Copyright by Michael Jones, Bill Elkus, Jim Lyles, and Lisa Lewis 1995, 1996 - All rights reserved worldwide.

The Widening Spectrum of Celiac Disease

by Joseph Murray, MD, PhD

This is a summary of the presentation made by Dr Joseph Murray to the Tri-County Celiac Sprue Support Group (TCCSSG) in October 1996 and summarized by Jim Lyles. The original article was published in the _The Sprue-nik Press_ and permission was granted to include it as a reference document for the members of the Celiac LISTSERVE.

Dr. Joseph Murray, one of the leading US physicians in the diagnosis of celiac disease (CD) and dermatitis herpetiformis (DH), spoke at our October meeting. Dr. Murray originally came from Ireland and got his medical degree and a doctorate from the National University of Ireland in Galway. His residency was at the University of Dublin and he completed his fellowship in gastroenterology at the University of Iowa College of Medicine, where he has been since 1988. What follows are some highlights of Dr. Murray's talk.

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The Standard Definition of CD

Dr. Murray gave us the "standard" definition of CD: "CD is a permanent intolerance to gluten that results in damage to the intestine and is reversible with avoidance of dietary gluten." There are some important parts in this definition:

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Effects of CD

"Classic" CD is what most medical students are taught about. It is characterized by diarrhea, steatorrhea (smelly, floating, pasty, fatty stools), weight loss, abdominal bloating or distention, and flatulence (farting [yes, he really did say that--ed.]).

Dr. Murray showed a lovely slide depicting steatorrhea, but warned that you can't identify it just from its appearance; it is the smell that distinguishes it. There is nothing that smells quite like steatorrhea. (Dr. Murray admitted that he sometimes has trouble keeping nurses in his clinic because he does frequently collect stool samples, which they find rather "challenging".) Steatorrhea (fat in the stool) was thought to be synonymous with CD. In fact, CD has also been called idiopathic steatorrhea, which refers specifically to this particular symptom. So it was thought that if you didn't have this symptom, you didn't have CD. Nothing could be further from the truth; Dr. Murray says fewer than a third of his celiac patients have ever produced this sort of stool.

What are the consequences of the damage to the small intestine?

Dr. Murray then showed a few pictures of a young woman who is one of his more unusual celiac patients: She was extremely obese. She was an inpatient at the hospital on the psychiatry floor (which is interesting in itself). She had complained of nighttime abdominal pain. The most common cause of this symptom is a regular duodenal ulcer, but medication to treat an ulcer wasn't working so the gastrointestinal (GI) department was consulted. They performed an endoscopy, expecting to find an ulcer. They also did a biopsy because that is Dr. Murray's habit whenever he does an endoscopy. They were surprised to find active CD. Her symptoms were chronic constipation (she had diarrhea as a child), malodorous flatus (smelly gas), had gained 200 lbs. in the preceding four years, and practiced lactose-avoidance. Being overweight and constipated, she was just about the exact opposite of what most people would conceive of as the typical celiac. She had completely normal serum chemistries. Routine blood tests were normal; there was no clue to the physician suggesting CD. Yet the biopsy showed completely flattened villi and an antiendomysial antibody test came back positive. She had a good clinical response to a gluten-free (GF) diet which included some weight loss.

The degree or type of symptoms that a person with CD presents with does NOT depend on the severity of the disease where you take the biopsy. In CD the damage starts in the intestine just after the stomach and works its way down. The small intestine is about 26 feet long and has a tremendous ability to compensate. So if the damage is mostly near the stomach (which is where biopsies are done) then you may never have diarrhea; the rest of the small intestine can compensate and absorb all the liquid and food that passes by the first few damaged feet.

When somebody presents with severe diarrhea and wasting, that means most of the small intestine is damaged and it is not able to compensate for the damage closer to the stomach. So it is the amount of the small intestine that is damaged which determines the symptoms. If you have all of the small intestine damaged you'll have diarrhea and weight loss. If only a small portion of the small intestine is damaged, you may have pain, bloating, and discomfort after eating but not diarrhea.

Dr. Murray discussed some of the different types of presentations that they see at the University of Iowa:

As we see, CD can present in its "classic" form with multiple symptoms such as steatorrhea, weight loss, typical blood test abnormalities, and a flat biopsy. But perhaps more often it presents in an "atypical" form with only one symptom such as anemia or bone problems. In atypical cases the biopsies are not always flat; there may be varying degrees of damage.

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Lactose Intolerance

Dr. Murray revisited the topic of lactose intolerance. About 50% of celiac patients are lactose intolerant at the time of diagnosis. Here is why:

Lactose is a double sugar. The small intestine has an enzyme called lactase which breaks that double sugar down into single sugars which your body can then absorb. Lactase is produced right at the tips of the villi. If the villi are damaged then you can't produce that enzyme to split that double sugar. So the lactose stays intact in the intestine, passes through it, and then acts as a laxative. You will get diarrhea, bloating, or gas, depending on the severity of the symptoms.

After you go on a GF diet and get healing in your intestine, usually those villi will regenerate and begin producing lactase again, allowing your body to break down the lactose and absorb it. Dr. Murray looks for improvement in lactose tolerance as a measure of healing. If you do not recover the ability to digest lactose, then either the intestine has not yet healed or you are one of the few celiacs that are also genetically-predetermined to never be able to break down lactose, as was discussed earlier. So continued lactose intolerance is not necessarily a sign of villi damage (though highly suggestive); but improvement in lactose tolerance is a sign of healing.

Dr. Murray tells patients who have a lot of problems with milk to wait about six months after starting a GF diet before trying it again. After about six months they should start testing themselves with a little skim milk first thing in the morning, to see if they get any symptoms. If they get symptoms (bloating, gas, or diarrhea) then they probably are still lactose intolerant. If that continues then they need to revisit their doctor to find out if there is still evidence of damage in the intestine.

The important point is that in most (90%+) newly-diagnosed celiacs with lactose intolerance, it should get better.

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Dermatitis Herpetiformis

Next Dr. Murray discussed dermatitis herpetiformis (DH). DH is an extremely itchy skin rash. There is nothing that is as itchy as DH; even poison ivy may not come close according to those who have had both. It effects the elbows, knees, buttocks, back of the head, and scalp. Dr. Murray even had one lady who got it in her outer ear canal. It comes on in waves. Crops of little bumps appear and soon turn into blisters that are extremely itchy.

DH is often thought of as a skin disease, but that is not strictly true. DH is a manifestation of intestinal intolerance to gluten. Research has been done in which gluten has been injected under the skin of DH patients, and it does not produce a blister. So DH is NOT a skin allergy to gluten.

However, if a DH patient takes gluten by the mouth, then it can come out as DH on the skin. In fact, Dr. Marsh in Manchester (England) has put gluten in the rectum and in a couple of cases he had DH patients claim that they got an attack of DH afterwards.

What happens when a DH patient ingests gluten? In the intestine the body's immune system mounts a response to the gluten. Part of that response is the production of antibodies, which are like little chemical messengers the body produces to attack things and help defend itself. In DH patients those antibodies often get dumped under the lining of the skin, where they just sit like little land mines for days, months, or years. Then one day something triggers them (sunlight, iodine in a cleanser, etc.) and you get this little bursting forth as the skin's immune system begins attacking these deposits thus forming the blisters. But the deposits occur originally due to the intestine being exposed to gluten.

So DH is the skin manifestation of intestinal gluten sensitivity which is indistinguishable from CD. Most, if not all, DH patients will have some degree of damage in their small intestines. They may have no GI symptoms but they have some degree of damage.

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Villi Damage

The villi are the most important part of the absorptive system in the small intestine. Normal villi are long and slender, giving a healthy small intestine the appearance of a deep pile carpet. All these villi give the small intestine an enormous absorptive surface; if laid out flat it would cover an area the size of a tennis court.

Now consider the "worst case" scenario for CD, where the villi are completely flattened. This decreases the absorptive surface down from a tennis court to about the size of a small table. So you have a dramatic reduction in the amount of area for digesting and absorbing nutrition from your food. But there are other factors to consider as well. The villi aren't just flattened, they are also inflamed; just like your skin is inflamed after being burned. It can produce pain. (But the pain is not as obvious and localized as it is for inflamed skin; you just know that there is pain in there somewhere.)

Often the villi are not completely flat. Dr. Murray showed a slide in which the villi were a little "stubby". In these cases the villi are still different enough to be classified as not fully formed. But then he showed a slide in which the villi appeared to be normal size. Many pathologists would look at such a case and be tempted to rule out CD as a possibility. However, if you carefully examine the surface of the villi you'll see that there is a marked increase in lymphocytes, the small immune cells that reside in the intestine. It is the lymphocytes which are mostly responsible for the damage in the small intestine. These are the cells that are responding to gluten.

Dr. Murray talked about five degrees of severity of villi damage:

    1. Healthy, undamaged villi.

    2. Infiltrated villi. The villi are still standing up long and straight, but the is an increase in the surface lymphocytes.

    3. Partially-shortened villi. The villi are somewhat short and stubby, and the crypts (the basement parts of the villi) are expanding and becoming inflamed.

    4. Flattened villi. This is the typical or classic form of CD, in which the villi are destroyed.

    5. Burned-out villi. This can occur in older celiacs, where the villi don't necessarily have the ability to recover on a GF diet.

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Causes of CD

There are three factors involved in CD:

The immune system comes into play through the lymphocytes we previously discussed. There are lymphocytes in the intestines of celiac patients that respond specifically to something in gluten. These are called T-cells, and are actually responsible for the damage in the villi. There are also cytokines, which are chemical messengers floating around that our bodies produce to fight infection. The lymphocytes also produce cytokines which cause even more damage.

The environment comes into play in the form of gluten. For example, in the early '70s there was a trend towards a macrobiotic diet, meaning a lot of grains. As a result, a lot of people presented with celiac disease. This was a result of challenging themselves with a lot of gluten, causing the damage in the intestine to become more extensive. So a gluten challenge can cause symptoms, though Dr. Murray does not think it triggers the disease itself. Instead, some other event may "trigger" the beginning of CD. Possible triggers of CD include:

There is a tissue type called HLA. This is similar in nature to blood types, where A, B, and O are the three standard blood types. Tissue typing takes that a whole generation further, taking it down to very specific subtypes of the genetic material in our white blood cells (and most other cells in the body). It identifies us as "self", because we have a specific genetic type in our cells. Our body uses this to avoid attacking anything that it can identify as "self"; anything else it readily attacks. This is what makes organ transplants difficult. The body automatically recognizes the transplanted organ as a foreign body and tries to attack it as an invader. It is the immune system that mounts this attack, and one of the things it uses to distinguish foreign bodies from "self" is the HLA typing in the body's cells.

Why is this relevant for celiacs? There is a very particular tissue type that is seen in most celiacs called DQ2. (Dr. Murray noted that the HLA names keep changing every year or two, so that a different term might be in use now; but DQ2 was what it was previously called.) Studies in the USA on this subject are sparse, but in studies in Czechoslovakia, the United Kingdom, and Italy 87% or more of the celiacs had this tissue type.

The risk of CD increases within the families of known celiacs. According to Dr. Murray, here are the approximate risk factors for various relatives of a diagnosed celiac:

Why is there a difference in risk factors for an identical twin and an HLA-matched sibling? Clearly there must be another gene involved besides the known DQ2 tissue type. Up until three months ago we didn't have any clue as to what that other gene might be. But at the symposium in Finland(1) a collaborative study done jointly in Galway, Ireland and Alabama, USA provided some new information. A series of families from the Galway group were studied. A new method of looking for gene site associations was used. They took some of the chromosomes from blood samples of these patients and looked for genetic similarities. [Human beings have 23 pairs of chromosomes. Each chromosome is composed of a multitude of genes.--editor] They found one spot on chromosome #6 which it seemed to be very highly associated with CD; in other words, those that have CD seem to have this "spot" on chromosome #6; those that did not have CD did not tend to have this "spot". It is not known what the genes in that "spot" do, because i t is one of those uncharted areas of human genetics. It is hoped that over the next two years we will learn which specific gene is involved and how it confers a risk for CD. So there are probably at least two separate genes that come together to result in a genetic predisposition towards CD.

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Prevalence of CD

How common is CD? A few years ago it was thought that the prevalence of CD in Europe varied from 1:300 (one out of 300 people) to 1:2000. Now the figures vary from 1:90 to 1:600, depending on which study you look at. These figures are mostly based on studies involving anonymous blood donors, or screening healthy populations such as school children. These figures are not based on going to hospitals and counting the number of diagnosed celiacs.

CD is rare in the Negroid and Asian races, though not unheard of. This may be because the major starch in China and Africa was not wheat until fairly recently. So until these populations are exposed to large amounts of wheat, we may not know what the true prevalence of CD is in those countries.

The rate of diagnosis of CD seems to be directly related to the level of suspicion of the doctor, hospital, or health care system. It has been well-studied in places like Scotland where the rate of diagnosis in one area is found to be high and then in another area it is much lower. Then someone with an interest in CD transfers to the second area and the rate of diagnosis of CD suddenly increases.

There are some population differences that have been noted. For instance, in Sweden CD is very common and mostly diagnosed in childhood. But in neighboring Finland CD tends to be diagnosed more often in adults than in children. In the USA the vast majority are diagnosed during adulthood. At the University of Iowa the rate is 30 or 40 adults diagnosed with CD for each child. How does one explain these differences. Is it because the adult doctors aren't looking for CD in Sweden and the pediatricians aren't looking for it in the USA? Dr. Murray doesn't think so; he believes there truly is a difference in the age at which CD is presenting in these countries. At the Finland symposium there was some discussion on this topic. In Sweden commercial baby food products have a lot of wheat in them. (In the past they had lots of milk protein in them, and they changed it 20-30 years ago due to the incidence of milk allergies.)

Incidentally, nearly the exact opposite happened in England & Ireland in the 1970's. It had been general practice to begin feeding some type of cereal such as oatmeal to a baby as early as two weeks of age. Breast feeding was done only in 10% of the children beyond the age of six weeks. As a result there were several very young celiacs diagnosed. However, due to the incidence of CD public health nurses began advising new mothers to avoid giving gluten to their babies before the age of one year, and to avoid solids altogether for the first four months or so. As a result the entire feeding patterns of infants changed within a year or two and diagnosis of CD in very young children dropped considerably.

So in Sweden the children are challenged with gluten early in life, so CD begins presenting early in life; whereas in Ireland gluten is now avoided early in life, so CD doesn't show up until a later age.

One question that arises: In families with a history of CD, does exposure to gluten at an early age increase the chances of getting CD? Nobody knows for sure. Dr. Murray generally advises families with a history of CD to not feed gluten to a child before the age of one. Then, once they are a year old, put them on a normal gluten-containing diet and see what happens. In these cases Dr. Murray recommends that the child then get the celiac antibody blood tests at age two, or a full GI evaluation if they develop symptoms or fail to grow.

Is CD really as rare as you might think in the USA? Probably not. Consider the following:

Dr. Jarmo Visakorpi is a Finnish researcher who has been studying CD for about 35 years. He gave the introductory talk at the Finland symposium and talked about the celiac "iceberg". The analogy is that the diagnosed cases of CD are like the portion of a floating iceberg which is above water, and the undiagnosed cases of CD are like the portion that is below the water. Dr. Visakorpi said that the goal is to get the entire iceberg above water. This is mostly a reality in Sweden. In Finland and the rest of Europe some of those peaks are sticking out of the water. Across the ocean [meaning in North America] most of the iceberg is underwater.

At the University of Iowa there are 14-17 full-time gastroenterologists on their staff. Prior to 1990 they diagnosed 2-3 cases of CD a year. Then the numbers started to jump up: 8 cases of CD diagnosed in 1990; 18 in 1992; 55 or so in 1995, and they are running at about the same rate again in 1996. Prior to 1990, most of their newly diagnosed celiac patients presented with either the "classic" celiac symptoms, DH, or lymphoma. In 1992, only a third of the newly-diagnosed celiacs fit the representation of classic CD. Most of them had a single symptom, not multiple symptoms. Half of them had no diarrhea, and never really had diarrhea at all. Two thirds of those tested did not have steatorrhea (fatty, smelly stools).

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Testing for CD

Many different tests have been used or proposed for CD screening:

In the past, three biopsies were required to diagnose CD. The European Society for Pediatric Gastroenterology and Nutrition (ESPGAN) developed criteria in 1969-1970 for defining CD. They said you needed three biopsies: The initial biopsy to show the damaged villi, a second biopsy after being on a GF diet showing that the villi have healed, and a third biopsy showing damaged villi after a gluten challenge.

In 1990 ESPGAN revised their criteria. They now say that in most cases only one biopsy is needed. If there is a clinical response to a GF diet (meaning the symptoms go away), so that there is some definable improvement, then no additional biopsies and no gluten challenge are necessary to make the diagnosis. Now there occasionally may still be a second biopsy to show healing, but it is not specifically to confirm diagnosis. The second biopsy is usually for a different reason, such as looking for a complication or making sure that healing has occurred (and sometimes it doesn't occur despite the best efforts of doctor and patient). The gluten challenge is now reserved for less than 10% of the cases that Dr. Murray sees; usually those that have minimal damage and in whom it is not easy to determine if the GF diet has really helped.

Older patients may respond to the GF diet but not completely heal. Why not? Well, they may be healing fully further down the small intestine but not in the area near the stomach, which has been exposed to the most gluten for the longest time. However, it is only in the area near the stomach that you can effectively take small intestine biopsies. So a biopsy might not show the true extent to which healing has occurred.

What about all the atypical cases; people who present, but don't yet have symptoms? Where do they fit in the ESPGAN criteria? And do milder degrees of damage cause problems? The other thing is the response to a gluten challenge. Some people don't get sick at all; they don't get any symptoms. They may have damage in their gut but no symptoms, sometimes even after six months. There was one patient that went 14 years on a gluten challenge before they developed intestinal damage. This tells us that if a celiac eats gluten there won't necessarily be any reaction, so you can't use how you react to judge whether or not an item is GF. On the other hand, Dr. Murray said that some people will get intestinal changes within two hours of ingesting gluten; this has been shown by taking a biopsy of a fast-reacting celiac before and two hours after some gluten was ingested.

If a celiac is having a gluten challenge Dr. Murray looks for symptoms to begin occurring again, or if not then he follows the antibody tests until they become positive. After the return of symptoms, or a positive antibody test, or after about six months, then Dr. Murray generally performs a biopsy.

There are two basic serological (blood) antibody tests: antigliadin (antibodies directed against a component of gluten) and connective tissue (antibodies directed against our own tissues). The antiendomysial test is an example of the second type of antibody test. It is very operator-dependent (unfortunately).

A study reported in Gut in 1992 suggests that the celiac antibody blood tests are 100% sensitive and 99% specific to CD. Some HMOs have pointed to these studies as proof that a biopsy is unnecessary. But there are some problems with that study. It was based on a serum bank saved from previously-diagnosed celiacs. These were celiacs who were originally found because of screening with these blood tests. So negative results would automatically not be found in the serum bank.

In September the University of Iowa tested seven reference labs in the USA. They took 20 serum samples from untreated celiacs, split them seven ways, and sent them to seven different labs across the country for analysis. All of the untreated celiacs were diagnosed by biopsy and had not previously had the antibody tests. They also sent 20 serum samples from people who were biopsy-proven to NOT have CD. Dr. Murray just got the data back in the last week. Each lab tested the samples blindly, using their own methods. The results:

However, there is one caveat with these test results: the 20 celiac samples were "classic" celiac cases. These were not patients with mild damage. So patients with mild damage might not have abnormal antibody levels. [Yet these are the very patients that are hard to diagnose, and for which better tests are needed!--editor] Some of the potentials for these antibody tests include:

There are problems with the blood tests. For example, there is no standardization between the various labs. None of the labs do these tests the same way, and none of them report the results the same way. A "high" positive from one lab is not necessarily going to be a "high" positive from another. That means you may not be able to compare results from one year to the next if the samples are sent to different labs. (This often happens as HMO's change contracts.)

Who should be screened? Dr. Murray usually screens people with Type I diabetes, unexplained iron-deficiency anemia (Dr. Murray does not accept heavy menstrual flow in women as an explanation), unexplained bone disease, functional diarrhea, irritable bowel syndrome, history of "transient" gluten-sensitivity ("Well, I had it as a child and outgrew it..."--you DON'T outgrow CD), or lactose intolerance (if Caucasian).

How should close relatives of a known celiac be screened? Obviously, a biopsy would be ideal as it would determine for sure whether or not villi damage is present. But a more reasonable first step is to use the celiac antibody blood tests to screen close relatives. Tissue typing could also be done to determine whether or not a relative is at risk for developing CD, but there is not enough information on the American population. The type of tissue you see in celiacs also occurs in about 20% of Caucasians.

You also have to follow up intermittently, since a relative might not develop CD until after the first screening. For example, suppose you are a celiac and you have a child. Dr. Murray recommends keeping the child GF the first year, then putting them on a gluten-containing diet. At the age of two, or at the appearance of any symptoms, they would then be screened for CD using the antibody tests. Then check them again at age 9 or 10, before they go into that pubertal growth spurt.

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Treating CD

Dr. Murray says that when he tells someone they have CD, and that the treatment is to avoid wheat, barley, rye, and oats, he expects a "grief" reaction. This reaction has some fairly standard stages: Shock, denial (this lasts a long time for some people), anger, and then (eventually) acceptance. The most dangerous of these stages are denial and anger. In the denial stage you just deny that this is really happening to you, or you deny that you are really that sensitive ("Well, I can get away with a little bit of gluten."). This reaction is especially common in men. In the anger stage you may be angry at the delay in getting diagnosed, or angry at why you got this disease ("God, why did you give this to me?"), anger at the food manufacturers for incomplete ingredient information, or anger at the difficulties of following the diet. It is good to channel the anger to something useful, but eventually you have to get to the acceptance stage.

Professional dietary advice is invaluable--if you can get it. Dietitians who are interested, knowledgeable, keep up-to-date, and learn as much from their celiac patients as the patients learn from them are invaluable, and there are a few. (Dr. Murray specifically referred to our own dietitian advisor, Dorothy Vaughan, as one of the few.)

The University of Iowa surveyed members of the Iowa Dietetic Association, asking how many celiac patients they have, what kind of information do they provide, do they routinely give information about support groups, etc. They found that most of them don't treat celiac patients, most don't even know what to do because it is so difficult. Most dietitians get their material from the American Dietetic Association, and up until several years ago it was woefully out-of-date. Dietitians can keep up on fat, cholesterol, and diabetic information; but it is the celiac information that keeps on changing. As a professional, it is very challenging for a dietitian to keep up, especially if you are only counseling one or two celiacs a year.

Local and national support groups are important for your immediate benefit. You don't have to reinvent the wheel all the time. Also, there is strength in numbers to advocate to bigger corporations and food providers, and perhaps get them to bend a little bit.

Nutritional supplementation to correct deficiencies is important. For example, if someone is very anemic they need something to correct it.

Dr. Murray advocates "champagne, not pessimism"(2). Initially the GF diet may be overwhelming and dominate a celiac's life. But after a few years to adjust celiacs should expect to have the attitude that they are on a healthy diet that is interesting and just happens to be free of gluten.

There are many other aspects of treatment. A bone density test may be important. You may want to screen family members for CD. Intense nutritional fluid intervention is sometimes necessary in the really sick patient. Consider coexisting malignancy or other disease, especially in the older patients.

Finally, there is the need of follow-up for compliance. Those that do well on the diet may need less follow-up. The doctor doesn't know at the time of diagnosis just how compliant the patient will be to the GF diet (though he may have his suspicions). By setting up a follow-up appointment six months down the road, you give the patient a goal to shoot for.

Most patients come back for a checkup doing very well. But Dr. Murray has had some come back looking terrible. In some cases he has had to admit them because they were suicidally depressed, somewhere between the denial and anger stages. They obviously needed help. (Trying to persuade the insurance company to admit them to the hospital for dietary management is nearly impossible.)

Dr. Murray advocates prudence, but not paranoia about what you eat. Some people do get to the point of paranoia, avoiding things that are reliably GF. You need to have a "safe haven", where you can simply eat without worrying about whether or not the food is GF. This could be your home, a celiac friend's house, whatever; someplace where you can completely relax and not worry about the diet. Some of the GF cruises that have been organized provided such a haven for the duration of the trip. [So did the CSA Conference--editor]

In Iowa they have about 150 people in their support group. They have split up into smaller subgroups that meet every two months or so in somebody's home. There is no real organization to it, but they know they can go to that person's home, bring their food, and then relax and not worry about the food being GF or explaining the diet to someone. This provides them with a "relief valve". You need to be able to do something like that from time to time.

Dr. Murray then spoke on monitoring the GF diet. Symptoms should go away when you are following the GF diet. Deficiency states (such as iron-deficient anemia) should become corrected. Dr. Murray asks his patients, "How many times in the last three months have you put anything in your mouth that you suspected beforehand contained gluten?" He says he can look at them as they answer this and know whether they have or not. The last person he asked answered, "well, maybe twice a week". This was a shock, and Dr. Murray told the patient that he really was not on a GF diet. Then he asks why. The answers include: "I was very hungry"; "I couldn't get anything else to eat"; "I was traveling". The advice he tries to give is to think of these situations before they happen and plan for them.

Antigliadin antibody tests can be helpful in monitoring compliance. How many times do you do them? Dr. Murray says nobody really has an answer; but he likes to see them become normal (negative). A follow-up biopsy is done occasionally, on a case by case basis.

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(1) Dr. Murray is referring to the "7th International Symposium on Coeliac Disease" held September 5-7 in Tampere Finland. See _The Sprue-nik Press_, Sept. '96, for a summary of this symposium.

(2) This quote came originally from Elaine Harstook, the late founder of the Gluten Intolerance Group of North America.

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