Wheat Belly (Revised and Expanded Edition)

by William Davis

  The more than one hundred million diabetics and prediabetics in the United States today are therefore getting old before their time with the excess baggage of high blood sugars and glycation.19 There are many more Americans who don’t yet meet the criteria for prediabetes but still experience plenty of high blood sugars after consuming carbohydrates that increase blood sugar—i.e., blood sugars high enough to trigger more AGEs than normal. (If you doubt that blood sugars increase after eating, say, an apple or a slice of pizza, just pick up a simple glucose meter from your pharmacy. Test your blood sugar one hour after consuming the food of interest. More often than not, you will be shocked to see how high your blood glucose soars. Remember my two slices of whole wheat bread “experiment”? Blood glucose 167 mg/dl. That’s not uncommon.)

  While eggs don’t increase blood sugar, nor do raw nuts, olive oil, pork chops, or salmon, carbohydrates do—all carbohydrates, from apples and oranges to jelly beans and seven-grain cereal. As we discussed earlier, from a blood sugar standpoint, wheat products are worse than nearly all other foods, skyrocketing blood sugar to levels that rival those of a fullblown diabetic—even if you’re non-diabetic.

  Remember, the “complex” carbohydrate contained in wheat is the unique variety of amylopectin, amylopectin A, a form distinct from amylopectin in other carbohydrate-rich foods such as black beans and bananas. The amylopectin of wheat is the form most readily digested by the enzyme amylase, thus explaining the greater blood sugar–increasing property of wheat products. The more rapid and efficient digestion of wheat amylopectin means higher blood sugars over the ensuing two hours after consumption of wheat products, which in turn means greater triggering of AGE formation. If AGE formation was a contest, wheat would win nearly all the time, beating out other carbohydrate sources such as apples, oranges, sweet potatoes, ice cream, and chocolate bars.

  Thus, wheat products such as your poppy seed muffin or roasted vegetable focaccia are triggers of extravagant AGE production. Put two and two together: Wheat, because of its unique blood glucose–increasing effect, makes you age faster. Via its blood sugar/AGE-increasing effects, wheat accelerates the rate at which you develop signs of skin aging, kidney dysfunction, dementia, atherosclerosis, and arthritis.

  AGES: INSIDE AND OUT

  While we’ve focused so far on AGEs that form in the body and are largely derived from consumption of carbohydrates, there is a second source of AGEs that come directly from diet: animal products cooked at high temperatures. This can get awfully confusing, so let’s start from the beginning.

  AGEs originate from two general sources:

  ENDOGENOUS AGES

  These are the AGEs that form within the body, as we’ve discussed. The main pathway to forming endogenous AGEs starts with blood glucose. Foods that increase blood glucose increase endogenous AGE formation. Foods that increase blood glucose the most trigger the greatest AGE formation. This means that all carbohydrates, all of which increase blood glucose, trigger endogenous AGE formation. Some carbohydrates increase blood glucose more than others. From an endogenous AGE viewpoint, a Snickers bar triggers AGE formation only modestly, while whole wheat bread triggers AGEs vigorously, given the greater blood glucose–increasing effect of whole wheat bread.

  Interestingly, fructose, another sugar that has exploded in popularity as an ingredient in modern processed foods, increases AGE formation within the body up to several hundredfold more than glucose.20 Occurring as high-fructose corn syrup, fructose often accompanies wheat in breads and baked products. You will be hard-pressed to find processed foods not containing fructose in some form, from barbecue sauce to dill pickles. Also note that table sugar, or sucrose, is 50 percent fructose, the other 50 percent being glucose. Maple syrup, honey, and agave syrup are other fructose-rich sweeteners.

  EXOGENOUS AGES

  In contrast to endogenous AGEs, exogenous AGEs are not formed in the body, but are ingested preformed in cooked food.

  Foods vary widely in their AGE content. In particular, meats and animal products heated to high temperature, e.g., broiling and frying, increase AGE content more than a thousandfold.21 Also, the longer an animal product food is cooked, the richer its AGE content becomes.

  An impressive demonstration of the power of exogenous AGEs to impair arterial function was demonstrated when identical diets of chicken breast, potatoes, carrots, tomatoes, and vegetable oil were consumed by two groups of diabetic volunteers. The only difference: The first group’s meal was cooked for 10 minutes by steaming or boiling, while the second group’s meal was cooked by frying or broiling at 450°F for 20 minutes. The group given food cooked longer and at a higher temperature showed 67 percent reduced capacity for arterial relaxation, along with higher AGE and oxidative markers in the blood.22

  Exogenous AGEs are found in meats that are also rich in saturated fat. It means that saturated fat was wrongly accused of being heart-unhealthy because it often occurred in the company of the real culprit: AGEs. Cured meats (i.e., containing sodium nitrite), such as bacon, sausage, pepperoni, and hot dogs, are unusually rich in AGEs. So meats are not intrinsically bad, but they can be made unhealthy through manipulations that increase AGE formation (and other high-temperature by-products).

  Beyond the diet prescription of the Wheat Belly philosophy, i.e., eliminate wheat while maintaining restricted intake of carbohydrates, it is wise to avoid sources of exogenous AGEs, namely meats containing sodium nitrite, meats heated to high temperature (>350°F) for prolonged periods, and anything deep-fried. Whenever possible, avoid well-done and choose meats cooked rare or medium. (Is sashimi the perfect meat?) Cooking in water-based, rather than oil-based, liquids also helps limit AGE exposure.

  All that said, AGE science is still in its infancy, with many details yet to be discovered. Given what we know about the potential long-term effects of AGEs on health and aging, however, I do not believe it is premature to start giving some thought to how to reduce your personal AGE exposure. Perhaps you’ll thank me on your hundredth birthday.

  THE GREAT GLYCATION RACE

  There is a widely available test that, while not capable of providing an index of biological age, provides a measure of the rate of biological aging due to glycation. Knowing how fast or slow you are glycating the proteins of your body helps you know whether biological aging is proceeding faster or slower than chronological age. While AGEs can be assessed via biopsy of the skin or internal organs, most people are understandably less than enthusiastic about a pair of forceps being inserted into some body cavity to snip a piece of tissue. Thankfully, a simple blood test can be used to gauge the ongoing rate of AGE formation: hemoglobin A1c, or HbA1c. HbA1c is a common blood test that, while usually used for the purpose of diabetes control, can also serve as a simple index of glycation.

  Hemoglobin is the protein residing within red blood cells that is responsible for carrying oxygen. Like all other proteins of the body, hemoglobin is subject to glycation, i.e., modification of the hemoglobin molecule by glucose. The reaction occurs readily and, like other AGE mechanisms, is irreversible. The higher the blood glucose, the greater the percentage of hemoglobin that becomes glycated.

  Red blood cells have an expected life span of sixty to ninety days. Measuring the percentage of glycated hemoglobin molecules in the blood provides an index of how high blood glucose has ranged over the preceding sixty to ninety days, a useful tool for assessing the adequacy of blood sugar control in diabetics, or to diagnose diabetes.

  A slender person with a normal insulin response who consumes a limited amount of carbohydrates will have approximately 4.0 to 4.8 percent of all hemoglobin glycated (i.e., an HbA1c of 4.0 to 4.8 percent), reflecting the unavoidable low-grade, normal rate of glycation. Diabetics commonly have 8, 9, even 12 percent or more glycated hemoglobin—twice or more the normal rate. The majority of non-diabetic Americans are somewhere in between, most living in the range of 5.0 to 6.4 per
cent, above the perfect range but still below the “official” diabetes threshold of 6.5 percent.23, 24 In fact, an incredible 70 percent of adults have an HbA1c between 5.0 percent and 6.9 percent.25

  HbA1c does not have to be 6.5 percent to generate adverse health consequences. HbA1c in the “normal” range is associated with an increased risk for heart attacks, cancer, and 28 percent increased mortality for every 1 percent increase in HbA1c.26, 27 That trip to the all-you-can-eat pasta bar, accompanied by a couple of slices of Italian bread and finished off with a little bread pudding, sends your blood glucose up toward 150 to 250 mg/dl or higher for three to four hours; high glucose for a sustained period glycates hemoglobin, reflected in higher HbA1c.

  HEY, IT’S KIND OF BLURRY IN HERE

  The lenses of your eyes are the wonderful, naturally engineered optical devices that are part of the ocular apparatus that allows you to view the world. The words you are now reading present images, focused by the lenses on your retina, then transposed into nervous system signals interpreted by your brain as black letter images on white background. Lenses are like diamonds: Without flaws, they are crystal clear, allowing the unimpeded passage of light. Pretty damn amazing, when you think about it.

  Flawed, however, and the passage of light will be distorted.

  Lenses consist of structural proteins called crystallins that, like all other proteins of the body, are subject to glycation. When proteins in the lenses become glycated and form AGEs, the AGEs cross-link and clump together. Like the little specks that can be seen in a flawed diamond, little defects accumulate in the lenses. Light scatters upon hitting the defects. Over years of AGE formation, accumulated defects cause opacity of the lenses, or cataracts.

  The relationship of blood glucose, AGEs, and cataracts is well-defined. Cataracts can be produced within as little as ninety days in lab animals just by keeping blood glucose high.28 Diabetics are especially prone to cataracts (no surprise), with as much as fivefold increased risk compared to non-diabetics.29

  In the United States, cataracts are common, affecting 42 percent of males and females between the ages of fifty-two and sixty-four, and increasing to 91 percent between the ages of seventy-five and eighty-five.30 In fact, no structure in the eye escapes the damaging effects of AGEs, including the retina (macular degeneration), the vitreous (the gel-like liquid filling the eyeball), and the cornea.31

  Any food that increases blood sugar therefore has the potential to glycate the crystallins of the lenses of your eyes. At some point, injury to the lens exceeds its limited capacity for defect resorption and crystallin renewal. That’s when the car in front of you is lost in a blurry haze, unimproved by putting on your glasses or squinting.

  HbA1c—i.e., glycated hemoglobin—therefore provides a running index of glucose control. It also reflects to what degree you are glycating body proteins beyond hemoglobin. The higher your HbA1c, the more you are also glycating the proteins in the lenses of your eyes, in kidney tissue, arteries, skin, etc.32 In effect, HbA1c provides an ongoing index of aging rate: The higher your HbA1c, the faster you are aging.

  HbA1c is much more than just a feedback tool for blood glucose control in diabetics. It also reflects the rate at which you are glycating proteins of the body, the rate at which you are aging. Stay at 5 percent or less, and you are aging at the normal rate; more than 5 percent, and time for you is moving faster than it should, taking you closer to the great nursing home in the sky.

  Foods that increase blood glucose levels the most and are consumed more frequently are reflected by higher levels of HbA1c that in turn reflect a faster rate of organ damage and aging. So if you hate your boss at work and you’d like to hasten his approach to old age and infirmity, bake him a nice coffee cake.

  WHEAT ELIMINATION IS AGE-REVERSING

  You’ll recall that foods made from wheat increase blood sugar more than nearly all other foods, including table sugar. Pitting wheat against most other foods in a blood sugar contest would be like putting Mike Tyson in the ring against Truman Capote: no contest, a blood sugar KO in no time. Unless you’re a premenopausal, size 2, twenty-three-year-old female longdistance runner who, by virtue of minimal visceral fat, vigorous insulin sensitivity, and the advantages of abundant estrogen, enjoys little increase in blood sugar, two slices of whole wheat bread will likely launch your blood sugar into the 150 mg/dl range or higher—more than enough to set the AGE-forming cascade in motion.

  If glycation accelerates aging, can not glycating slow aging?

  Such a study has been performed in an experimental mouse model, with an AGE-rich diet yielding more atherosclerosis, cataracts, kidney disease, diabetes, and shorter life spans compared to longer-lived and healthier mice consuming an AGE-poor diet.33

  The clinical trial required for final proof of this concept in humans has not yet been performed, i.e., AGE-rich versus AGE-poor diet followed by examination of organs for the damage of aging. This is a practical stumbling block to virtually all anti-aging research. Imagine the pitch: “Sir, we will enroll you in one of two ‘arms’ of the study: You will either follow a high-AGE diet or a low-AGE diet. After five years, we are going to assess your biological age.” Would you accept potential enrollment in the high-AGE group? And how do we assess biological age?

  It seems plausible that, if glycation and AGE formation underlie many of the phenomena of aging, and if some foods trigger AGE formation more vigorously than others, a diet low in those foods should slow the aging process, or at least the facets of aging that advance through the process of glycation. A low HbA1c value signifies that less age-promoting endogenous glycation is ongoing. You will be less prone to cataracts, kidney disease, wrinkles, arthritis, atherosclerosis, and all the other phenomena of glycation that plague humans, especially those of the wheat-consuming kind.

  Indeed, the real-world Wheat Belly experience has illustrated the age-reversing effects of this lifestyle. Combine glycation-slowing effects with the inflammation-reversing effects of banishing wheat, and wonderful and spectacular changes occur: Around-the-eye puffiness reverses, yielding bigger eyes; reduction in facial edema, especially around the cheeks, alters and thins the proportions of the face; skin redness and rashes recede; numerous forms of gastrointestinal irritation are reversed, no more mad rushes to the toilet; and HbA1c plummets, signifying that the rate of aging has been slowed. People report reductions in leg edema, increased flexibility, increased strength, greater energy, increased libido, smoother skin—many of the trappings of youth. Photo comparisons of before and after “selfies” are often startling, posted on Wheat Belly social media, many of them sufficiently dramatic to prompt comments that we are finding mothers and daughters and posting them as “befores” and “afters.”

  Perhaps this lifestyle will even allow you to be honest about your age.

  CHAPTER 10

  MY PARTICLES ARE BIGGER THAN YOURS: WHEAT AND HEART DISEASE

  IN BIOLOGY, SIZE is everything.

  Filter-feeding shrimp, measuring just a couple of inches in length, feast on microscopic algae and plankton suspended in ocean water. Larger predatory fish and birds, in turn, consume the shrimp.

  In the plant world, the tallest plants, such as two-hundred-foot kapok trees of the tropical forest, obtain advantage with height, reaching high above the jungle canopy for sunlight required for photosynthesis, casting shadows on struggling trees and plants below.

  And so it goes, all the way from carnivorous predator to herbivorous prey. This simple principle predates humans, precedes the first primate who walked the earth, and dates back over a billion years since multi-cellular organisms gained evolutionary advantage over single-celled organisms, clawing their way through the primordial seas. In countless situations in nature, bigger is better.

  The Law of Big in the ocean and plant worlds also applies within the microcosm of the human body. In the human bloodstream, low-density lipoprotein (LDL) particles, wha
t most of the world wrongly recognizes as “LDL cholesterol,” follow the same size rules as shrimp and plankton.

  Large LDL particles are, as their name suggests, relatively large. Small LDL particles are—you guessed it—small. Within the human body, large LDL particles provide a survival advantage to the host human. We’re talking about size differences on a nanometer (nm) level, a billionth of a meter. Large LDL particles are 25.5 nm in diameter or larger, while small LDL particles are less than 25.5 nm in diameter. (This means LDL particles, big and small, are thousands of times smaller than a red blood cell but larger than a cholesterol molecule. Around ten thousand LDL particles would fit within the period at the end of this sentence.)

  For LDL particles, size of course does not make the difference between eating or being eaten. It determines whether LDL particles will accumulate in the walls of arteries, such as those of your heart (coronary arteries) or neck and brain (carotid and cerebral arteries) or not. In short, LDL size determines to a large degree whether you will have a heart attack or stroke at age fifty-seven or whether you’ll continue to pull the handle on casino slot machines at age eighty-seven.

  Small LDL particles are, in fact, an exceptionally common cause of heart disease, showing up as heart attacks, angioplasty, stents, bypass, and many other manifestations of atherosclerotic coronary disease.1 In my personal experience with thousands of patients with heart disease, over 90 percent express the small LDL pattern to at least a moderate, if not severe, degree.

  The drug industry has found it convenient and profitable to classify this phenomenon in the much-easier-to-explain category of “high cholesterol.” But cholesterol has little to do with the disease of atherosclerosis; cholesterol is a convenience of measurement, a remnant of a time when it was not possible to characterize and measure the various lipoproteins (i.e., lipid-carrying proteins) in the bloodstream that cause injury, atherosclerotic plaque accumulation, and, eventually, heart attack and stroke. But, like hula hoops and American Bandstand, cholesterol’s time has come and gone.