- The prevalence, pathogenesis and diagnostics of celiac disease
- Celiac disease
- Disease pathogenesis
- CD-specific antibodies and diagnosis
- The prolamin trigger
- New ESPGHAN diagnostic guidelines
- The current diagnostic landscape
- The Many Faces of Celiac Disease
- Celiac Disease
- What causes celiac disease?
- What are the symptoms of celiac disease?
- How is celiac disease diagnosed?
- What is the treatment for celiac disease?
- Celiac disease rate is growing, particularly among elderly, study reveals
- New Treatment for Celiac Disease?
- A Vaccine for Celiac Disease?
- Doctors caution that gluten-free is not for everyone
The prevalence, pathogenesis and diagnostics of celiac disease
While biopsies for celiac disease (CD) remain the standard screening practice in the United States, European gastroenterologists and laboratories are steadily moving away from this invasive procedure, except to clarify particularly difficult cases.
One of the key reasons for this change in diagnostic approach is the multitude of different serological assay methods now available to labs. Many of these blood-based assays have been developed with greater specificity and sensitivity than ever before, enabling standard diagnostic criteria to be detecting CD-specific antibodies.
Specifically, those against tissue transglutaminase (tTG-IgA) and deamidated (modified) gliadin peptides (DGP), immunoglobulin (Ig)A and IgG.
CD is a lifelong, gluten-sensitive autoimmune disease deriving from environmental (gluten) and genetic factors (human leukocyte antigen [HLA] and non-HLA genes). CD is becoming more prevalent and common in developed regions of the world, such as the U.S. and Europe, as increased awareness and detection of the disease continues to grow.
The disease presents with gastrointestinal symptoms, non-gastrointestinal symptoms or no symptoms at all. It usually manifests with severe gastrointestinal problems such as diarrhea, vomiting, abdominal pains and cramps.
However, about half of CD patients present with non-gastrointestinal symptoms, which can include anemia, osteoporosis, skin conditions and weight loss.
CD was originally thought to affect European populations exclusively but is currently prevalent around the world. Areas such as South America, Asia, the Middle East and Africa, previously thought to be unaffected by CD, are now believed to have been underdiagnosed, contributing to the notion that CD is becoming one of the most common autoimmune and genetic diseases.
It is thought that CD generally followed humans’ evolutionary migratory and dietary flows—from once feeding primarily on meat, fruits and vegetables, to the development and prominence of farming, when gluten-containing cereals such as wheat, barley and rye became an integral part of a diet. As human expansion continued, farming became more of a staple way of life and agricultural practices, as well as the gradual replacement of indigenous inhabitants, introduced genetic anomalies into the population leading to increased gluten sensitivity.
CD is typically activated by a combination of environmental and genetic causes. The main genetic factor derives from the HLA-DQ genes, DQ2 and DQ8. In genetically pre-disposed individuals, disease of the intestinal tract (enteropathy) is triggered by the immune system’s over-response to the prolamins within gluten, particularly gliadin.
Gliadin peptides are not fully digested in the small intestine, enabling the gliadin remnants to be taken up into the intestinal wall and the surrounding intestinal connective tissue. At this point, the enzyme tTG deamidates (modifies) the gliadin by converting the amino acid glutamine into glutamate.
The DGP affect intestinal permeability causing an immune reaction in CD patients because of their resistance to gastrointestinal enzymes. This process results in the production of antibodies against DGP and the bodies’ own tTG, and the secretion of inflammatory cytokines. The inflammation of the small-intestinal epithelium leads to atrophy of the intestinal villi.
This cascade results in swelling of the small intestine and the variety of gastrointestinal symptoms mentioned above.
CD-specific antibodies and diagnosis
Pathogenesis of celiac disease.In addition to HLA genetic predisposition, tTG autoantigens play a crucial role in CD pathogenesis. Autoantibodies against tTG are a very sensitive and specific marker for CD.
They can be detected by monospecific immunoassays, such as antigen-coated ELISA or immunoblot, or indirect immunofluorescence tests (IIFT). tTG mediates deamidation of gliadins, creating an epitope that binds efficiently to DQ2 and is recognized by gut-derived T-cells.
Antibodies against these deamidated epitopes of gliadin fragments are specific for CD. Antibodies against native gliadin, however, are less specific and are no longer a determinant as they are frequently also found in healthy individuals.
Anti-DGP antibodies can be determined by ELISA, immunoblot or monospecific IIFT assays.
The prolamin trigger
Gluten is a protein found in cereals such as wheat, barley, rye and oat, amalgamating the proteins prolamin and glutelin. Most of the proteins in food that are responsible for immune reactions in CD are the prolamins.
Because of their high glutamine content and certain specific sequence patterns, prolamins are resistant to gastrointestinal enzymes that protect the small intestine from autoimmune response. The incomplete gastrointestinal digestion of the gluten leads to the presence of gluten-derived gliadin peptides.
The ingestion of prolamins from cereals causes changes in the small intestine mucous membrane of celiac patients leading to a syndrome of poor absorption, causing an autoimmune response after the ingestion of gluten.
When screening for CD, it is mandatory that the individuals are on a regular gluten-containing diet as the CD-specific antibodies disappear when on a gluten-free diet.
New ESPGHAN diagnostic guidelines
Detection of EmA by IFA on liver tissue.In September 2019, the European Society of Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) published updated guidelines for the diagnosis of CD.
Since guidelines were last released in 2012, there has been the development of more sensitive and specific assays to detect antibodies leading to a refinement in thinking about diagnostics testing for CD.
Among the new guidelines are recommendations that, for initial testing, consider the combination of total IgA and IgA-class antibodies against transglutaminase 2 (TGA-IgA) to be more accurate than other test combinations. If the test is positive, then a confirmatory test is encouraged; if both tests are positive, then a biopsy is no longer recommended.
Detection of EmA by IFA on small intestine tissue.Regarding pediatrics, a no-biopsy approach for CD diagnosis is safe in children with high TGA-IgA values (≥10 times the upper limit of normal) with appropriate tests and positive endomysial antibodies (EMA-IgA) in a second serum sample.
If TGA-IgA is ≥10 times the upper limit of normal (10xULN) and the family agrees, a no-biopsy diagnosis need be applied, provided that endomysial antibodies (EMA-IgA) test positive in a second blood sample.
However, children with positive TGA-IgA but lower titers (
HLA testing and presence of symptoms are not compulsory criteria for a serology-based diagnosis. Presence of HLA-DQ2 and/or DQ8 does not constitute a diagnosis of CD, nor does it mean one will ever develop it.
However, carrying HLA-DQ2/DQ8 increases the risk of developing CD from the overall average of one to three percent of the population.
The current diagnostic landscape
The current environment of laboratory testing can be quite challenging for laboratories in the diagnosis of CD simply because of the recent burgeoning and availability of a variety of methods and approaches.
Very different testing systems now exist with diverse diagnostic algorithms to test for the disease, so it becomes increasingly difficult for labs to decide how to implement various modalities into their routines.
For example, the highly specific indirect immunofluorescence test (IIFT) allows for the use of a variety of different tissues, including small intestine and liver. Different tissues may require a different set of experiences and skills in reading the fluorescent patterns from the tissues.
In monospecific assays, such as ELISA and immunoblot, there are different parameters including the anti-tTG and anti-DGP testing, as well as different combinations of these parameters. Assays that specifically test for antibodies against deamidated gliadins also represent a major advance in diagnostic testing.
These tests are more sensitive and accurate in determining CD in that deamidated gliadin antibodies are more ly found in CD patients than native gliadin antibodies.
One of the biggest challenges gastroenterologists and laboratories still face, however, is diagnosing patients who exhibit all the symptoms of CD yet have no antibodies.
At this time, there are no real criteria that would help physicians in diagnosing these types of patients. In response, researchers are trying to determine a biomarker, but as of yet none have been found.
This situation remains an obstacle.
It is expected that the ESPGHAN guidelines will become more widespread outside of Europe, resulting in fewer biopsies over time—making it easier for both patients and gastroenterologists. With screening of serological markers becoming more sensitive and accurate, these guidelines would inevitably be the standard of diagnosis for the detection of CD, globally.
The Many Faces of Celiac Disease
Ranier von Coelln, MD2
Joseph Savitt, MD2
Linda A. Lee, MD1
1Department of Medicine, Division of Gastroenterology & Hepatology, 2Department of Neurology,
Johns Hopkins Hospital, Baltimore, Maryland
Address correspondence to:
Dr. Vivian Asamoah, Department of Medicine, Division of Gastroenterology & Hepatology, Johns Hopkins Hospital, 600 N. Wolfe Street, Baltimore, MD 21287; Tel: 410-955-4916; Fax: 410-614-8799; E-mail: firstname.lastname@example.org
Celiac disease (CD) is the most common food intolerance in Western populations. However, recent studies have shown that the prevalence of CD in individuals of non-European descent is similar to that of Western populations.
Currently, this disorder represents a major health issue that is globally underdiagnosed. CD has a broad clinical spectrum, with signs and symptoms including iron-deficiency anemia, constipation, diarrhea, malabsorption, and weight loss.
Extraintestinal manifestations have also been described, including dermatologic and neurologic disorders. To our knowledge, this case is the first report of a Middle Eastern woman with celiac enteropathy who presented with skin rash and gait ataxia.
This case highlights the prevalence of CD in non-Western populations, and it illustrates the importance of considering CD in the differential diagnosis of patients with atypical gastrointestinal and neurologic symptoms.
A 37-year-old woman from the United Arab Emirates presented to our institution’s Movement Disorder Center with a 5-year history of undiagnosed gait disturbance, imbalance, and dysarthria. She described a slowly progressive course over several years; for the last 3 years, she had used a wheelchair when traveling longer distances due to concerns about frequent falls.
The patient reported moderate impairment in fine motor skills and some visual disturbances, but she denied numbness and tingling in her extremities. She admitted to increased urinary frequency and urge incontinence beginning after the onset of her gait disturbance.
Initial blood laboratory analysis showed profound iron-deficiency anemia, and the patient was referred to the gastroenterology clinic for further evaluation. Except for chronic constipation and weight gain, she had no other gastrointestinal symptoms. She also reported an undiagnosed pruritic skin rash that had appeared 3 years prior to presentation.
She had no other significant past medical history and no family history of any neurologic disorder. However, her parents were first cousins.
On physical examination, the patientappeared weak and unsteady on her feet. She was alert and oriented to person, place, and time. Her vitals were stable, and there was no evidence of orthostatic hypotension. She was not jaundiced.
A healing, symmetric, papulovesicular rash was noted on her trunk and extremities (Figures 1 and 2). Cardiac and pulmonary examination results were normal.
Her abdomen was benign, with no hepatosplenomegaly or other mass found on palpation.
Pertinent neurologic findings included prominent cerebellar oculomotor dysfunction as evidenced by saccadic pursuit, hypermetric saccades, impaired suppression of the vestibulo-ocular reflex, and mild gaze-evoked nystagmus. Her speech was consistent with cerebellar dysarthria. She had normal muscle tone with no weakness or tremor.
She had 2+ symmetric reflexes and downgoing toes. Her sensation was intact to light touch, proprioception, and vibration. Rapid alternating movements were slow and dysrhythmic. There was moderate dysmetria on finger-to-nose and heel-to-shin testing. Her walk was wide-based and unsteady.
Her score on the scale for the assessment and rating of ataxia was 15/40.
Neurologic work-up for sporadic ataxia, including a paraneoplastic antibody panel, was negative.
Vitamin E, vitamin B12, thyroid-stimulating hormone, rapid plasma reagin, methylmalonic acid, coenzyme Q10, anti–glutamic acid decarboxylase 65 antibodies, and hexosaminidase levels were all within normal limits.
A lumbar puncture was performed; cerebrospinal fluid revealed a normal cell count, protein content, and negative cytopathology. The patient refused genetic testing. Brain magnetic resonance imaging revealed significant cerebellar and borderline pontine atrophy (Figure 3).
Blood analysis was notable for profound iron-deficiency anemia, with a hemoglobin level of 9 g/dL, mean corpuscular volume of 68 fL, and ferritin level less than 3 ng/mL. A celiac serology panel was positive: Her gliadin antibody immunoglobulin (Ig)G level was
34 mg/dL (normal,
Celiac disease is a digestive problem that hurts your small intestine. It stops your body from taking in nutrients from food.
You may have celiac disease if you are sensitive to gluten. Gluten is a kind of protein found in wheat, rye, barley, and sometimes in small amounts in mixed oats.
When you have celiac disease and you eat foods with gluten, your body has a reaction that is not normal. The part of your body that fights disease (the immune system) starts to hurt your small intestine. It attacks the tiny bumps (villi) that line your small intestine.
The villi help your body take in nutrients from food into your bloodstream. Without the villi, your small intestine can’t get enough nutrients, no matter how much food you eat.
Celiac disease is genetic. This means it can be passed down from parent to child.
More than 2 million Americans have been diagnosed with celiac disease. Studies show that as many as 1 in every 133 Americans may have it. They may not know they have it.
Celiac disease is more common in people:
- Whose ancestors came from Europe
- Who are white
- Who have type 1 diabetes
- Who have Down syndrome
- Who have other autoimmune diseases
- Who are infertile
- Who have irritable bowel syndrome with diarrhea
What causes celiac disease?
Celiac disease is a genetic disease that runs in families. You may have celiac disease and not know it because you don’t have any symptoms.
Some things that may make symptoms start to appear are:
- Too much stress
- Physical injury
What are the symptoms of celiac disease?
Celiac disease affects people in different ways. Some have symptoms as children. Others have symptoms only as adults. Some people have diarrhea and belly (abdominal) pain. Others may feel moody or depressed.
Each person’s symptoms may vary. Common signs of celiac disease include:
- Constant (chronic) diarrhea or constipation
- Weight loss
- Pale, bad-smelling stool
- Unexplained low blood count that makes you feel tired (anemia)
- Tingling, numb feeling in the legs
- Missed menstrual periods (linked to too much weight loss)
- Early osteoporosis or fractures
- Teeth changing color or losing their enamel
Celiac disease can be painful. Some common pain symptoms are:
- Stomach pain or swelling (bloating) that keeps coming back
- Muscle cramps or bone pain
- Pain in the joints
- Painful, itchy skin rash
Children who have celiac disease may not grow at a normal rate.
You may have celiac disease but not have any symptoms. That is because the part of your small intestine that is not hurt can still take in enough nutrients. But you may still be at risk for problems of the disease.
Celiac disease symptoms may look other health problems. Always see your healthcare provider to be sure.
How is celiac disease diagnosed?
Celiac disease can be hard to diagnose. Its symptoms may look symptoms of other digestive problems such as:
- Crohn's disease
- Irritable bowel syndrome
- Ulcerative colitis
- Infected colon (diverticulitis)
- Intestinal infections
- Small intestinal bacterial overgrowth
To see if you have celiac disease, your healthcare provider will look at your past health and do a physical exam. You may also have tests such as:
- Blood work. This is done to check the level of infection-fighting cells (antibodies) you have to gluten in your blood. People with celiac disease have higher than normal levels of these cells. Your immune system makes these cells to help fight things (such as gluten) that the body feels are a danger.
- Biopsy. This is the most accurate way to tell if you have celiac disease. A tissue sample (biopsy) is taken from your small intestine to check for damage to the villi. To do this, a long, thin tube (endoscope) is placed in your mouth, down to your stomach and into your small intestine. A tissue sample is taken using tools passed through the tube. The sample is checked in a lab.
What is the treatment for celiac disease?
If you have celiac disease, you must stop eating gluten. Eating gluten will do more damage to your small intestine. Eliminating gluten is the only treatment for this disease. You must not eat gluten for the rest of your life. In most cases, taking gluten your diet will stop your symptoms.
And, any damage to your intestine will heal. It will also stop any more damage from happening.Removing gluten from your diet can be difficult. This is because gluten can contaminate many foods. It can be found in condiments, salad dressings, and other unexpected places.
For this reason, your healthcare provider may refer you to a dietitian who specializes in celiac disease.
After you stop eating foods with gluten, your symptoms will ly get better in a few days. Your small intestine should heal completely in 3 to 6 months. Your villi will be back and working again. If you are older, it may take up to 2 years for your body to heal.
Celiac disease rate is growing, particularly among elderly, study reveals
Working to solve the puzzle of when people develop celiac disease has led researchers from the University of Maryland School of Medicine Center for Celiac Research to some surprising findings.
They have found that the autoimmune disorder is on the rise with evidence of increasing cases in the elderly.
An epidemiological study published September 27 in the Annals of Medicine supports both trends — with interesting implications for possible treatment and prevention.
“You're never too old to develop celiac disease,” says Alessio Fasano, M.D., director of the University of Maryland's Mucosal Biology Research Center and the celiac research center, which led the study.
The Universita Politecnica delle Marche in Ancona, Italy; the Johns Hopkins Bloomberg School of Public Health; the Women & Children's Hospital of Buffalo; and Quest Diagnostics Inc. of San Juan Capistrano, Calif.
, also participated.
Celiac disease is triggered by consuming gluten, a protein found in wheat, barley and rye. Classic symptoms include diarrhea, intestinal bloating and stomach cramps. Left untreated, it can lead to the malabsorption of nutrients, damage to the small intestine and other medical complications.
Since 1974, in the U.S., the incidence of the disorder has doubled every 15 years.
Using blood samples from more than 3,500 adults, the researchers found that the number of people with blood markers for celiac disease increased steadily from one in 501 in 1974 to one in 219 in 1989.
In 2003, a widely cited study conducted by the celiac research center placed the number of people with celiac disease in the U.S. at one in 133.
As the people in the study aged, the incidence of celiac disease rose, echoing the findings of a 2008 Finnish study in Digestive and Liver Disease that found the prevalence of celiac disease in the elderly to be nearly two and a half times higher than the general population. The recent findings challenge the common speculation that the loss of gluten tolerance resulting in the disease usually develops in childhood.
“You're not necessarily born with celiac disease,” says Carlo Catassi, M.D., of the Universita Politecnica delle Marche in Italy. Dr.
Catassi is the lead author of the paper and co-director of the Center for Celiac Research. “Our findings show that some people develop celiac disease quite late in life.
” The trend is supported by clinical data from the center, notes Dr. Catassi, who urges physicians to consider screening their elderly patients.
Although researchers have identified specific genetic markers for the development of celiac disease, exactly how and why an individual loses tolerance to gluten remains a mystery.
“Even if you have these genetic markers, it's not your destiny to develop an autoimmune disease,” adds Dr. Fasano.
“Our study shows that environmental factors cause an individual's immune system to lose tolerance to gluten, given the fact that genetics was not a factor in our study since we followed the same individuals over time.”
The finding contradicts the common wisdom that nothing can be done to prevent autoimmune disease unless the triggers that cause autoimmunity are identified and removed.
Gluten is one of the triggers for celiac disease.
But if individuals can tolerate gluten for many decades before developing celiac disease, some environmental factor or factors other than gluten must be in play, notes Dr. Fasano.
Identifying and manipulating those factors could lead to novel treatment and possible prevention of celiac disease and other autoimmune disorders including type 1 diabetes, rheumatoid arthritis and multiple sclerosis.
Researchers at the University of Maryland Center for Celiac Research are working toward that goal, says Dr. Fasano. As the third most common disease category after cancer and heart disease, autoimmune disorders affect approximately five to eight percent of the U.S.
population, according to the National Institutes of Health.
“The groundbreaking research of Dr.
Fasano and his team sheds new light on the development of celiac disease, a complex disorder that continues to present challenges to physicians and their patients,” says E. Albert Reece, M.D., Ph.D., M.B.
A, vice president for medical affairs, University of Maryland, and John Z. and Akiko K. Bowers Distinguished Professor and dean, University of Maryland School of Medicine.
Diagnosis of celiac disease can be a challenge as patients who test positive for the disease may not display the classic symptoms of gastrointestinal distress linked to the disease.
Atypical symptoms include joint pain, chronic fatigue and depression.
In the study, only 11 percent of people identified as positive for celiac disease autoimmunity through blood samples had actually been diagnosed with the disease.
Materials provided by University of Maryland Medical Center. Note: Content may be edited for style and length.
New Treatment for Celiac Disease?
From the WebMD Archives
Feb. 9, 2011 — Blocking an inflammatory protein called interleukin-15 (IL-15) may help treat the symptoms of celiac disease and prevent the development of celiac disease in certain at-risk people, according to new research in mice published in Nature.
Celiac disease is an autoimmune and inflammatory condition that is triggered by gluten, the protein found in wheat, barley, and rye. When people with celiac disease eat gluten, it triggers an inflammatory response that damages the lining of the small intestine. Symptoms include gas, bloating, cramping, and constipation.
People with celiac disease are also at risk for nutritional shortfalls including vitamin B12, vitamin B1 (thiamine), vitamin K, vitamin D, calcium, iron, and folate.
Risk factors for developing celiac disease include family history of celiac disease and/or a personal or family history of other autoimmune diseases, including rheumatoid arthritis (RA).
Gluten-free diets are the treatment of choice for celiac disease. Such foods are becoming increasingly available because of the dramatic uptick in rates of celiac disease and other conditions that may respond to gluten-free diets.
In the new study, researchers blocked IL-5 in mice genetically altered to have celiac disease and found that the disease symptoms were reversed, and the mice were once again able to eat gluten.
“We have identified one mechanism by which people lose tolerance to gluten,” says author Bana Jabri, MD, PhD, an associate professor of medicine and pathology and co-director of the Digestive Disease Research Core Center at the University of Chicago. “IL-15 may be a critical element that drives the loss of tolerance to gluten, and we can now think about pathways to block it and potentially develop therapies for celiac disease.”
Medications that block IL-15 are being developed for other inflammatory diseases, including RA.
The new research also shows that retinoic acid, a vitamin-A derivative found in acne treatments such as Retin-A and Accutane, may be complicit in the onset of celiac disease.
“Vitamin A in these patients is a bad idea,” she says. “Patients at risk should be careful about using retinoids.” This may even include topical retinoids if they can enter the bloodstream, she says.
Those two molecules act together to promote inflammation, she says. “The vitamin A derivative seems to fuel the IL-15, but if you block IL-15, retinoids are OK,” she says.
“In the U.S., we need to increase awareness and diagnosis of celiac disease because less than 10% of patients are diagnosed,” she says. “A gluten-free diet is currently the treatment of choice, but some patients only respond partially, and it is still socially a handicap.”
The race is on to develop new therapies to treat or prevent celiac disease, she says.
“At this point, the new study holds theoretic promise,” says Gerard Mullin, MD, an associate professor of medicine at Johns Hopkins School of Medicine and the director of Integrative Nutrition Services at the Johns Hopkins Hospital in Baltimore.“IL-15 may be a major player in driving the inflammatory response in celiac disease, and if we block it, you can tolerate gluten.
“A drug that blocks IL-15 may be most beneficial in people with really aggressive disease that doesn’t respond to conventional dietary measures,” Mullin says. For people with celiac disease, “today’s day and age is better to live in than 10 years ago due to increased availability of gluten-free foods and gluten-free menu options.”
Celiac disease is on the rise in the U.S., he says.
“The prevalence has jumped four to five times since the 1940s, but we are not clear why,” Mullin says. “Many food experts have speculated that it is the way grains are processed here, but we do see it in Italy and other places.”
Diagnosing celiac disease is not always straightforward, he says. Blood tests that look for the presence of certain antibodies are the first step. If the results are positive, many doctors will order a biopsy of the small intestine to confirm the diagnosis. This biopsy can also help assess the degree of damage, but “even the biopsy can miss it,” he says.
Richard Desi, MD, a gastroenterologist at the Melissa L. Posner Institute for Digestive Health and Liver Disease at Mercy Medical Center in Baltimore, says that blocking IL-15 may well help some people with celiac disease.
“This may not be it for everybody, but maybe it can help some people,” he says. “We are starting to understand celiac disease a lot more and diagnose it a lot more. The hope is that we will be able to come up with a treatment that doesn’t just involve a gluten-free diet.”
Richard Desi , MD, gastroenterologist, Melissa L. Posner Institute for Digestive Health and Liver Disease, Mercy Medical Center, Baltimore.
Gerard Mullin, MD, associate professor of medicine, Johns Hopkins School of Medicine, Baltimore.
Bana Jabri, MD, PhD, associate professor of medicine and pathology; co-director, Digestive Disease Research Core Center, University of Chicago.
DePalo, R. Nature, 2011, manuscript received ahead of print.
© 2011 WebMD, LLC. All rights reserved.
A Vaccine for Celiac Disease?
- Health & Wellness
- Body, Mind & Spirit
- Disease & Disorders
Celiac disease is an inherited, autoimmune disorder that is characterized by damage to the small intestine when the diet contains gluten, the protein in wheat that makes dough elastic. Gluten is also is found in rye, barley and, possibly, oats. Celiac disease affects about one percent of the U.S. population. It leads to the loss of villi, the tiny protrusions in the small intestines, which are essential to the proper absorption of nutrients from food. This can cause malnutrition, no matter how well an affected person eats. Celiac disease has a genetic component, and, other autoimmune conditions, is often triggered by physical stress such as surgery, pregnancy, childbirth and viral infection. Severe emotional stress can also set it off.
Celiac disease manifests differently from person to person, with many and varied symptoms both in and the gastrointestinal system. These include recurring abdominal bloating and pain, chronic diarrhea, weight loss, anemia, bone pain, fatigue, and in children and infants, delayed growth and failure to thrive.
The only reliable treatment thus far is going gluten-free for life. Consuming even a small amount of this protein can cause intestinal damage. However, I’ve read about two new approaches to treating celiac disease that are in development:
- A vaccine that would target three components (peptides) of gluten that are believed to set off the reaction to the protein. The vaccine, called Nexvax2, is designed to train the immune system to tolerate the three peptides. According to the developers, initial study results indicate that they have identified the right components, and that Nexvax2 is safe to take. However, they report that since volunteers who have taken part in studies have been on gluten-free diets, it isn’t yet clear how well the vaccine will work once people start to consume gluten. If the vaccine proves effective in celiac patients (or some subset of them), its success might lead to vaccines for other autoimmune diseases, such as type 1 diabetes and rheumatoid arthritis.
- Pills to counteract accidental consumption of gluten by celiac disease patients. These approaches come from two different companies. One of the medications in development is aimed at a protein called zonulin, which is believed to contribute to “leaks” in the gut that allow gluten to get the GI tract. The other is designed to neutralize the effect of accidental ingestion of gluten by influencing an enzyme that breaks the protein into harmless particles before it reaches the gut. The developers report that little or no intestinal damage was seen in patients who tested the pill for six weeks while consuming gluten and that the symptoms of some participants improved during the study. Both companies are preparing for trials to test whether their drugs work in a larger population and at what dosage.
I discussed these new approaches to celiac disease with Gerard Mullin, M.D., associate professor of medicine and an integrative gastroenterologist at Johns Hopkins Hospital.
He notes that the two pill approaches are designed to work with a gluten-free diet and wouldn’t enable patients to eat normally. He adds that the most exciting option is a vaccine that can build the body’s tolerance to gluten and retrain the immune system not to react to it.
Since both of the new approaches are in early stages of testing, even if they work, I wouldn’t expect them to be available for some years.
Andrew Weil, M.D.
Doctors caution that gluten-free is not for everyone
After battling stomach problems for years, Sarah Croessmann took action. On the advice of her doctor, she tried eating fewer fats, then removing dairy. Four years ago, she hit on a winner: She cut gluten from her diet.
Croessmann, a 25-year-old Baltimore resident, is one of 1.6 million Americans on gluten-free diets who have not been diagnosed with celiac disease, according to a recent study published in the American Journal of Gastroenterology.
Celiac disease is triggered by the gluten found in wheat, barley, rye and possibly oats, which causes an autoimmune reaction and can lead to damage to the small intestine. Gluten sensitivity, from which Croessmann suffers, is much vaguer.
A 2011 study in the journal BMC Medicine determined that individuals with gluten sensitivity, as is the case with those who have celiac disease, cannot tolerate gluten, but the overall clinical picture is less severe, and the condition generally does not lead to intestinal damage.
Dr. Joseph Murray, professor of medicine and a consultant in gastroenterology and immunology at the Mayo Clinic in Minnesota and co-author of the recently published study on the prevalence of celiac disease, says gluten sensitivity is ly one of many reasons the 1.6 million who have cut gluten without a celiac diagnosis are on the restricted diet.
Others reasons may include advice from practitioners of alternative medicine practitioner, a desire to lose weight, or simply the prevalence of gluten-free products on shelves at health stores.
Whatever the reason, doctors say, going on a gluten-free diet should be done only after careful consideration. It's not necessarily bad for you, but it's not for everyone, either.
Dr. Gerard Mullin, an associate professor at Johns Hopkins Hospital and author of “The Inside Tract,” says that while there's not a particular component of gluten that your body will lack or need to have replaced if it's removed from your diet, it's best to take a highly individualized approach when determining whether a gluten-free diet is right for you.
While celebrities often promote a gluten-free diet as a great way to slim down, Mullin says it's far from an easy or sure way to lose weight.
“A lot of convenience foods are gluten-laden,” he says. In removing gluten, you're taking away a lot of easily accessible and caloric snack foods — bagels, pizza, cereal and the , he says.
Murray agrees, saying that those who lose weight on a gluten-free diet are ly shedding pounds because they're simply eating less.
However, if dieters are simply replacing the snack foods with their gluten-free counterparts, they're probably not seeing results.
“Gluten-free cookies are still full of sugar,” Mullin says.
Croessmann says that often, friends think that gluten-free foods can be labeled as good for you because they are sold at stores Trader Joe's and Whole Foods, which tend to be associated with healthful lifestyles.
“Most of the gluten-free products are actually denser and higher in calories,” she says.
Murray says it's also important to note that many of the foods you are removing from your diet, cereals and breads, are fortified with vitamins that their gluten-free counterparts lack.
Gluten-free products also tend to be pricier.
“It's a lot more expensive,” Croessmann says. “If you want gluten-free bread, crackers or pretzels, sometimes it's three or four times the cost.”
While gluten sensitivity is certainly a good reason to remove gluten from your diet, Murray says it's a tricky diagnosis that's arrived at only by the process of elimination.
Symptoms of gluten sensitivity, stomachaches, fatigue, bloating and diarrhea, are identical or similar to those of celiac disease, irritable bowel syndrome and lactose intolerance.
Though it's tempting to remove gluten — and, if you feel better, keep it your diet — Murray says it could delay diagnosis of other conditions, celiac disease, intestinal obstruction or Crohn's disease.
Celiac disease, in particular, often goes undiagnosed. Murray's study determined that of the 1.8 million Americans that have it, 1.4 million are unaware.
“If you think you have celiac, go on a gluten-free diet and then ask to be tested, your blood test may be negative,” he says. “So we're faced with putting patients back on gluten to make them sick again.”
Murray says that if you experience celiac symptoms, you should go to your doctor and ask to be tested before altering your diet.