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.

Wheat brain

Among the most common effects of wheat are those on the brain.

Consume wheat and susceptible individuals will experience a subtle euphoria. Others experience mental cloudiness or sleepiness. (This is what I personally get.)

It gets worse. Children with ADHD and autism have difficulty concentrating on a task and have behavioral outbursts after a cookie. Schizophrenics experience paranoid delusions, auditory hallucinations, and worsening of social detachment. People with bipolar disorder can have the manic phase triggered by a breadcrumb. All these effects are blocked by administering drugs that block the brain's opiate receptors. (This is why, by the way, a drug company is planning to release an oral agent, naltrexone, formerly administered to heroin addicts to help control addiction, for weight loss: block the euphoric effect, take away the temptation, lose weight.)

Here is Heart Scan Blog reader, Nicole's, mental fog story:

I have been grain-free (no gluten free grains either) for quite a long time (about a year and a half). Earlier this week, I decided to try white bread and pasta. The experiment only lasted two days. I had horrible terminal insomnia both nights, causing me on the second night to wake up at 2:30 am unable to get back to sleep at all. I felt drugged and in a mind-fog all the next day and even dozed off a few times! Luckily I had the day off work.

I had very bad forgetfulness also. I forgot that I left my bag and groceries at work, so I had to go back for them. Then I had to use my husband's keys to get in because I thought my keys were in my bag, but it turns out they were in my pocket. Then I got my bag, set the alarm, locked the door and then realized I forgot my groceries. So I had to re-open the door, unset the alarm, and go back for the groceries. Then I locked the door, forgetting to set the alarm, so I had to unlock it, open up and set the alarm. It was just ridiculous, I am NEVER like that!

In addition to the insomnia and forgetfulness, I also had horrible anxiety and paranoia, almost to the point of panic. Which I NEVER have, I am usually very easy-going, even-tempered, and worry-free. But this was horrible, I really was quite paranoid and anxious about everything. Weird!

And the worst, was that in just two days of eating wheat, I gained 4 lbs and 2% bodyfat!! It's two days wheat-free now, and it's finally going back down, but wow. Just two days of wheat-eating caused that much weight and fat gain!

Anyway, I've learned my lesson and will continue to avoid grains (including gluten free grains) entirely.


Eat more "healthy whole grains"? Modern dwarf Triticum aestivum, perverted even further by agricultural geneticists and modern agribusiness, subsidized by the U.S. government to permit $5 pizza, is better than any terrorist plot to discombobulate the health and performance of the American people.

The Westman Diet

Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek.

Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days).

Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables.

After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications.

That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal.

Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes.

This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.

These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics.

All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes.

(This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)

Handy dandy carb index

There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences.

One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet.

Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test.

For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c.

HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.)

HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less.

HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)

HbA1c of diabetics: 6.5% or greater.

Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics.

With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar.

Battery acid and oatmeal

Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."

Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus.

Know what food is the most potent source of sulfuric acid in the body? Oats.

Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.

Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic.

The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases.

Here's one reference for this effect.

What'll it be: Olive oil or bread?

We frequently discuss the advisability of consuming fats, carbohydrates, and various types within each category.

But what's the worst of all? Combining fats with carbohydrates.

Putting aside the wheat-is-worst form of carbohydrate issue and treating bread as a prototypical carbohydrate, let's play out a typical scenario, a make-believe feeding study in which a theoretical person is fed specific foods.

John is our test person, a 40-year old, 5 ft 10 inch, 210 lb, BMI 27.7 (roughly the mean for the U.S.) He starts with an average American diet of approximately 55% carbohydrates and 30% fat. Starting lipoproteins (NMR):

LDL particle number 1800 nmol/L
Small LDL 923 nmol/L


(The LDL particle number of 1800 nmol/L translates to measured LDL cholesterol of 180 mg/dl, i.e., drop last digit or divide by 10.)

Also, calculated LDL cholesterol is 167 mg/dl (yes, underestimating "true" measured LDL), HDL 42 mg/dl, triglycerides 170 mg/dl.

We feed him a diet increased in carbohydrates and reduced in fat, especially saturated fat, with more breakfast cereals, breads and other wheat products, pasta, fruit juices and fruit, and potatoes. After four weeks:

LDL particle number 2200 nmol/L
Small LDL 1378 nmol/L

Note that LDL particle number has increased by 400 nmol/L due entirely to the increase in small LDL particles triggered by carbohydrate consumption. Lipids show calculated LDL cholesterol 159 mg/dl--yes, a decrease, HDL 40 mg/dl, triglycerides 189 mg/dl. (At this point, if John's primary care doctor saw these numbers, he would congratulate John on reducing his LDL cholesterol and/or suggest a fibrate drug to reduce triglycerides.)

John takes a rest for four weeks during which his lipoproteins revert back to their starting values. We then repeat the process, this time replacing most carbohydrate calories with fats, weighed heavily in favor of saturated fats like fatty red meats, butter and other full-fat dairy products. After four weeks:

LDL particle number 2400 nmol/L


Let's

Chocolate peanut butter cup smoothie

Here's a simple recipe for chocolate peanut butter cup smoothie.

The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa.


Ingredients:
1/2 cup coconut milk
1 cup unsweetened almond milk
2 tablespoons cocoa powder (without alkali)
2 tablespoons shredded coconut (unsweetened)
1 tablespoon ground flaxseed
1 teaspoon almond extract
1 1/2 tablespoons natural peanut, almond, or sunflower seed butter
Non-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)
4 ice cubes

Combine ingredients in blender. Blend and serve.

If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand.

For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener.

The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe.

Letter from the insurance company

Claudia got this letter from her health insurance company:

Dear Ms. ------,

Based on a recent review of your cholesterol panel of January 12, 2011, we feel that you should strongly consider speaking to your doctor about cholesterol treatment.

Reducing cholesterol values to healthy levels has been shown to reduce heart attack risk . . .


Okay. So the health insurer wants Claudia to take a cholesterol drug in the hopes that it will reduce their exposure to the costs for her future heart catheterization, angioplasty and stent, or bypass surgery. This is understandable, given the extraordinary costs of such hospital services, typically running from $40,000 for a several hour-long outpatient catheterization procedure, to as much as $200,000 for a several day long stay for coronary bypass surgery.

So what's the problem?

Here are Claudia's most recent lipid values:

LDL cholesterol 196 mg/dl
HDL 88 mg/dl
Triglycerides 37 mg/dl
Total cholesterol 291 mg/dl

By the criteria followed by her health insurer, both total and LDL cholesterol are much too high. Note, of course, that LDL cholesterol was a calculated value, not measured.

Here are Claudia's lipoproteins, drawn simultaneously with her lipids:

LDL particle number 898 nmol/L
Small LDL particle number less than 90 nmol/L (Values less than 90 are not reported by Liposcience)

LDL particle number is, by far and away, the best measure of LDL particles, an actual count of particles, rather than a guesstimate of LDL particles gauged by measuring cholesterol in the low-density fraction of lipoproteins (i.e., LDL cholesterol). It is also measured and is highly reproducible.

To convert LDL particle number in nmol/L to an LDL cholesterol-like value in mg/dl, divide by ten (or just drop the last digit).

Claudia's measured LDL is therefore 89 mg/dl--54% lower than the crude calculated LDL suggests.

This is because virtually all of Claudia's LDL particles are large, with little or no small. This situation throws off the crude assumptions built into the LDL calculation, making it appear that she has very high LDL cholesterol.

Do you think that Big Pharma advertises this phenomenon?

Healthy smoothies

I've now seen several people who have either caused themselves to be diabetic or to have other phenomena associated with excessive consumption of carbohydrates, all by innocently indulging in a carbohydrate-packed smoothie every morning.

Kay, for instance, has a smoothie of a half-pint blueberries, a banana, a scoop of whey, low-fat yogurt, a cup of milk every morning. The rest of her diet was fairly healthy: salads with oil-based dressing for lunch, salmon and asparagus for dinner, only an occasional carbohydrate indulgence outside of her morning smoothie ritual. Yet she had a HbA1c (a reflection of prior 60 to 90 days average blood sugar) at the near-diabetic range of 5.9%.

The mistake most people make when making smoothies is relying too heavily on carbohydrates like fruit. A smoothie like the one made by Kay can easily top 50, 60, or 70 grams carbohydrates per serving, more than sufficient to send blood sugars up to 150 mg/dl or more.

So what can you put in your smoothie and not send you over the edge to diabetes, small LDL, and all the other undesirable phenomena of excessive carbohydrates? Here's a list:

--coconut milk, unsweetened almond milk. Less desirable: milk, full-fat soymilk
--ground flaxseed
--oils: flaxseed oil, coconut oil (melted), extra-light olive oil, walnut oil
--dried coconut
--extracts: vanilla, almond, coconut, cherry, hazelnut
--spices: cinnamon, nutmeg, ginger
--herbs: mint leaves, cilantro
--cocoa powder (unsweetened)
--nut or seed butters (peanut butter, almond butter, sunflower seed butter)
--tofu
--exotic ingredients (ingredients you wouldn't expect in a smoothie): spinach, kale, cucumber

How do you sweeten a smoothie? This is what trips up most people. If you resort to fruit like bananas, pineapple, or apple, you will readily send your blood sugar skyward. Honey, agave syrup, and sugar, of course, all increase blood sugar and/or have the adverse effects of fructose. Be careful of yogurt, also, for similar reasons.

Therefore, to sweeten your smoothie, consider:

--Small servings of berries, e.g., 8-10 blueberries, 2 strawberries, a few wedges of apple, half a kiwi
--Non-nutritive sweeteners like stevia, Truvia, sucralose, xylitol, erythritol. Also, sugar-free (sucralose-based) syrups like those from DaVinci and Torani are useful. (Just be aware that non-nutritive sweeteners can increase appetite--use sparingly.)

Also, note that, if you have divorced yourself from wheat, cornstarch, and sugars, your desire for sweet should be much reduced. Foods other people find just right will taste sickeningly sweet to you. You might therefore find that foods like peanut butter or coconut milk have a mild natural sweetness; added sweetness is only minimally necessary.

Coming next: I'll share a smoothie recipe or two of mine. Anyone want to share a recipe?

Insulin secretagogue

Dairy products have the peculiar property of triggering pancreatic release of insulin. The research group at Lund University in Sweden have contributed the most to documenting this phenomenon:




Mean (±SEM) incremental changes (?) in serum insulin in response to equal amounts of carbohydrate from a white-wheat-bread reference meal (x) and test meals of whey (?), milk (?), cheese (?), cod (?), gluten-low (?), and gluten-high (?) meals. From Nilsson 2004.

Note that it is the area under the curve (AUC), not the peak value, that assumes greatest importance.

Dairy products, especially milk, whey, and yogurt, are insulin secretagogues: they stimulate pancreatic release of insulin. The effect is likely due to amino acids and/or polypeptides in dairy products. (The effect is less prominent with cheese. Also see this study.)

By conventional wisdom, this may be a good thing, since the excess insulin will blunt the glucose rise after consumption. However, in my book, this is not such a good thing, since most of us have tired, beaten, overworked pancreatic beta cells from our decades of carbohydrate overconsumption. I fear that the effect of dairy products just take us a bit closer to beta cell failure: diabetes.

Good news: The effect is least with cheese.

Be gluten-free without "gluten-free"

While I've discussed this before, it is such a confusing issue that I'd like to discuss it again.

I advocate wheat elimination because consumption of products made from modern dwarf Triticum aestivum:

--Triggers formation of extravagant quantities of small LDL and LDL particle number (or apoprotein B)
--Triggers inflammatory phenomena like c-reactive protein, increases leptin resistance, and reduction of the protective adipocytokine, adiponectin.
--Encourages accumulation of deep visceral fat ("wheat belly") that is inflammatory and causes resistance to insulin
--Increases blood sugar more than nearly all other foods--higher than a Milky Way bar, higher than a Snickers bar, higher than table sugar.
--Is being linked to a growing number of immune-mediated diseases, including celiac disease (quadrupled over past 50 years), type 1 diabetes in children, and cerebellar ataxia and peripheral neuropathies.

This last group of wheat-related phenomena are primarily due to gluten, the collection of 50+ proteins found in each wheat plant. For this reason, people diagnosed with celiac disease are advised to eliminate gluten from wheat and other sources (barley, rye, triticale, bulgur) and to eat gluten-free foods.

Gluten-free has therefore come to be viewed as wheat-free and problem-free. It ain't so.

Among the few foods that increase blood glucose higher than wheat: cornstarch, rice starch, potato starch, and tapioca starch--Yup: the ingredients commonly used to replace wheat in gluten-free foods. They are also flagrant triggers of the small LDL pattern, along with increased triglycerides, reduced HDL, increased visceral fat, increased blood pressure. In short, gluten-free foods lack the immune and brain effects of wheat gluten, but still make you fat, hypertensive, and diabetic.

I tell patients to view gluten-free foods like jelly beans: Gluten-free pancakes, muffins, breads, etc. are indulgences, not healthy replacements for wheat. It's okay to have a few jelly beans now and then. But they should not be part of a frequent or daily routine. Same with gluten-free foods.
All posts by william-davis

What to eat: Part I

I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.



The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.



One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

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.