Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health (12 page)
Read Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health Online
Authors: William Davis
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 age 30 provided blood samples for celiac markers from 1978 to 1980. Twenty years later, in 2000-01, another 6,700 male and female Finns, also over 30, 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.
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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.
Antigliadin antibodies.
The short-lived IgA antibody and the longer-lived IgG antigliadin 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.
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Transglutaminase antibody.
Gluten damage to the intestinal lining uncovers muscle proteins that trigger antibody formation. Transglutamin-ase 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.
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Endomysium antibody.
Like the transglutaminase antibody test, the endomysium antibody identifies another intestinal tissue protein that triggers an antibody response. Introduced in the mid-nineties, this test is emerging as the most accurate antibody test, identifying more than 90 percent of celiac cases.
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If you have already divorced yourself from wheat, note that these tests can turn negative within a few months, and almost certainly negative or reduced after six months. So the tests have value only for people currently consuming wheat products or only for those recently having stopped consuming wheat products. Fortunately, there are some other tests available.
HLA DQ2, HLA DQ8.
These are not antibodies, but genetic markers for human leukocyte antigens, or HLA, that, if present, make the bearer more likely to develop celiac disease. More than 90 percent of people who have celiac disease diagnosed by intestinal biopsy have either of these two HLA markers, most commonly the DQ2.
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A dilemma: Forty percent of the population have one of the HLA markers and/or antibody markers that predispose them to celiac, yet express no symptoms or other evidence of an immune system gone awry. However, this latter group has been shown to experience better
health when wheat gluten is eliminated.
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It means that a very substantial portion of the population is potentially sensitive to wheat gluten.
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 logistical challenges of this four-hour test limit its usefulness.
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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.
Most celiac disease experts advocate starting with an endomysium and/or transglutaminase antibody test, followed by intestinal biopsy if the antibody test is positive. In the occasional situation in which symptoms are highly suggestive of celiac disease but antibody tests are negative, intestinal biopsy might still be considered.
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 of these so-called gluten-sensitive or latent celiac disease sufferers will either develop celiac disease over time, or will develop some other manifestation of celiac disease, such as neurological impairment or rheumatoid arthritis.
Another perspective: If you are committed to this notion of removing wheat from your diet, along with other sources of gluten such as rye and barley, then testing may be unnecessary. The only time testing is a necessity is 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 (or at least the immune markers to gluten) 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.
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Emerging evidence suggests that the greater exposure to 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 gluten protein structures that trigger celiac, researchers found that celiac-triggering gluten proteins were expressed to higher levels in modern wheat, while non-celiac-triggering proteins were expressed less.
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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 dwarf wheat.
The gliadin protein of wheat gluten, present in all forms of wheat from spongy Wonder Bread to the coarsest organic multigrain loaf, has the unique ability to make your intestine permeable.
Intestines are not meant to be freely permeable. You already know that the human intestinal tract is home to all manner of odd things, many of which you observe during your morning ritual on the toilet. The wondrous transformation of ham sandwich or pep-peroni pizza into the components of your body, the remainder discarded, is truly fascinating. But the process needs to be tightly regulated, allowing entry of only selected components of ingested foods and liquids into the bloodstream.
So what happens if various obnoxious compounds mistakenly gain entry into the bloodstream? One of the undesirable effects is autoimmunity—i.e., the body’s immune response is “tricked” into activation and attacks normal organs such as the thyroid gland or joint tissue. This can lead to autoimmune conditions such as Hashimoto’s thyroiditis and rheumatoid arthritis.
Regulating intestinal permeability is therefore a fundamental function of the cells lining the fragile intestinal wall. Recent research has fingered wheat gliadin as a trigger of intestinal release of a protein called zonulin, a regulator of intestinal permeability.
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Zonulins have the peculiar effect of disassembling tight junctions, the normally secure barrier between intestinal cells. When gliadin triggers zonulin release, intestinal tight junctions are disrupted, and unwanted proteins such as gliadin and other wheat protein fractions gain entry to the bloodstream. Immune-activating lymphocytes, such as T-cells, are then triggered to begin an inflammatory process against various “self” proteins, thus initiating wheat gluten- and gliadin-initiated conditions such as celiac disease, thyroid disease, joint diseases, and asthma. Gliadin wheat proteins are akin to being able to pick the lock on any door, allowing unwanted intruders to gain entry into places they don’t belong.
Outside of gliadin, few things share such a lock-picking, intestinal-disrupting talent. Other factors that trigger zonulin and disrupt intestinal permeability include the infectious agents that cause cholera and dysentery.
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The difference, of course, is that you contract cholera or amoebic dysentery by ingesting
feces-contaminated food or water; you contract diseases of wheat by eating some nicely packaged pretzels or devil’s food cupcakes.
After you read about some of the potential long-term effects of celiac disease, you just might find yourself
wishing
for diarrhea.
Traditional notions of celiac disease revolve around the presence of diarrhea: No diarrhea, no celiac. Not true. Celiac disease is more than an intestinal condition with diarrhea. It can extend beyond the intestinal tract and show itself in many other varied ways.
The range of diseases associated with celiac is truly astonishing, from childhood (type 1) diabetes to dementia to scleroderma. These associations are also among the least understood. It is therefore not clear whether
anticipation
of gluten sensitivity with removal of all gluten will, for instance, reduce or eliminate the development of childhood diabetes—certainly a tantalizing prospect. These conditions, like celiac disease, test positive for the various celiac antibody markers and are triggered by the immune and inflammatory phenomena set in motion by genetic predisposition (presence of the HLA DQ2 and HLA DQ8 markers) and exposure to wheat gluten.
One of the most bothersome aspects of the conditions associated with celiac disease is that intestinal symptoms of celiac may not be expressed. In other words, the celiac sufferer might have neurological impairment, such as loss of balance and dementia, yet be spared the characteristic cramping, diarrhea, and weight loss. Lack of telltale intestinal symptoms also means that the correct diagnosis is rarely made.
Rather than calling it celiac disease without the intestinal expression of the condition, it would be more accurate to speak about
immune-mediated gluten intolerance.
But because these non-intestinal conditions of gluten sensitivity were first identified
because they share the same HLA and immune markers with intestinal celiac disease, the convention is to speak about “latent” celiac disease or celiac disease without intestinal involvement. I predict that, as the medical world begins to better recognize that immune-mediated gluten intolerance is much more than celiac disease, we will be calling it something like immune-mediated gluten intolerance, of which celiac disease will be a subtype.
Conditions associated with celiac disease—i.e., immune-mediated gluten intolerance—include the following:
- Dermatitis herpetiformis
—This characteristic rash is among the more common manifestations of celiac disease or immune-mediated gluten intolerance. Dermatitis herpeti-formis is an itchy, bumpy rash that usually occurs over the elbows, knees, or back. The rash disappears upon gluten removal.
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—Liver diseases associated with celiac can assume many forms, from mild abnormalities on liver tests to chronic active hepatitis to primary biliary cirrhosis to biliary cancer.
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Like other forms of immune-mediated gluten intolerance, intestinal involvement and symptoms such as diarrhea are often not present, despite the fact that the liver is part of the gastrointestinal system. - Autoimmune diseases
—Diseases associated with immune attacks against various organs, known as autoimmune diseases, are more common in people with celiac. People with celiac disease are more likely to develop rheumatoid arthritis, Hashimoto’s thyroiditis, connective tissue diseases such as lupus, asthma, inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease, as well as other inflammatory and immune disorders. Rheumatoid arthritis, a painful, disfiguring joint arthritis treated with anti-inflammatory agents, has been shown to improve, and occasionally remit entirely, with gluten removal.
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The risk for autoimmune inflammatory bowel disease, ulcerative colitis, and Crohn’s disease is especially high; incidence is sixty-eight-fold compared to nonceliacs.
29 - Insulin-dependent diabetes—
Children with insulin-dependent type 1 diabetes have an unusually high likelihood of having positive antibody markers for celiac disease, with up to twenty-fold greater risk for developing it.
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It is not clear whether wheat gluten is the
cause
of diabetes, but investigators have speculated that a subgroup of type 1 diabetics develop the disease triggered by gluten exposure.
31 - Neurological impairment
—There are neurological conditions associated with gluten exposure that we will consider in greater detail later in the book. There is a curiously high incidence (50 percent) of celiac markers among people who develop otherwise unexplained loss of balance and coordination (ataxia) or loss of feeling and muscle control in the legs (peripheral neuropathy).
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There is even a frightening condition called gluten encephalopathy, characterized by brain impairment with headaches, ataxia, and dementia, eventually fatal; abnormalities are seen in the white matter of the brain by MRI.
33 - Nutritional deficiencies
—Iron-deficiency anemia is unusually common among celiac sufferers, affecting up to 69 percent. Deficiencies of vitamin B
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, folic acid, zinc, and fat-soluble vitamins A, D, E, and K are also common.
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