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.
CHAPTER 6
HELLO, INTESTINE. IT’S ME, WHEAT. WHEAT AND CELIAC DISEASE
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 healthcare benefits. Deviled eggs, roast chicken, or spinach salad are all transformed into the familiar product of digestion, the bilirubin-tinted, semi-solid waste that, in our modern society, you just flush away, no questions asked.
Enter an intruder that can disrupt the entire happy system: wheat.
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—three hundred generations—was insufficient to allow all humans to make the adaptation to this unique grass. Among the most dramatic evidence of failed adaptation to wheat is celiac disease, the disruption of small intestinal health by the gliadin protein within 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, ways as varied as headaches, joint pain, and paranoid delusions. 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 his 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 mussel-only diet in the 1880s and Dr. Sidney Haas’s 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: BEWARE THE MIGHTY BREAD CRUMB
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 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 of protein, fatty acids, and vitamins B12, D, E, K, folate, iron, and zinc.3 And it doesn’t take much. Just a bread crumb or the residue of pancake batter on a sloppily washed utensil is enough to trigger the abnormal response, abdominal pain, diarrhea, and other misery.
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 used to diagnose the condition: Antibodies against wheat gliadin 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 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 disease 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 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 classic symptoms of cramping, diarrhea, and weight loss over time, the other half experience 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. 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 glut
en 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 more reliable 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 semi-dwarf wheat’s developer, Dr. Norman Borlaug, to roll over in his grave, but there are 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 U.S. 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 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.
I asked Dr. Joseph Murray, lead researcher in the study, if he expected to find the marked increase in the incidence of celiac disease. “No. My initial assumption was that celiac disease was there all along and we just weren’t finding it. While that was partly true, the data taught me otherwise: It really is increasing. Other studies showing that celiac disease occurs for the first time in elderly patients back up the imputation that something is affecting the population at any age, not just infant feeding patterns.”
A similarly constructed study was conducted by a group in Finland, part of a larger effort to chronicle health changes over time. Some 7,200 male and female Finns over the age of thirty provided blood samples for celiac markers from 1978 to 1980. Twenty years later, in 2000–2001, another 6,700 male and female Finns, also over thirty, provided blood samples. Measuring transglutaminase and endomysial antibody levels in both groups, the frequency of abnormal celiac markers increased from 1.05 percent in the earlier participants to 1.99 percent, a near doubling.13
NAME THAT ANTIBODY
Three groups of antibody blood tests are now widely available to diagnose celiac disease, or at least strongly suggest that an immune response against gluten has been triggered.
ANTI-GLIADIN ANTIBODIES
The short-lived IgA antibody and the longer-lived IgG anti-gliadin antibodies are often used to screen people for celiac. While widely available, they are less likely to make the diagnosis in all people with the disease, failing to diagnose approximately 20 to 50 percent of true celiac sufferers.14 Anti-gliadin antibodies are proving to be helpful, however, in diagnosing wheat- and grain-induced health conditions beyond celiac disease, such as Hashimoto’s thyroiditis (autoimmune inflammation of the thyroid), cerebellar ataxia (autoimmune deterioration of the cerebellum of the brain, leading to incoordination, incontinence, and death), some of the phenomena associated with schizophrenia, and peripheral neuropathy (loss of muscle control and/or sensation, typically in the legs).
TRANSGLUTAMINASE ANTIBODY
Gluten damage to the intestinal lining uncovers muscle proteins that trigger antibody formation. Transglutaminase is one such protein. The antibody against this protein can be measured in the bloodstream and used to gauge the ongoing autoimmune response. Compared to intestinal biopsy, the transglutaminase antibody test identifies approximately 86 to 89 percent of celiac cases.15, 16
ENDOMYSIUM ANTIBODY
Like the transglutaminase antibody test, the endomysium antibody identifies another abnormal antibody response to an intestinal tissue protein. Introduced in the mid-nineties, this test is emerging as the most accurate antibody test, identifying more than 90 percent of celiac cases.17, 18
If you have already divorced yourself from wheat, note that these tests can turn negative within a few months, almost certainly negative or reduced after six months. So the tests have value only for people currently consuming wheat products or only for those who have recently stopped consuming wheat products. Fortunately, there are some other tests available that can be helpful even after you’ve banished the evil grain from your life.
HLA DQ2, HLA DQ8
These are not antibodies, but genetic markers for human leukocyte antigens, or HLA, that, if present, make the bearer more genetically likely to develop celiac disease. More than 90 percent of people with celiac disease have either of these two HLA markers, most commonly the HLA DQ2.19
A dilemma: 40 percent of the population has one of the HLA markers and/or antibody markers that pre-dispose them to celiac, yet express no symptoms or other evidence of an immune system gone awry. However, this group has been shown to experience better health when wheat and grains are eliminated.20
RECTAL CHALLENGE
Not a new TV game show, but a test involving the placement of a sample of gluten into the rectum to see whether an inflammatory response is triggered. While quite accurate, the obvious logistical challenges of this four-hour test limit its usefulness.21
SMALL INTESTINE BIOPSY
Biopsy of the jejunum, the uppermost part of the small intestine, performed via an endoscope, is the “gold standard” by which all other tests are measured. The positive: The diagnosis can be made confidently. Negatives: An endoscopy and biopsies are required. Most gastroenterologists advise a small intestinal biopsy to confirm the diagnosis if suggestive symptoms, such as chronic cramping and diarrhea, are present and antibody tests suggest celiac disease. However, some experts have argued (and I agree) that the increasing reliability of antibody tests, such as the endomysium antibody test, potentially make intestinal biopsy less necessary, perhaps unnecessary. (In my view, the push for endoscopy is driven more by an interest in the considerable fees for the gastroenterologist rather than genuine need.)
Conventional wisdom holds that, if one or more antibody tests are abnormal but intestinal biopsy is negative for celiac, then gluten elimination is not necessary. I believe this is dead wrong, since many gluten-sensitive or latent celiac disease sufferers will either develop celiac disease over time or, even more likely, will develop some other manifestation of wheat and grain consumption such as neurological impairment, rheumatoid arthritis, Hashimoto’s thyroiditis, acid reflux, irritable bowel syndrome, type 2 diabetes, seborrhea, migraine headaches, or weight gain with visceral fat.
Keep in mind that if you are committed to removing wheat from your diet, along with other sources of gluten such as rye and barley, then testing may be altogether unnecessary. Testing
is only a necessity when serious symptoms or potential signs of wheat intolerance are present and documentation would be useful to help eliminate the possibility of other causes. Knowing that you harbor the markers for celiac might also increase your resolve to be meticulously gluten-free.
We therefore have good evidence that the apparent increase in celiac disease is not just due to better testing: The disease itself has increased in frequency, fourfold over the past fifty years, doubling in just the past twenty years. To make matters worse, the increase in celiac disease has been paralleled by an increase in type 1 diabetes, autoimmune diseases such as multiple sclerosis and Crohn’s disease, and allergies, many cases of which can be traced back to pretzels, bagels, and sandwiches.22
Emerging evidence suggests that the greater exposure to new forms of the gliadin protein within gluten that now occurs with modern wheat may underlie at least part of the explanation for the increased incidence of celiac disease. A study from the Netherlands compared thirty-six modern strains of wheat with fifty strains representative of wheat grown up until a century ago. By looking for the gliadin protein structures that trigger celiac, researchers found that celiac-triggering gliadin proteins were expressed at higher levels in modern wheat, while non-celiac-triggering proteins were expressed less.23
In short, while celiac disease is usually diagnosed in people complaining of weight loss, diarrhea, and abdominal pain, in the twenty-first century you can be fat and constipated, or even thin and regular, and still have the disease. And you are more likely to have the disease than your grandparents were.
While twenty to fifty years may be a long time in terms of wine or mortgages, it is far too little time for humans to have changed genetically. The timing of the two studies chronicling the increasing incidence of celiac antibodies, one in 1948 and the other in 1978, also parallel changes in the type of wheat that now populates most of the world’s farms, namely semi-dwarf wheat.
Wheat Belly (Revised and Expanded Edition) Page 10
