Wheat Belly (Revised and Expanded Edition)

by William Davis

  While the gastrointestinal system is ground zero in the human body’s battle against grains, it is by no means the only battleground. Let’s discuss the rest of the battered, barren, land mine–strewn desolation that wheat and related grains leave behind.

  CHAPTER 8

  DIABETES NATION: WHEAT AND INSULIN RESISTANCE

  I’VE KICKED IT in the jaw, beaten it, and called it names. Let’s now look this thing called diabetes square in the eye.

  PRESIDENT OF THE SOUP BONE CLUB

  When I was a kid growing up in Lake Hiawatha, New Jersey, my mother used to point to one person or another and declare him or her the “president of the soup bone club.” That’s the title she gave local people who thought they were big shots in our little town of five thousand. One time, for instance, the husband of a friend of hers droned on about how he could fix all the ills of the country if only he were elected president—though he was unemployed, was missing two front teeth, and had been arrested twice for drunk driving over the past two years. Thus, my mother’s gracious appointment of the man as president of the soup bone club.

  Wheat, too, is the leader of an unenviable group, the worst carbohydrate in the bunch, the one most likely to lead us down the path of diabetes. Wheat is president of its own little soup bone club, chief among carbohydrates. Drunk, foul-mouthed, and unbathed, still wearing last week’s T-shirt, it gets elevated to special “fiber-rich,” “complex carbohydrate,” and “healthy whole grain” status by all the agencies that dispense dietary advice and food manufacturers who profit from it.

  Because of wheat’s incredible capacity to send blood sugar levels straight up, initiate the glucose-insulin roller coaster ride that drives appetite, yield addictive brain-active exorphins, and grow visceral fat, it is the one essential food to eliminate in a serious effort to prevent, reduce, or eliminate diabetes. You could eliminate walnuts or pecans, but it will have no impact on diabetic risk. You could eliminate spinach or cucumbers, miss them in your salads, yet see no effect on diabetic risk. You could banish all pork or beef from your table and still experience no effect.

  But you could remove wheat and have an entire domino effect of changes develop: less blood sugar rises, no exorphins to drive the impulse to consume more, no initiation of the glucose-insulin cycle of appetite. And if there are no opiates nor wild glucose-insulin cycles, there’s little to drive appetite except genuine physiologic need for sustenance. If appetite shrinks, caloric intake is effortlessly reduced, visceral fat disappears, insulin resistance improves, and blood sugars fall. Diabetics can become non-diabetics, prediabetics can become non-prediabetics. All the phenomena associated with poor glucose metabolism recede, including high blood pressure, inflammation, glycation, small LDL particles, triglycerides, and pants or skirts from last year too tight to wear this year.

  In short, remove wheat and thereby reverse a constellation of phenomena that would otherwise result in diabetes and all its associated health consequences, three or four medications if not seven, and years shaved off your life.

  Think about that for a moment: The personal and societal costs of developing diabetes are substantial. On average, one person with diabetes incurs $180,000 to $250,000 in direct and indirect healthcare costs if diagnosed at age fifty1 and dies eight years earlier than someone without diabetes.2 That’s as much as a quarter of a million dollars and half the time spent watching your children grow up that you sacrifice to this disease, a disease caused in large part by food—in particular, a specific list of foods that government agencies, doctors, and dietitians urge you to eat. President of this soup bone club: wheat.

  Typically, health-conscious people who follow conventional dietary advice to reduce fat and eat more “healthy whole grains” consume approximately 75 percent of their carbohydrate calories from wheat products. That’s more than enough hobnobbing with the soup bone club to take you down the road to the increased medical costs, health complications, and shortened life span of diabetes. But it also means that, if you knock off the top dog, the pack disperses.

  PASSING WATER THAT TASTES LIKE HONEY

  Wheat and diabetes are closely interwoven. In many ways, the history of wheat is also the history of diabetes. Where there’s wheat, there’s diabetes. Where there’s diabetes, there’s wheat. It’s a relationship as cozy as McDonald’s and hamburgers. But it wasn’t until the modern age that diabetes became not just a disease of the idle rich but of every level of society. Diabetes has become Everyman’s Disease.

  Diabetes was virtually unknown in the Neolithic Age, when Natufians first began to harvest wild einkorn wheat. It was certainly unknown in the Paleolithic Age, the millions of years preceding the agricultural ambitions of Neolithic Natufians. The archaeological record and observations of modern hunter-gatherer societies suggest that humans almost never developed diabetes nor died of diabetic complications before grains were present in the diet.3, 4 The adoption of grains into the human diet was followed by archaeological evidence of increased infections, bone diseases such as osteoporosis and arthritis, increased infant mortality, and reduction in life span, as well as diabetes.5

  For example, the 1534 BC Egyptian “Eber’s papyrus,” discovered in the Necropolis of Thebes and harking back to the period when Egyptians incorporated ancient wheat into their diet, describes the excessive urine production of diabetes. Adult diabetes (type 2) was described by the Indian physician Sushruta in the fifth century BC, who called it madhumeha, or “honey-like urine,” due to its sweet taste (yes, he diagnosed diabetes by tasting urine) and the way the urine of diabetics attracted ants and flies. Sushruta also presciently ascribed diabetes to obesity and inactivity and advised treatment with exercise.

  The Greek physician Aretaeus called this mysterious condition diabetes, meaning “passing water like a siphon.” Many centuries later, another urine-tasting diagnostician, Dr. Thomas Willis, added “mellitus,” meaning “tasting like honey.” Yes, passing water that tastes like honey like a siphon. You’ll never look at your diabetic aunt the same way again.

  Starting in the 1920s, diabetes treatment took a huge leap forward with the administration of insulin, which proved lifesaving for diabetic children. Child diabetics experience damage to insulin-producing beta cells of the pancreas, impairing its ability to make insulin. Unchecked, blood glucose climbs to dangerous levels, acting as a diuretic (causing urinary water loss). Metabolism is impaired, since glucose is unable to enter the body’s cells due to lack of insulin. Unless insulin is administered, a condition called diabetic ketoacidosis develops, followed by coma and death. The discovery of insulin earned Canadian physician Sir Frederick Banting the Nobel Prize in 1923, spawning an era in which all diabetics, children and adults, were administered insulin.

  While the discovery of insulin was truly lifesaving for children, it sent the understanding of adult diabetes off course for many decades. After insulin was discovered, the distinction between type 1 and type 2 diabetes remained blurred. It was therefore a surprise in the fifties when it was discovered that adult type 2 diabetics don’t lack insulin until advanced phases of the disease. In fact, most adult type 2 diabetics have high quantities of insulin (several times greater than normal). Only in the eighties was the concept of insulin resistance discovered, explaining why abnormally high levels of insulin were present in adult diabetics.6

  Unfortunately, the discovery of insulin resistance failed to enlighten the medical world when the eighties’ notion of reducing fat and saturated fat in the diet led to a nationwide embrace of carbohydrates. In particular, it led to the idea that “healthy whole grains” would salvage the health of Americans believed to be threatened by overconsumption of fats. It inadvertently led to a fifty-year experiment in what can happen to people who reduce fats but replace lost fat calories with “healthy whole grains” such as wheat.

  The result: weight gain, obesity, bulging abdomens of visceral fat, prediabetes and diabetes on a scale never bef
ore witnessed, affecting males and females alike, rich and poor, herbivores and carnivores, reaching across all races and ages, all “passing water that tastes like honey like a siphon.”

  WHOLE GRAIN NATION

  Adult diabetes through the ages was mostly the domain of the privileged who didn’t have to hunt for their food, farm the land, or prepare their own meals. Think Henry VIII, gouty and obese, sporting a 54-inch waistline, gorging nightly on banquets topped off with loaves of bread, sweet puddings, marzipan, and ale. Only during the last half of the nineteenth century and into the twentieth century, when sucrose (table sugar) consumption increased across all societal levels, common laborer on up, did diabetes become more widespread.7

  The transition of the nineteenth into the twentieth century therefore witnessed an increase in diabetes, which then stabilized for many years. For most of the twentieth century, the incidence of adult diabetes in the United States remained relatively constant—until the mid-eighties.

  Then things took an abrupt turn for the worse (fig. 8.1).

  Fig. 8.1. Trends in adult overweight, obesity, and extreme obesity among men and women aged 20 to 74: United States, selected years 1960–1962 through 2011–2012

  NOTES: Age-adjusted by the direct method to the year 2000 U.S. Census Bureau estimates using age groups 20–39, 40–59, and 60–74. Pregnant females were excluded. Overweight is a body mass index (BMI) of 25 or greater but less than 30; obesity is a BMI greater than or equal to 30; and extreme obesity is a BMI greater than or equal to 40. SOURCE: CDC/NCHS. National Health Examination Survey 1960–1962; and National Health and Nutrition Examination Surveys 1971–1974, 1976–1980, 1988–1994, 1999–2000, 2001–2002, 2003–2004, 2005–2006, 2007–2008, 2009–2010, and 2011–2015.

  Today diabetes is epidemic, as common as tabloid gossip. In 2015, thirty million Americans were diabetic, a number representing explosive growth compared to just a few years earlier.8 The number of Americans with diabetes is growing faster than any other disease condition with the exception of obesity (if you call obesity a disease). If you’re not diabetic yourself, then you likely have friends who are diabetic, co-workers who are diabetic, neighbors who are diabetic. Given the exceptionally high incidence in the elderly, your parents are (or were) likely to be diabetic.

  And diabetes is just the tip of the iceberg. For every diabetic, there are three people with prediabetes (encompassing the conditions impaired fasting glucose, impaired glucose tolerance, and metabolic syndrome) waiting in the wings. This means that 29.3 percent of all women have prediabetes and 36.6 percent of all men. The combined total of people with prediabetes in 2015 was eighty-four million, or one in three adults over eighteen years of age, putting the total number of people with diabetes or prediabetes at well over one hundred million.9 That’s more than the total number of people, adults and children, diabetic and non-diabetic, living in the entire United States in 1900.

  If you also count the people who don’t yet meet full criteria for prediabetes but just show high after-meal blood sugars, high triglycerides, small LDL particles, and poor responsiveness to insulin (insulin resistance)—phenomena that can still lead to heart disease, cataracts, kidney disease, and eventually diabetes—you would find few people in the modern age who are not in this group, children included.

  This disease is not just about being fat and having to take medications; it leads to serious complications, such as kidney failure (40 percent of all kidney failure is caused by diabetes) and limb amputation (more limb amputations are performed for diabetes than any other non-traumatic disease). We’re talking real serious.

  It’s a frightening modern phenomenon, the widespread democratization of a formerly uncommon disease. The widely broadcast advice to put a stop to it? Exercise more, snack less…and eat more “healthy whole grains.”

  PANCREATIC ASSAULT AND BATTERY

  The explosion of diabetes and prediabetes has been paralleled by an increase in people who are overweight and obese.

  Actually, it would be more accurate to say that the explosion of diabetes and prediabetes has been in large part caused by the explosion in overweight and obesity, since weight gain leads to impaired insulin sensitivity and greater likelihood that excess visceral fat accumulates, the fundamental conditions required to create diabetes.10 The fatter Americans become, the greater the number that develop prediabetes and diabetes. In 2013–2014, 36.5 percent of American adults, or 119 million people, met the criteria for obesity—i.e., a body mass index (BMI) of 30 or greater—with an even greater number falling into the overweight (BMI 25 to 29.9) category.11 No state has yet met, nor is any approaching, the 15 percent goal for obesity set by the U.S. Surgeon General’s Call to Action to Prevent and Decrease Overweight and Obesity. (As a result, the Surgeon General’s office has repeatedly emphasized that Americans need to increase their level of physical activity, eat more reduced-fat foods, and, yes, increase consumption of whole grains.)

  Weight gain is predictably accompanied by diabetes and prediabetes (fig. 8.2), though the precise weight point at which they develop can vary from individual to individual, a genetic component of risk. One 5-foot-5 woman might develop diabetes at a weight of 240 pounds, while another 5-foot-5 woman might show diabetes at 140 pounds. Such variation is determined genetically as well as by other factors such as vitamin D status and bowel flora.

  The economic costs of such trends are staggering. Gaining weight is exceptionally costly, both in terms of healthcare costs and the personal toll on health.12 Some estimates show that, over the next twenty years, an incredible 16 to 18 percent of all healthcare costs will be consumed by health issues arising from excessive weight: not genetic misfortune, birth defects, psychiatric illness, burns, or post-traumatic stress disorder from the horrors of war—no, just getting fat. The cost of Americans becoming obese dwarfs the sum spent on cancer. More money will be spent on health consequences of obesity than education.

  Fig. 8.2. Number and percentage of U.S. population with diagnosed diabetes, 1958–2015

  CDC’s Division of Diabetes Translation. United States Diabetes Surveillance System available at http://www.cdc.gov/diabetes/data.

  Yet another factor parallels the trends in diabetes, prediabetes, and weight gain. You guessed it: wheat consumption. Whether it’s for convenience, taste, or in the name of “health,” Americans have become helpless wheataholics, with per capita annual consumption of wheat products (white and wheat bread, durum pasta) having increased by 22 pounds since 1972.13 If national wheat consumption is calculated across all Americans—babies, children, teenagers, adults, the elderly—the average American consumes 133 pounds of wheat per year. (Note that 133 pounds of wheat flour is equal to approximately 200 loaves of bread, or a bit more than half a loaf of bread per day.) Of course, this means that many adults eat far more than that amount, since no baby or young child included in the averaging process eats 133 pounds of wheat per year.

  That said, babies eat wheat, children eat wheat, teenagers eat wheat, adults eat wheat, the elderly eat wheat. Each group has its own preferred forms—baby food and animal crackers, cookies and peanut butter sandwiches, pizza and Oreos, whole wheat pasta and whole grain bread, dry toast and Ritz crackers—but, in the end, it’s all the same. In parallel with increased consumption, we also have the silent replacement of wheat from five-foot-tall Triticum aestivum with high-yield semi-dwarf strains and new gliadin/gluten structures not previously consumed by humans.

  Physiologically, the relationship of wheat to diabetes makes perfect sense. Products made with wheat dominate our diet and push blood sugar higher than virtually all other foods. This sends measures such as HbA1c (reflecting the average preceding sixty to ninety days’ blood glucose) higher. The cycle of glucose-insulin reaching high levels several times every day provokes growth of visceral fat. Visceral fat—wheat belly—is closely aligned with resistance to insulin that, in turn, leads to even highe
r levels of glucose and insulin.14

  The early phase of growing visceral fat and diabetes is accompanied by a 50 percent increase in pancreatic beta cells responsible for producing insulin, a physiologic adaptation to meet the enormous demands of a body that is resistant to insulin. But beta cell adaptation has limits.

  High blood sugars, such as those occurring after a nice cranberry muffin consumed on the car ride to work, provoke the phenomenon of “glucotoxicity,” damage to pancreatic insulin–producing beta cells that results from high blood sugars.15 The higher the blood sugar, the more damage to beta cells. The effect is progressive and starts at a glucose level of 100 mg/dl, a value many doctors call normal. After two slices of whole wheat bread with low-fat turkey breast, a typical blood glucose would be 140 to 180 mg/dl in a non-diabetic adult, more than sufficient to do away with a few precious beta cells—which are never replaced.

  Your poor, vulnerable pancreatic beta cells are also damaged by the process of lipotoxicity, loss of beta cells due to increased triglycerides and fatty acids, such as those developing from repeated carbohydrate ingestion. A diet weighted toward carbohydrates results in increased triglycerides that persist in both the after-meal and between-meal periods, further exacerbating attrition of pancreatic beta cells.