survivors. Evolution has likely served to select Lp(a) people for their superior survival characteristics.

But wait a minute: Isn't Lp(a) a risk for heart attack and stroke? Don't we call Lp(a) "the most aggressive known cause for heart disease and stroke that nobody gives a damn about"?

Yes. So what allows this evolutionary advantage for survival to become a survival disadvantage?

Carbohydrates, especially those from grains and sugars. Let me explain.

More so than other people, Lp(a) people express the small LDL pattern readily when they consume carbohydrates such as those from "healthy whole grains." Recall that the gene for Lp(a) is really the gene for apoprotein(a), the protein that, once produced by the liver and released into the bloodstream, binds to an available LDL particle to create the combination Lp(a) molecule. If the LDL particle component of Lp(a) is small, it confers greater atherogenicity (greater plaque-causing potential). Thus, carbohydrate consumption makes Lp(a) a more aggressive cause for atherosclerotic plaque. The situation can be made worse by exposure to vegetable oils, such as those from sunflower or corn, which increases production of apo(a).

Also, more than other people, Lp(a) people tend to show diabetic tendencies with consumption of carbohydrates. Eat "healthy whole grains," for instance, or if a marathoner carb-loads, he/she will show diabetic-range blood sugars. I have seen long-distance runners or triathletes, for instance, have a 6 ounce container of sugary yogurt and have blood sugars of 200 mg/dl or higher. The extreme exercise provides no protection from the diabetic potential.

Because carbohydrates are so destructive to the Lp(a) type, it means that people with this pattern do best by 1) absolutely minimizing exposure to carbohydrates and vegetable oils, ideally grain-free and sugar-free, and 2) rely on a diet rich in fats and proteins.

The perfect diet for the Lp(a) type? It would be a diet of feasting on the spoils of the hunt, devouring the wild boar captured and slaughtered and eating the snout, hindquarters, spleen, kidneys, heart, and bone marrow, then eating mushrooms, leaves, nuts, coconut, berries, small rodents, reptiles, fish, birds, and insects when the hunt is unproductive.

Capable hunter, survivor, consumer of muscle and organ meats: I call people with Lp(a) "The Perfect Carnivores."

Track Your Plaque in the news

The NPR Health Blog contacted me, as they were interested in learning more about health strategies and tools that are being used by individuals without their doctors. The Track Your Plaque website and program came up in their quest, as it is the only program available for self-empowerment in heart disease.

Several Track Your Plaque Members spoke up to add their insights. The full text of the article can be viewed here.

How's Your Cholesterol? The Crowd Wants To Know
Mainstream medicine isn't in favor of self-analysis, or seeking advice from non-professionals, of course. And anyone who does so is running a risk.

But there are folks who want to change the course of their heart health with a combination of professional and peer support. Some are bent on tackling the plaque that forms in arteries that can lead to heart disease. They gather online at Track Your Plaque, or "TYP" to the initiates.

"We test, test, test ... and basically experiment on ourselves and have through trial and error came up with the TYP program, which is tailored to the individual," Patrick Theut, a veteran of the site who tells Shots he has watched his plaque slow, stop and regress.

The site was created in 2004 by Bill Davis, a preventive cardiologist in Milwaukee, Wisc. Davis is also the author of Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health, which argues that wheat is addictive and bad for most people's health. Davis recommends eliminating wheat from the diet to most new members of Track Your Plaque.

"The heart is one of the hardest things to self-manage but when you let people take the reins of control, you get far better results and far fewer catastrophes like heart attacks," Davis tells Shots.

Doctors typically give patients diagnosed with heart disease two options: take cholesterol-lowering statin drugs, or make lifestyle changes, like diet. It's usually far easier for both parties — the doctor and the patient — to go with the drugs than manage the much more difficult lifestyle changes, Davis says.

"Doctors say take the Lipitor, cut the fat and call me if you have chest pain," he explains. "But that's an awful way to manage care."

TYP has members submit their scores from heart CT scans, cholesterol values, lipoproteins and other heart health factors to a panel of doctors, nutritionists and exercise specialists. Then they receive advice in the form of an individualized plaque-control program. But the online forum, where users share their results with other members and exchange tips, is where most of the TYP action happens.

The community currently has about 2,400 members who pay $39.95 for a quarterly membership, or $89.75 for a yearly membership. Davis says all proceeds go towards maintaining the website.

Ilaine Upton is a 60-year-old bankruptcy lawyer from Fairfax, Va., and a TYP member. At a friend's suggestion, Upton decided to get a heart CT scan in July. Her score was higher than it should have been (22 instead of 0), so she decided to get her blood lipids and cholesterol tested, too, and sent a sample off to MyMedLabs.com.

She learned that her LDL particle count was over 2,000 ("crazy high," she says), and she posted her results on TYP. Davis advised her that a low-carb diet would reduce it, so she decided to try it.

Since July, she says she has had "excellent results" with the program, and her LDL counts are coming down.

"It would be nice to have a [personal] physician involved in this, but [my insurer] Blue Cross won't pay if you are not symptomatic, and I am trying to prevent becoming symptomatic," says Upton. "I feel very empowered by this knowledge and the ability to take better control of my health by getting feedback on the decisions I make."

Pecan Streusel Coffee Cake


This is about as decadent as it gets around here!

Here’s a recreation of an old-fashioned coffee cake, a version with a delicious chewy-crunchy streusel topping.

I’ve specified xylitol as the sweetener in the topping, as it is the most compatible sweetener for the streusel “crumb” effect and browning.

Variations are easy. For example, for an apple pecan coffee cake, add a layer of finely-chopped or sliced apples to the cake batter and topping.

Additional potential carbohydrate exposure comes from the garbanzo bean flour and molasses. However, distributed into 10 slices, each slice provides 7.2 grams “net” carbs (total carbs minus fiber), a perfectly tolerable amount. Be careful not to exceed two slices!

Yield 10 slices

Cake:
2½ cups almond flour
½ cup garbanzo bean flour
1 tablespoon ground cinnamon
1 teaspoon baking soda
Sweetener equivalent to ¾ cup sugar
Dash sea salt

3 eggs separated
3/8 teaspoon cream of tartar
1 tablespoon vanilla extract
4 ounces butter, melted
Juice of ½ lemon

Topping:
½ cup almond flour
¼ cup pecans, finely chopped
1 tablespoon ground cinnamon
½ cup xylitol
1 tablespoon molasses
6 ounces butter, cut into ½-inch widths, at room temperature

Preheat oven to 325º F. Grease bread pan.

In bowl, combine almond flour, garbanzo flour, cinnamon, baking soda, sweetener, salt, and mix.

In small bowl, whip egg whites and cream of tartar until stiff peaks form. At low speed, blend in egg yolks, vanilla, melted butter, and lemon juice.

Pour liquid mixture into almond mixture and mix thoroughly. Pour into microwave-safe bread pan and microwave on high for 3 minutes. Remove and set aside.

To make topping, combine almond flour, pecans, cinnamon, xylitol, and molasses in small bowl and mix. Mix in butter

Spread topping on cake. Bake for 20 minutes or until toothpick withdraws dry.

Recipe: Peanut Butter and Jelly Macaroons



If you miss peanut butter and jelly sandwiches, you’re going to absolutely love these peanut butter and jelly macaroons!

Not everybody loves the taste or texture of coconut. This issue is solved by the first step: toasting shredded coconut, then reducing them down to a granular consistency. This yields a macaroon consistency without the dominant coconut taste, replaced instead with the flavors of PB & J.

I’ve specified liquid stevia as the sweetener, but this is easily replaced by your choice of sweetener. Note that, regardless of which sweetener used, they vary in sweetness from brand to brand and the quantity required to equal the ½ cup of sugar equivalent can vary. It always helps to taste your batter and adjust sweetness.

Also, I used Swerve in this recipe, the erythritol-inulin mix that enhances texture, but its use is optional.

As written, each macaroon contains just over 3 grams “net” carbohydrates (total carbs minus fiber), meaning you can have several before doing any damage!

Makes 24 macaroons

3 cups shredded unsweetened coconut
2 tablespoons vanilla extract
1 teaspoon almond extract
¼ cup coconut flour
¼ cup dried unsweetened cherries (or other unsweetened berries)
2 tablespoons coconut oil
¼ cup natural peanut butter, room temperature
2 egg whites
½ teaspoon liquid stevia or sweetener equivalent to ½ cup sugar
2 tablespoons Swerve


Preheat oven to 300° F.

In large bowl, combine coconut, vanilla and almond extracts, and mix.

Spread mixture on baking sheet and bake for 10 minutes, stirring occasionally, until very lightly browned. Be careful not to burn. Remove and cool. (Leave oven at 300° F.)

When cooled, using food chopper, food processor, or coffee grinder, pulse coconut mixture until coconut reduced to consistency of coffee grounds. Pour back into bowl. Stir in coconut flour.

Place cherries or other berries in food chopper, food processor, or coffee grinder and pulse until reduced to small granules or paste. Remove with spatula and add to coconut mixture. Set aside.

Place egg whites in bowl and whip until frothy and stiff peaks form.

In small microwave-safe bowl, combine coconut oil and peanut butter and microwave in 10-second increments until warm (not hot) liquid. Stir in egg whites, followed by stevia and Swerve, and blend thoroughly.

Dispense dough onto a parchment paper-lined baking sheet using a 1 ½-inch cookie scooper or spoons.

Bake for 15 minutes or until lightly browned.

I Wish I Had Lipoprotein(a)!

Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.


In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.
All posts by william-davis

Wheat "debate" on CBC

"Many Canadians plan warm buns, stuffing and pie for their Thanksgiving meals tonight. But I'll speak with a cardiologist who thinks we have no reason to be thankful for any food that contains wheat. William Davis says our daily bread is making us fat and sick."

That's the introduction to my recent interview and debate on CBC, the Canadian public radio system, aired on the Canadian Thanksgiving. Arguing the other side was Dr. Susan Whiting, an academic nutritionist. (I use the word "arguing" loosely, since she hardly argued the issues, certainly hadn't read the book, but was content to echo the conventional line that whole grains are healthy and cutting out a food group is unhealthy.)

I do have to give credit to the Canadian media, including the CBC, who have been hosting some rough-and-tumble discussions about the entire wheat question despite Canada being a world exporter of wheat. I recently participated in another debate with a PhD nutrition expert from Montreal who, in response to my assertion that the genetically-altered high-yield, semi-dwarf strains have changed the basic composition of wheat, argued that the creation of the 2-foot tall semi-dwarf strain was a convenience created so that farmers could see above their fields--no kidding. I stifled my laugh. (The semi-dwarf variants were actually created to compensate for the heavy seed head that develops with vigorous nitrate fertilization that buckles 4 1/2-foot tall wheat stalk, making harvesting and threshing impossible, a process farmers call "lodging." The 2-foot tall semi-dwarf thick, stocky stalk is strong enough to resist lodging.)

In short, debating the nutrition "experts" on this question has been tantamount to arguing with a school age child on the finer points of quantum physics. There has not yet been any real objection raised on the basic arguments against modern genetically-altered wheat. Modern semi-dwarf wheat is, and remains, an incredibly bad creation of the genetics laboratories of the 1970s. It has no business on the shelves of your grocery store nor on the cupboards in your home.

Carrot Cake

This is among my favorite recipes from the Wheat Belly book. I reproduce it here for those of you who read the Kindle or audio version and therefore didn't get the recipes.

I made this most recently this past weekend. It was gone very quickly, as even the 13-year old gobbled it up.

(I reduced the sour cream in this version from 8 to 6 oz to reduce cooking time. Also, note that anyone trying to avoid dairy can substitute more coconut milk, i.e., the thicker variety, in equivalent quantities.)

Makes 8-10 servings



 

 

 

 

 

 

Ingredients:
Cake:
2 cups carrots, finely grated
1 cup chopped pecans
1 cup coconut flour
1 tablespoon ground flaxseed
2 teaspoons ground cinnamon
1 teaspoon allspice
1 teaspoon nutmeg
1 teaspoon baking powder
2 tablespoons freshly grated orange peel
Sweetener equivalent to ½ cup sugar (e.g., 4 tablespoons Truvia)
½ teaspoon sea salt
4 eggs
1/2 cup butter or coconut oil, melted
2 teaspoons vanilla extract
½ cup coconut milk
6 ounces sour cream

Icing:
8 ounces cream cheese or Neufchâtel cheese, softened
1 teaspoon lemon juice
1 tablespoon Truvía or 1/8 teaspoon stevia extract powder or ¼ cup Splenda

Preheat oven to 325° degrees F. Grate carrots and set aside.

Combine coconut flour, flaxseed, cinnamon, nutmeg, baking powder, orange peel, sweetener, and salt in large bowl and mix by hand.

Put eggs, butter or coconut oil, vanilla coconut milk, and sour cream in mixing bowl; mix by hand. Pour liquid mixture into dry pecan/coconut flour mixture and blend with power mixer until thoroughly mixed. Stir carrots and pecans in by hand with spoon. Pour mixture into greased 9- or 10-inch square cake pan.

Bake for 60 minutes or until toothpick withdraws dry. Allow to cool 30 minutes.

Place Neufchâtel cheese in bowl. Add lemon juice and sweetener and mix thoroughly. Spread on cake.

Why wheat makes you fat

How is it that a blueberry muffin or onion bagel can trigger weight gain? Why do people who exercise, soccer Moms, and other everyday people who cut their fat and eat more "healthy whole grains" get fatter and fatter? And why weight gain specifically in the abdomen, the deep visceral fat that I call a "wheat belly"?

There are several fairly straightforward ways that wheat in all its varied forms--whole wheat bread, white bread, multigrain bread, sprouted bread, sourdough bread, pasta, noodles, bagels, ciabatta, pizza, etc. etc.--lead to substantial weight gain:

High glucose and high insulin--This effect is not unique to wheat, but shared with other high-glycemic index foods (yes: whole wheat has a very high-glycemic index) like cornstarch and rice starch (yes, the stuff used to make gluten-free foods). The high-glycemic index means high blood glucose triggers high blood insulin. This occurs in 90- to 120-minute cycles. The high insulin that inevitably accompanies high blood sugar, over time and occurring repeatedly, induces insulin resistance in the tissues of the body. Insulin resistance causes fat accumulation, specifically in abdominal visceral fat, as well as diabetes and pre-diabetes. The more visceral fat you accumulate, the worse insulin resistance becomes; thus the vicious cycle ensues.

Cycles of satiety and hunger--The 90- to 120-minute glucose/insulin cycle is concluded with a precipitous drop in blood sugar. This is the foggy, irritable, hungry hypoglycemia that occurs 2 hours after your breakfast cereal or English muffin. The hypoglyemia is remedied with another dose of carbohydrate, starting the cycle over again . . . and again, and again, and again.

Gliadin proteins--The gliadin proteins unique to wheat, now increased in quantity and altered in amino acid structure from their non-genetically-altered predecessors, act as appetite stimulants. This is because gliadins are degraded to exorphins, morphine-like polypeptides that enter the brain. Exorphins can be blocked by opiate-blocking drugs like naltrexone. A drug company has filed an application with the FDA for a weight loss indication for naltrexone based on their clinical studies demonstrating 22 pounds weight loss after 6 months treatment. Overweight people given an opiate blocker reduce calorie intake 400 calories per day. But why? There's only one food that yields substantial quantities of opiate-like compounds in the bloodstream and brain: wheat gliadin.

Leptin resistance--Though the data are preliminary, the lectin in wheat, wheat germ agglutinin, has the potential to block the leptin receptor. Leptin resistance is increasingly looking like a fundamental reason why people struggle to lose weight. This might explain why eliminating, say, 500 calories of wheat consumption per day yields 3500 calories of weight loss.

And, as in many things wheat, the whole is greater than the sum of the parts. Despite all we know about this re-engineered thing called wheat, eliminating it yields health benefits, including weight loss, that seem to be larger than what you'd predict with knowledge of all its nasty little individual pieces.

Just who is "Real Facts 2000"?

This is an example of what seems to be developing over at Amazon.com, posted as a "book review":

The author has no credentials, no credibility, just a small cult of terribly misinformed followers. Don't be fooled by the high volume screech against wheat and grains. Allegations of "secret ingredients in wheat" to make you eat more, or comparisons to cigerettes. Seriously?! For over 8000 years wheat has sustained and grown human kind, oh and it tastes good when mixed with a little water and yeast. Every nutritionist and serious medical professional will tell you that bread is the most economical and safe source of essential nutrients. In fact, bread is handed out in natural disasters because it sustains life without food safety issues or requiring refrigeration. And now, suddenly it will kill you. Comical! This book is such a bone headed, misinformed way to just scare people into not eating.

As for secret ingredients, humm, apparently the author is ignorant of the food laws that regulate everything that goes into food and on food labels. Unlike some enforcement agencies, the FDA has some serious teeth behind its enforcement. As for frankenwheat, again seriously?! Wheat, due to its ubiquitous presence in the world is treated as sacrosant from any GMO research or development.

If you need real, science based information on healthy eating, check out [...] and leave this book and its cult in the compound.


If you recognize the wording and tone, you will readily recognize the footprints of the Wheat Lobby here. "Terribly misinformed followers"? . . . Hmmm. "Food laws"? I didn't realize that eating more "healthy whole grains" was a . . . law?

Make no mistake: There are people and organizations who have a heavy stake in your continued consumption of the equivalent of 300 loaves of bread per year. There are people and organizations (read: pharmaceutical industry) who have a big stake on the "payoff" of your continued consumption of "healthy whole grains."

This is not a book review; this is part of a concerted, organized campaign to discredit a message that needs to be heard.

Anybody from the media listening?

Almonds are the new wheat

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

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

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

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

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

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

Being regular is dangerous to your health

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

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

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

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

The ideal response is:

1) increase in heart rate with inspiration

2) decrease in heart rate with expiration.

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

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

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

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

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

You mean weight loss is hazardous to your health?

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

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

I experienced this very thing.

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

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

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

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


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

What is this wacky thing called "weight loss"?

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

What happens when you lose weight?

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

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

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

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

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

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

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

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

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

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

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

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

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

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

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

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

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

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

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

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

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

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

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

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

Even moore from Jimmy Moore

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

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

Food (non-wheat-containing, of course) for thought.
All posts by william-davis

Medicine ain't what it used to be

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

For instance:

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

Normal cholesterol panel . . . no heart disease?

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

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

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

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

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

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

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

 

Idiot farm

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

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

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

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

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

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

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

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

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

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

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

Eat triglycerides

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

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

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

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

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

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

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

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

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

 

 

 

 

 

 

 

You've come a long way, baby

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



 

 

 

 

 

 

 

 

 

 

 

 

 

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

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



 

 

 

 

 

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

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

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

 

 

Fasting with green tea

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

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

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

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

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

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

Dreamfields pasta is wheat

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

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



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

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

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

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

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

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

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

Bet you can't fast

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

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

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

Among its many physiological benefits, fasting can:

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

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

  • Reduce inflammatory measures

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

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


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

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

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

More on fasting to come . . .

Total cholesterol 220

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

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

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

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

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

Rearranging the equation:

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

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

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

(a relatively low-risk pattern for heart disease)

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

(an indeterminate risk pattern, potentially moderate risk)

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

(a potentially high-risk pattern)

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

(an indeterminate risk pattern)

 

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

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

Scientists are freakin' liars

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

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

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

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

 

Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.