Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health (11 page)

Gluten is the main protein of wheat, and as I have explained, it is responsible for some, though not all, of the adverse effects of
wheat consumption. Gluten is the culprit underlying inflammatory damage to the intestinal tract in celiac disease. People with celiac disease must meticulously avoid food containing gluten. This means the elimination of wheat, as well as gluten-containing grains such as barley, rye, spelt, triticale, kamut, and perhaps oats. People with celiac disease often seek out “gluten-free” foods that mimic wheat-containing products. An entire industry has developed to meet their gluten-free desires, from gluten-free bread to gluten-free cakes and desserts.

However, many gluten-free foods are made by replacing wheat flour with cornstarch, rice starch, potato starch, or tapioca starch (starch extracted from the root of the cassava plant). This is especially hazardous for anybody looking to drop twenty, thirty, or more pounds, since gluten-free foods, though they do not trigger the immune or neurological response of wheat gluten, still trigger the glucose-insulin response that causes you to gain weight. Wheat products increase blood sugar and insulin more than most other foods. But remember: Foods made with cornstarch, rice starch, potato starch, and tapioca starch are among the few foods that increase blood sugar even
more
than wheat products.

So gluten-free foods are not
problem-free.
Gluten-free foods are the likely explanation for the overweight celiac sufferers who eliminate wheat and fail to lose weight. In my view, there is no role for gluten-free foods beyond the occasional indulgence, since the metabolic effect of these foods is little different from eating a bowl of jelly beans.

Thus, wheat elimination is not just about eliminating gluten. Eliminating wheat means eliminating the amylopectin A of wheat, the form of complex carbohydrate that actually increases blood sugar higher than table sugar and candy bars. But you don’t want to replace wheat’s amylopectin A with the rapidly absorbed carbohydrates of powdered rice starch, cornstarch, potato starch, and tapioca starch. In short, don’t replace wheat calories with rapidly
absorbed carbohydrates of the sort that trigger insulin and visceral fat deposition. And avoid gluten-free foods if you are gluten-free.

Later in the book, I will discuss the ins and outs of wheat removal, how to navigate everything from choosing healthy replacement foods to wheat withdrawal. I provide a view from the trenches, having witnessed thousands of people do it successfully.

But before we get to the details of wheat elimination, let’s talk about celiac disease. Even if you do
not
suffer from this devastating disease, understanding its causes and cures provides a useful framework for thinking about wheat and its role in the human diet. Beyond teaching us lessons about weight loss, celiac disease can provide other useful health insights to those of us without this condition.

So put down that Cinnabon and let’s talk about celiac.

YOUR POOR, UNSUSPECTING
intestine. There it is, doing its job every day, pushing along the partially digested remains of your last meal through twenty-some feet of small intestine, four feet of large intestine, eventually yielding the stuff that dominates the conversations of most retired people. It never stops for a rest but just does its thing, never asking for a raise or health care benefits. Deviled eggs, roast chicken, or spinach salad are all transformed into the familiar product of digestion, the bilirubin-tinted, semisolid waste that, in our modern society, you just flush away, no questions asked.

Enter an intruder that can disrupt the entire happy system: wheat gluten.

After
Homo sapiens
and our immediate predecessors spent millions of years eating from the limited menu of hunting and gathering, wheat entered the human diet, a practice that developed only during the past ten thousand years. This relatively brief
time—300 generations—was insufficient to allow all humans to make the adaptation to this unique plant. The most dramatic evidence of failed adaptation to wheat is celiac disease, the disruption of small intestinal health by wheat gluten. There are other examples of failed adaptation to foods, such as lactose intolerance, but celiac disease stands alone in the severity of the response and its incredibly varied expression.

Even if you don’t have celiac disease, I urge you to read on.
Wheat Belly
is not a book about celiac disease. But it is impossible to talk about the effects of wheat on health without talking about celiac disease. Celiac disease is the prototype for wheat intolerance, a standard against which we compare all other forms of wheat intolerance. Celiac disease is also on the rise, increasing fourfold over the past fifty years, a fact that, I believe, reflects the changes that wheat itself has undergone. Not having celiac disease at age twenty-five does not mean you cannot develop it at age forty-five, and it is increasingly showing itself in a variety of new ways besides disruption of intestinal function. So, even if you have happy intestinal health and can match success stories of regularity with your grandmother, you can’t be sure that some other body system is not being affected in a celiac-like way.

Flowery descriptions of the characteristic diarrheal struggles of celiac sufferers started with the ancient Greek physician Aretaeus in
AD
100, who advised celiac patients to fast. No lack of theories issued over the ensuing centuries to try to explain why celiac sufferers had intractable diarrhea, cramping, and malnutrition. It led to useless treatments such as castor oil, frequent enemas, and eating bread only if toasted. There were even treatments that enjoyed some degree of success, including Dr. Samuel Gee’s use of the mussel-only diet in the 1880s and Dr. Sidney Haas’ eight-bananas-a-day diet.
¹

The connection between celiac disease and wheat consumption was first made in 1953 by Dutch pediatrician Dr. Willem-Karel Dicke. It was the chance observation of the mother of a celiac child, who observed that her son’s rash improved when she did not feed
him bread, that first sparked his suspicion. During food shortages toward the end of World War II, bread became scarce and Dicke witnessed improvements of celiac symptoms in children, only to witness deterioration when Swedish relief planes dropped bread into the Netherlands. Dr. Dicke subsequently made meticulous measurements of children’s growth and stool fat content that finally confirmed that the gluten of wheat, barley, and rye was the source of the life-threatening struggles. Gluten elimination yielded dramatic cures, major improvements over the banana and mussel regimens.
²

While celiac disease is not the most common expression of wheat intolerance, it provides a vivid and dramatic illustration of what wheat is capable of doing when it encounters the unprepared human intestine.

Celiac disease is serious stuff. It’s truly incredible that a disease so debilitating, potentially fatal, can be triggered by something as small and seemingly innocent as a bread crumb or a crouton.

About 1 percent of the population is unable to tolerate wheat gluten, even in small quantities. Feed gluten to these people, and the lining of the small intestine, the delicate barrier separating incipient fecal matter from the rest of you, breaks down. It leads to cramping, diarrhea, and yellow-colored stools that float in the toilet bowl because of undigested fats. If this is allowed to progress over years, the celiac sufferer becomes unable to absorb nutrients, loses weight, and develops nutritional deficiencies, such as deficiencies of protein, fatty acids, and vitamins B
₁₂
, D, E, K, folate, iron, and zinc.
³

The broken-down intestinal lining allows various components of wheat to gain entry to places they don’t belong, such as the bloodstream, a phenomenon that is used to diagnose the condition:
Antibodies against wheat gliadin, one of the components of gluten, can be found in the blood. It also causes the body to generate antibodies against components of the disrupted intestinal lining itself, such as transglutaminase and endomysium, two proteins of intestinal muscle that also provide the basis for the two other antibody tests for diagnosis of celiac, transglutaminase and endomysium antibodies. Otherwise “friendly” bacteria that normally inhabit the intestinal tract are also permitted to send their products into the bloodstream, initiating another range of abnormal inflammatory and immune responses.
⁴

Until a few years ago, celiac was believed to be rare, affecting only one per several thousand people. As the means to diagnose the disease have improved, the number of people with it has expanded to 1 per 133. Immediate relatives of people with celiac disease have a 4.5 percent likelihood of also developing it. Those with suggestive intestinal symptoms have as high as 17 percent likelihood.
⁵

As we shall see, not only has more celiac disease been uncovered by better diagnostic testing, but the incidence of the disease itself has increased. Nonetheless, celiac disease is a well-kept secret. In the United States, 1 in 133 equates to just over two million people who have celiac disease, yet less than 10 percent of them know it. One of the reasons 1,800,000 Americans don’t know that they have celiac disease is that it is “The Great Imitator” (an honor previously bestowed on syphilis), expressing itself in so many varied ways. While 50 percent will experience the classic cramping, diarrhea, and weight loss over time, the other half show anemia, migraine headaches, arthritis, neurological symptoms, infertility, short stature (in children), depression, chronic fatigue, or a variety of other symptoms and disorders that, at first glance, seem to have nothing to do with celiac disease.
⁶
In others, it may cause no symptoms whatsoever but shows up later in life as neurological impairment, incontinence, dementia, or gastrointestinal cancer.

The ways that celiac disease shows itself are also changing. Until the mid-eighties, children were usually diagnosed with symptoms of
”failure to thrive” (weight loss, poor growth), diarrhea, and abdominal distention before age two. More recently, children are more likely to be diagnosed because of anemia, chronic abdominal pain, or with no symptoms at all, and not until age eight or older.
^7,
8,
9
In one large clinical study at the Stollery Children’s Hospital in Edmonton, Alberta, the number of children diagnosed with celiac disease increased elevenfold from 1998 to 2007.
¹⁰
Interestingly, 53 percent of children at the hospital who were diagnosed with antibody testing yet displayed no symptoms of celiac nonetheless reported feeling better with gluten elimination.

Parallel changes in celiac have been observed in adults, with fewer complaining of “classic” symptoms of diarrhea and abdominal pain, more being diagnosed with anemia, more complaining of skin rashes such as dermatitis herpetiformis and allergies, and more showing no symptoms at all.
¹¹

Researchers have failed to agree on why celiac disease may have changed or why it is on the rise. The most popular theory currently: More mothers are breastfeeding. (Yeah, I laughed, too.)

Much of the changing face of celiac disease can certainly be attributed to earlier diagnosis aided by the widely available antibody blood tests. But there also seems to be a fundamental change in the disease. Could the changing face of celiac disease be due to a change in wheat itself? It might cause dwarf wheat’s developer, Dr. Norman Borlaug, to roll over in his grave, but there is data suggesting that something in wheat itself indeed changed sometime during the past fifty years.

A fascinating study performed at the Mayo Clinic provides a unique snapshot of celiac incidence in US residents from half a century ago, the closest we will come to having a time machine to answer our question. The researchers acquired blood samples drawn fifty years ago for a streptococcal infection study, and kept frozen since. The frozen samples were collected during the period from 1948 to 1954 from more than 9,000 male recruits at Warren Air Force Base (WAFB) in Wyoming. After establishing the reliability of the long-frozen samples, they tested them for celiac markers
(transglutaminase and endomysium antibodies) and compared results to samples from two modern groups. A modern “control” group was chosen that consisted of 5,500 men with similar birth years to the military recruits, with samples obtained starting in 2006 (mean age 70 years). A second modern control group consisted of 7,200 men of similar age (mean age 37 years) at the time of the blood draw of the Air Force recruits.
¹²

While abnormal celiac antibody markers were identified in 0.2 percent of the WAFB recruits, 0.8 percent of men with similar birth ages and 0.9 percent of modern young men had abnormal celiac markers. It suggests that the incidence of celiac increased
fourfold
since 1948 in men as they age, and has increased fourfold in modern young men. (The incidence is likely to be even higher in females, since women outnumber men in celiac disease, but all the recruits enrolled in the original study were male.) Recruits with positive celiac markers were also four times more likely to die, usually from cancer, over the fifty years since providing blood samples.