Celiac.com 12/02/2021 - Summer is the perfect time of year for having guests over because, with the warmer weather, it expands your living space to the outdoors and everything is generally more casual.  If you don’t entertain much, the thought of creating gluten-free appetizers that your guests will genuinely enjoy may seem intimidating

As guests gather casually on your patio, deck or lawn, they will like to ‘nibble’.  Prepare gluten-free ‘nibbles’ that you, too, can enjoy.  There is no sense in putting forth the added energy and expense of making ‘their’ foods and ‘your’ foods when the gluten-free versions can be so delicious.  

Summer appetizers should be big on flavor, loaded with color, use seasonal ingredients, and be simple to prepare.  The buzzword for summer entertaining is ‘casual’.  

Be creative in your food choices.  Balance hot and cold dishes, rich and mild foods, and try to include at least one vegetarian offering.  The assortment is the key.  Pick foods that are ‘party-friendly’—guests will likely be walking around so you don’t want to serve too many foods that are sticky, messy or greasy.  The best choices are items that are easily picked up and can be eaten with two fingers.

Avoid dishes that require painstaking serving techniques or last-minute preparation.  Many party foods may be made in advance, frozen, and then heated up as the guests arrive.  As you plan, you need to weigh practical matters such as how much refrigerator or freezer space is available and how many appetizers you can heat at one time.  Prepare one or two hot appetizers ahead of time and simply heat them up at the last minute.  For the rest of your menu, choose foods you can prepare ahead and serve without last-minute attention.  You can also serve foods that require the participation of your guests (like assembling mini tacos on gluten-free corn tortillas or in corn taco shells) and let them add their own toppings, fillings, or condiments.

Presentation still counts—even with casual entertaining.  Serve your foods on a picnic table that is decorated with several pots of fresh flowers, or set the appetizers on small tables throughout the yard to encourage people to move around and mingle.  

Almost any appetizer can be successfully converted to a gluten-free version.  Cold dips are always a favorite, but try new concoctions like artichoke hummus or asparagus guacamole.  Other viable cold foods may include antipasto kabobs (with cubes of gluten-free salami, ham and cheeses), or a bowl of tuna salad made with lots of green peppers and green onions—served with gluten-free crackers.  Cold foods that may be made ahead include pickled shrimp, deviled eggs, sushi, and homemade cheese balls.  A simple appetizer is to spread cream cheese on a platter, top it with shredded crabmeat (not gluten-containing imitation crabmeat), then top with a layer of gluten-free cocktail sauce and a sprinkling of chopped parsley—a garnish of sliced lemon wedges around the edge of the dish completes the creation.  Serve with gluten-free crackers.  There are gluten-free crackers on the market today that are every bit as good as their wheat counterparts—or even better!

Rice papers (soaked for a few minutes first to make them pliable) are so versatile.  Fill them, roll them, then cover and refrigerate until serving time.  Make mini Reuben wraps with pastrami, Swiss cheese, Cole slaw and a dab of gluten-free brown mustard.  Or spread the papers with cream cheese then top with chunky salsa, shredded lettuce, crisp-cooked bacon and guacamole.  

To keep the hot appetizers hot, be sure to heat just one round of appetizers at a time.  This way, another batch of hot appetizers will be coming from the oven as the last batch is eaten.  An electric skillet, hot tray, griddle, fondue pot, chafing dish, or crockery cooker is handy for keeping appetizers hot.  If foods cool as they sit out on the table, pop them into the microwave for a quick reheating.  Baked appetizers may include pizza (made on gluten-free pizza crusts) and topped with fresh-grilled veggies, hot crab dip, cheese and bacon potato skins, and/or teriyaki chicken drumettes.  An electric skillet is convenient for frying spring rolls (rolled in gluten-free rice papers).  Perfect crock-pot appetizers are taco bean dip or mini meatballs in a sweet and sour glaze.

Don’t forget to make use of your microwave.  This oven is perfect for melting the cheese on homemade Nachos Grande.  A great assemble-ahead appetizer is Eggplant Pizza.  Brown slices of eggplant in your broiler, top with a small amount of gluten-free spaghetti sauce, sprinkle with Italian seasoning, then top off with a slice of provolone cheese or shredded Romano cheese before heating in the microwave to melt the cheese.

Nothing says ‘summer’ more than grilling outdoors.  The grill doubles both as a cooking unit and a social hub.  Foods conducive to grilling include BBQ shrimp, mini marinated chicken or beef kabobs, and grilled Quesadillas.  Also try wrapping mushrooms in bacon, then brushing them with gluten-free BBQ sauce and cooking them on the grill.  You can also stuff Poblano chili peppers with cheese and one tablespoon of gluten-free salsa, then grill them.

While you enjoy your friends and have fun entertaining, you also deserve to enjoy the food.  Stop making “their appetizers” and “your appetizers”—ALL of the appetizers can be deliciously gluten-free!

Salmon Cheesecake

From her “Wheat-free Gluten-free Recipes for Special Diets” Cookbook.

Ingredients:

• 1 cup dry gluten-free bread crumbs
• ½ teaspoon dill
• ¼ teaspoon paprika
• 1 teaspoon dried parsley flakes
• 3 tablespoons butter, melted
• 24 ounces gluten-free cream cheese, softened
• ½ teaspoon lemon juice
• 4 eggs, at room temperature
• ½ cup Swiss cheese, shredded
• ½ cup green onions, minced
• ½ teaspoon dill
• ½ pound smoked salmon, chopped fine

Directions:
In a bowl, mix together first 4 ingredients.  With a fork, blend in butter till crumbs are evenly moistened.  Spread mixture onto bottom of a 9-inch spring form pan.  Bake at 325 degrees for 10 minutes.  Whip cream cheese, lemon juice and eggs in a large bowl till well blended.  Stir in remaining ingredients; pour over crust.  Bake at 325 degrees for 1 hour until center is almost set.  Run a knife around edge of pan to loosen cake; cool completely before removing sides.  When cool, cover and refrigerate several hours.  Let cheesecake stand at room temperature 15 minutes before serving.  Serve with gluten-free crackers.  Makes 14 (1 inch) wedges.

Calories: 286; Total fat: 24g; Saturated fat: 12g; Cholesterol: 130mg; Sodium: 392mg; Carbohydrates: 7.5g; Fiber: 0.2g; Sugar: 0g; Protein: 10.4g

Celiac.com 09/21/2018 - The English as a Second Language (ESL) pie is so large in countries such as South Korea that there seem to be enough helpings for anyone interested. However, these generous slices may be off limits to individuals with severe food allergies or intolerances, including those with celiac disease. If you have diet restrictions and are thinking of heading to South Korea or another Asian country, the following information will help you decide whether or not this move is a good idea.

One might think that Asia, the land of rice-based meals, would be a celiac’s paradise. As one naïve dietician told me before I moved to Seoul, “You couldn’t be going to a better place.” This assumption could not be further from the truth. If cooked with traditional ingredients, many local dishes are gluten-free. However, in Korea, wheat flour is now cheaper than other kinds of flour, despite the fact that it has to be imported. Wheat flour and barley are currently the two most common ingredients in Korean food products.

In Korea, eleven major food allergens must be included on product labels: poultry eggs, milk, buckwheat, peanuts, soybean, wheat, mackerel, crab, pork, peaches, and tomatoes. As for anything else, the Korean Food and Drug Administration states that only the five major ingredients in a product have to be labeled. Furthermore, a label need only include intentional ingredients, not things accidentally mixed into a product through cross-contamination. So you can say goodbye to warnings like: “this product may contain traces of peanuts.” Stricter labeling regulations will be put into effect in September 2006. However, these laws will remain less stringent than those in North America and Europe. According to a source at the KFDA, labeling restrictions are similar in Japan and more lax in China and South East Asia.

One can easily learn Korean for “I’m allergic to ____” in any phrasebook or from a Korean coworker, friend, or even the guy in the next seat on your Korean Air flight. Yet it is the cultural barrier, not the language barrier, which poses the most difficulties for a celiac.

Korean culture revolves around the sharing of food due to food shortages during the Japanese occupation; Koreans do not ask, “How are you?” but, “Have you had your meal?” Co-workers, friends, and even the occasional stranger will offer to share food. The politest way to refuse is by saying, “Thank you, but I can’t. I’m allergic.” Also, rather than saying you are allergic to something in Korean—allerugi—it is much more effective to say you cannot have it. (see the list of useful phrases). Unfortunately, even these statements are unlikely to be fully effective when eating Korean food. Many Koreans are completely unaware that frequently-used ingredients such as tashida soup flavouring and soybean powder contain wheat.

Most Koreans I spoke with were shocked to hear that, as a celiac, I could not eat food which had so much as touched gluten. Generally, they assume that people with food allergies are still able to consume a product with a 1-2% trace of the allergen. Food allergies, celiac disease, vegetarianism, and other kinds of diet restrictions are rare in this country and are not taken very seriously. Furthermore, according to gastroenterologist Dr. Kim of Severance Hospital in Seoul, only two people were ever diagnosed with celiac disease in Korea.

The world of North American restaurants, where servers cater to those with food allergies, food sensitivities, and plain old picky eaters, is very far away. Koreans generally order what is on the menu without making any special requests. Even Westerners who learn enough of the Korean language to explain their diets often end up being served something they asked specifically not to have. Furthermore, Korean food is not served on personal plates: everyone at the table reaches his or her chopsticks into the various communal dishes, causing cross-contamination.

I was at a restaurant with some Korean friends and was trying to explain my gluten-intolerance to them, when one young man told me he was so sensitive to peaches that he could not so much as touch a peach without breaking out into a rash. Five minutes later I saw him eat a dish containing peach slices. This is the attitude of Koreans to food allergies—both theirs and yours.

The gluten-free meal which is safest and easiest to find in Korea is samgyupsal. This dish features fatty, thick slices of pork cooked over a clean grill right at your table. Just make sure that all sauces are kept off the grill. Bibimbop is a rice, vegetable, and egg dish usually served with kochujang, a red pepper paste which unfortunately contains wheat. Bibimbop can be ordered, however, with the kochujang on the side.

Most foreigners are in Korea to work rather than visit, and having an apartment provides the extra advantage of having one’s own cooking space. There are a few of us who have managed the gluten-free diet in Korea. However, it has not been easy. If you have celiac disease or food allergies and are thinking of moving to this part of the world, I can guarantee you that it will be a monumental challenge.

Useful Korean phrases:

• Thank you, but I can’t. I’m allergic: kamsa hamnida man, allerugi issoyo.
• I cannot have barley, rye, or wheat: chonun pori hago homil hago mil motmuhgeyo.
• Barley: pori
• Wheat: mil
• Rye: homil
• Bibimbop with the red pepper paste on the side: bibimbop kochujang garu
• Grilled Pork: samgyupsal

Celiac.com 09/15/2018 - People have a love/hate relationship with the purple fruit called ‘eggplant’. Eggplants, first cultivated in southern India and Sri Lanka, are also known as aubergine, Guinea squash, melazana, and ‘poor-man’s caviar’. Like potatoes they are members of the nightshade family, and despite the fact that we all consider eggplant to be a vegetable, biologically it is defined as a berry, and therefore it is a fruit.

When selecting the fruit, select ones that are firm to the touch, have a smooth and shiny skin and are heavy. Avoid those with brown or soft spots and have a dull color. Gently push with your thumb or forefinger. If the flesh gives slightly but then bounces back, it is ripe. If the indentation remains, it is overripe and the insides will be mushy. If there is no give at all, the eggplant was picked too early. Once you bring it home, avoid placing it near tomatoes and apples, as they give off a gas that quickens the ripening process. Try to use the eggplant within two days of purchase.

There are several cooking hints that will make your ‘eggplant experience’ more tasteful. Do not cook this fruit in an aluminum pan as it may cause discoloration (both of the pan and the fruit!). The skin is edible on small, younger plants, but should be removed on coarser, older ones. Once you cut the eggplant and cook it right away because the flesh will brown (similar to cut bananas). This fruit absorbs oil very easily, so it is recommended that you coat the slices with cornmeal before frying or baking. To help reduce the bitter flavor in older plants, ‘de-gorge’ the eggplant—Slice the eggplant into ½-inch pieces, salt well, then weigh down each slice in a colander to allow the liquid to drain out of the eggplant for 30 minutes—then rinse with cold water and pat dry.

Equivalents and Nutritional Value—one pound of eggplant equals 3½ cups of diced eggplant and 1¾ cups cooked eggplant. One medium eggplant weights about 1 pound. It contains vitamin C and potassium, has anti-bacterial and diuretic effects, as well as flavanoids (cancer fighting antioxidants). One cup cooked eggplant contains 25 calories.

The different ways to prepare eggplant are limited only by your imagination. Cut it into matchsticks to add to a stir-fry. Cube it for vegetable stews (Ratatouille). Shred it to make fritters, or puree it for a hummus-style dip. You can also slice it lengthwise and grill it.

This fruit is probably most famous for the Italian rendition of Eggplant Parmigiana. But the Greeks have taken this dish one step further, ‘Moussaka’. If you have never eaten this, it is a delight to savor. Lean ground beef may be substituted for the ground lamb. Three zucchini may be used in place of the eggplant (if you prefer). Even if you hate eggplant, you will love Moussaka.

The beauty of Moussaka is that this casserole may be made in advance, then covered and refrigerated overnight, or covered with foil and frozen—before you bake it (thaw in the refrigerator completely before baking). Time is precious for us all, and this concoction does take some time to assemble, but every moment is worth it. This makes an impressive side dish for company, it is perfect for a buffet table, or it can be used as a main dish for a family dinner.

The following recipe is from my “Wheat-free Gluten-free Reduced Calorie Cookbook”. Traditional Moussaka is ‘loaded’ with calories and fat and cholesterol. This version is lower in calories and fat without sacrificing any of the delicious taste.

Moussaka (Greek Casserole Dinner)

Ingredients:

• 1 large eggplant, peeled
• 2 teaspoons olive oil
• 1 large onion, chopped
• ½ pound lean ground lamb
• 5 teaspoons tomato paste
• ¼ cup white wine
• ¼ cup chopped fresh parsley
• 1/8 teaspoon cinnamon
• 18 teaspoon salt
• 1/8 teaspoon pepper
• 1 tablespoon margarine
• 1 ½ tablespoon cornstarch
• 1 cup scalded 1% milk
• 1 egg beaten until frothy
• 1/8 teaspoon nutmeg
• ½ cup gluten-free lowfat cottage cheese
• 1/3 cup gluten-free corn muffin crumbs, dried
• 1/3 cup Parmesan cheese, shredded

Directions:

Preheat broiler. Cut the peeled eggplant lengthwise into ½-inch thick slices. Spray both sides of the slices with gluten-free nonstick spray; set on a broiler pan and broil until browned, turning once. Preheat oven to 350F. Heat olive oil in a skillet; add onion and sauté until lightly browned. Add the lamb and cook, breaking meat up with a fork, for 10 minutes or until the meat is browned. In a small bowl, stir together the tomato paste, wine, parsley, cinnamon, salt and pepper; add to the meat and simmer, stirring frequently, until all liquid has been absorbed. Remove from heat. Melt the margarine in a medium-size saucepan; blend in the cornstarch with a whisk. Slowly stir the hot milk into the cornstarch; cook over medium heat, stirring constantly, until thickened. Cool slightly, and then stir in the beaten egg, nutmeg, and cottage cheese. Spray a 9-inch square pan with gluten-free nonstick spray. Sprinkle the bottom lightly with 2 tablespoons of the corn muffin crumbs. Arrange alternate layers of eggplant slices and meat mixture in the pan. Sprinkle each meat layer with the Parmesan cheese and remaining corn muffin crumbs. Pour the cottage cheese mixture over the top. Bake 45 minutes or until the top is golden. Cool slightly before cutting. Makes 6 (4 ½ X3-inch) serving.

Celiac.com 09/14/2018 - If it is really true that nobody really wants to see a grown man cry, then certainly nobody would have wanted to hang around me near the onset of a long illness whose mystery would take 14 years to solve.

It began subtly and mildly in 1989, my 43rd year. I had just finished a long and exhausting malpractice suit on behalf of my daughter, an attractive, genetically-normal child who had contracted quadriplegic cerebral palsy in a completely avoidable incident of post-natal asphyxia which had radically changed the nature of life for my spouse and I. By the time 1989 rolled around, I was thoroughly exhausted and carrying a toxic load of anger directed at an incompetent member of the medical profession who had never learned the importance of state-of-the-art skills in a profession that literally has the power of life, death, and disability.

From late 1989 on through 1990, I experienced strange episodes of profound sadness, usually of one to two hours duration, that became increasingly disruptive to my ability to handle a job and child-care duties. Initially, these episodes seemed to come from nowhere. Later on, I found that playing certain pieces of music of which I was fond, would send me into such intense sobbing that I would be forced to pull over if this occurred while driving.

By the time 1991 rolled around, something was to be added to these periodic bouts of intense sadness. Early in that year, my daughter became very ill, keeping both my spouse and I awake at night for weeks on end. By the time the problem was diagnosed to be a dental infection and dental surgery was done, I had begun to have a sensation of “hollowness”, as though I really weren’t part of this world, most of the time. In late summer of that year, a series of events in which my subconscious had informed me that a friend had a serious illness, sent me into a final “dive”: I simply stopped sleeping more than about two hours per night. When I first stopped sleeping, I soon noticed that even low-level use of alcoholic beverages would further interrupt sleep and throw me into a state in which I couldn’t think of anything but how terrible I felt. This state of pronounced alcohol intolerance would continue for 14 years.

The final blow came in November 1991, when I went into a completely disabling panic/anxiety attack that sent me to bed, cowering. I had no alternative but to seek treatment from the psychiatric profession. Unfortunately, the first two psychiatrists prescribed drugs which either had no effects, or had effects that seemed worse than the problem they were supposed to solve. The third psychiatrist, whom I stuck with for about six months, came up with a treatment plan that was partially effective (but certainly not restorative). I stayed with this psychiatrist until it became clear that his treatment was equivalent to Jefferson Airplane singing “one pill makes you larger, and one pill makes you small”. I was being jacked up every morning by a toxic, activating SSRI anti-depressant so I could semi-function, and then dropped by benzodiazepenes every night into a non-restorative twilight sleep state.

In retrospect, the most amazing thing about these first three psychiatrists was that not one of them ordered any tests of my endocrine function. Treatment consisted solely of a series of benzodiazepenes, anti-depressants, mood stabilizers, and anti-psychotics, administered in a trial-and-error fashion that yanked my psyche and body chemistry around like a manic pit bull on a two-foot leash.

Throughout the latter part of 1992, I transitioned to care with my primary-care physician, mostly because I trusted him more than any of the psychiatrists I had seen up to that time. He was able to stabilize me with one of the old tri-cyclic anti-depressants, doxepin, along with low doses of valium. Although doxepin packs a big morning hangover for many who use it, and has very strong anti-cholinergic effects, its ability to put me out at night helped me function satisfactorily for much of the 1990s, even at doses as low as 10mg, once daily in the evening.

In 1993 I consulted a highly-recommended psychiatrist, who was the first psychiatrist who actually looked at my thyroid function. When my TSH was measured at 3.5, without also checking my FT3 and FT4, that doctor concluded that thyroid was not my problem. Of course, standards of thyroid diagnosis and treatment have changed radically in the 12 years since. Under the new AACE guidelines, a TSH of 3.5 would now be suspect, because studies of patients with TSH over 3.0 have shown that most progress to hypothyroidism (i.e., TSH greater than 5.5). The new AACE guidelines would mean that further testing and evaluation should be done.

Until the fall of 1997, I continued treatment with doxepin and intermittent valium, adding the practice of meditation to help calm myself. At that time, I came back to my primary-care physician with the symptom of profound exhaustion on top of the symptoms of insomnia, anxiety, and depression I had suffered for years. Fortunately, my GP was suspicious of thyroid function, and found that my TSH was floating above 8. Since this was well above the old/traditional limit of 5.5, he was ready to start treatment, with (as would be expected of most GPs) T4-only replacement.

I began taking thyroxine (T4) shortly thereafter with high hopes. Initially, the treatment was successful: getting the added thyroxine into my system caused an immediate improvement in quality of sleep.

However, the use of T4 did not turn out to be an unqualified success. After use of T4 for about a month, it was apparent that use of thyroxine alone did not produce a full recovery—I still suffered from anxiety, which the medication seemed to be increasing.

In the meantime, hair loss became an issue. Several years earlier, I had noticed that running my fingers through my hair would produce an unpleasant sensation, almost as though the hair roots were tender. By the time of my 50th birthday, in 1996, I had noticed that my pillow was virtually coated with hair by the time I would remove it for washing. Unfortunately, nobody, including my GP, reminded me that hair loss is a prime symptom of hypothyroidism; and, like most males, I was ready to assume it was plain old male pattern baldness. By the time I was treated correctly and the hair loss stopped, I had pronounced thinning on the crown which was too advanced to be reversed in response to the treatment of the thyroid problem.

In about 1998, I began experimentation with amino acids which was to last for almost seven years. I found that use of tryptopan, 5-HTP, and GABA could reduce (but not correct) the worst of my symptoms. In retrospect, though, use of amino acids is a poor substitute for a well-functioning thyroid, as well as being expensive and inconvenient.

By the summer of 1999, I had reached a paradoxical situation. Experimentation had shown that my body needed on the order of 100 micrograms of thyroxine (T4) to keep my TSH down to a reasonable level; yet taking that much T4 was causing intense anxiety, requiring me to use strong sleeping medications. By late summer 1999, I had noticed another distressing symptom—my acute sense of hearing was being increasingly impacted by tinnitus. Evidently, the root cause that drove me into hypothyroidism, could also impact hearing.

It was soon after a household move in the spring of 2000, that I had a partially-disabling attack of severe epicondylitis (more commonly known as tennis elbow). It was obvious that my body was no longer able to handle the short-term stresses of the hard physical work required by a move. This obvious physical symptom, accompanied by increasing periodontal issues and continuing mental issues, prompted me to seek other treatment.

In September 2000, I began seeing a prominent “metabolic” doctor (M.D.) who is well known for his treatment of the metabolic disorders of diabetics. This doctor has written a number of books related to dietary changes and supplements needed to stave off metabolic degeneration as one ages. I was switched to Armour thyroid, and began treatment with other hormones (primarily hydrocortisone in low doses to supplement adrenal function, and pregnenolone). I took an enormous range of nutritional supplements recommended by this doctor, and also made radical changes in diet, which I maintained for nearly two years. Unfortunately, nothing seemed to really work—I did not obtain substantial relief of my symptoms. A thyroid test in Sep 2001 still showed unsatisfactory results—my TSH was 4.7, and my FT3 was below the bottom of the normal range.

By the spring of 2002, I had decided I would have to take my care elsewhere if there were to be progress. After doing a brief telephone consult with a naturopath outside my home state, I began seeing a naturopath in my home town for whom I had obtained very positive recommendations via a web search. By March 2002, the naturopath had informed me that testing showed my hypothyroidism was due to anti-thyroid antibodies, i.e., my body was attacking its own thyroid gland. This condition is officially known as Hashimoto’s Autoimmune Thyroiditis (HAIT—as I now know, HAIT is the leading cause of hypothyroidism). I found this discovery quite amazing; how come the three endocrinologists I had seen between 1998 and 2002, had not given me this information? I was started on Thyrolar (synthetic combination T3/T4) by the naturopath, because she said that my body’s ability to make T3 may have been compromised by HAIT.

Soon after beginning to see the naturopath, I learned that Dr. Stephen Langer of Berkeley, CA might have additional information on the problem I had been having with thyroid hormone causing anxiety in a hypothyroid patient. I had searched for information about this syndrome in a number of places but found nothing; for instance, the well-known book “Thyroid Solution”, by Ridha Arem M.D., contains no information on the condition. So, I consulted with Dr. Langer and learned that a small percentage of people with Hashimoto’s are exquisitely sensitive to even low doses of Thyrolar. In fact, the condition is rare enough that virtually no GPs, and only a few endocrinologists, know of its existence. Apparently, it does not have an official name attached to it. I decided to refer to it as “HAIT anxiety syndrome”, although there are a few doctors who prefer to refer to any neurological symptoms accompanying HAIT as “Hashimoto’s Encephalopathy”.

I began to feel a little better between March 2002 and June 2003. I’m not sure why the message about gluten grains had not penetrated before, but by June 2003, the naturopath reminded me again that she had seen a positive result to a test for antibodies to gliadin (one of the two major proteins in gluten grains) in 2002, and that I really should consider removing gluten grains from my diet. This recommendation was based on three factors:

1. I had antibodies to the protein gliadin found in wheat and other gluten grains such as rye and barley;
2. I had anti-thyroid antibodies which were over the threshold that defines HAIT;
3. Medicine really is an experimental science, and this experiment, in spite of its inconvenience, appeared to be worth a try.

In a numbers sense, the response of my anti-thyroid antibodies to the removal of gluten grains from my diet was slow, but gratifying. My thyroperox test started off at 25, dropped to 19 within 6 months, 7 within 10 months, and became zero in less than 2 years. I eventually concluded that the removal of gluten grains from my diet was not all that difficult, partly because I wasn’t a celiac who had to worry about that last 1%. I also concluded that removal of gluten would have a positive health effect in terms of the reduced glycemic index of the foods I consumed.

My symptomatic improvement thereafter was not immediate. It soon became obvious that T3/T4 treatment is not an exact science, and the proportion of T3 to T4 needs to be closer to the human body’s need, not the pig’s need (Both Armour and Thyrolar have the T3/T4 ratio of one part T3 for every four parts T4, typical of the pig’s biochemistry). For instance, in late 2003, my TSH had dropped very low, i.e. I had become clinically hyperthyroid due to excess T3 as revealed by a free T3 test. I have since gone through a couple more of these “yo-yo” episodes while being treated, which is a not uncommon event—thyroid treatment is as much art as science.

Cost of treatment also became a problem. By June 2004, I began seeing a highly-recommended Physician’s Assistant (P.A.), who was known locally to be very good at thyroid treatment, and whose clinic would accept my health insurance. I continued to see the naturopath, although at less frequent intervals, since my insurance (like most) would pay nothing for naturopathy. The P.A. and the naturopath did not completely agree on treatment methods, particularly the use of adrenal supplements (hydrocortisone and DHEA in low/biologic doses) along with thyroid supplements; but they were both in agreement that I should continue to pursue combination T3/T4 therapy. So, I blended recommendations from the two for awhile, transitioning to T3 and T4 in separate tablets of Cytomel and Synthroid, so the percentage of T3 could be altered.

I gradually transitioned off adrenal supplements during 2005, and very gradually increased my T3/T4 supplementation over the course of the year. Finally, by September 2005, I began to realize that I truly had recovered my health—I had episodes of feeling really good again! Still, my sleep was not perfect—I had discovered what Ridha Arem M.D. has documented in the book Thyroid Solution: a return to the euthyroid state may not immediately eliminate all symptoms. After going to a small dose of the atypical anti-depressant mirtazapine, I finally could feel, every day, like I had in my 30s. Unfortunately, it had taken an agonizing 14 years to get there.

Today, I religiously take my 10 micrograms T3, and 75 micrograms T4, split into two doses each day. I also religiously avoid all traces of gluten grains in my diet because I now understand that the gluey, hard-to-digest proteins in them are a substance which can cause major metabolic disruption. Like the co-author of the book “Dangerous Grains”, Ron Hoggan, with whom I have corresponded, I have come to realize that our society’s over-use of a potentially toxic substance isn’t just dangerous to the 1 in 133 people who have full-blown celiac disease—it can cause a very poor quality of life for the approximately 1 in 5 who have gluten intolerance. I have also come to the realization that, to those few who are unlucky enough to encounter the HAIT Anxiety Syndrome, you may require combination T3/T4 therapy to feel better; and, you may never feel as well as you did when you were young, unless you find a way to stop your immune system from waging war on your thyroid.

Most of all, 14 years after it started, I feel as though a significant part of my life has been taken from me. I was unable get joy or pleasure from life, I was unable to work effectively, and I was unable to be the kind of parent I could have been between my 45th and 59th years of life.

I never imagine that I would be looking forward to the relatively advanced age of 60. However, given that I now feel better than I did at anytime between the ages of 43 and 59, 60 looks like a good place to be.

Summary:

In retrospect, the most important things I ended up learning from 14 years of very unpleasant experience are:

• If you have psychiatric symptoms, e.g., depression, anxiety, panic disorder, etc., make sure your endocrine system is evaluated, with thyroid testing as the cornerstone. Beware of doctors who offer an antidepressant first thing, without endocrine evaluation.
• The emotional/psychiatric effects of hypothyroidism are just as important, and just as damaging, as the physical ones. Unfortunately, many MD’s focus on the physical.
• If you want to get well, you have to apply all your skills and intelligence to investigating your problem, which most MD’s may not understand. You may also have to turn to “alternative” practitioners.
• If your TSH is above 3.0, or maybe even 2.5, and your doctor will not do more comprehensive testing (e.g. FT3/FT4), and/or try a test run of thyroid supplementation, find another doctor.
• If your doctor diagnoses you as hypothyroid, demand that a test for anti-thyroid antibodies be done. If you have any antibodies, even if they are under the threshold where HAIT is considered to start, get testing for allergy to foods, and testing for allergy to common environmental toxins if food testing reveals nothing. You may find, as did I, that you won’t feel as well as possible until you free your body from antibodies.

Celiac.com 09/08/2018 - On a recent trip to Hawaii I was often attracted to a particular entrée on the menu of several restaurants. It went by many different names, but basically the dish was fish dredged in a mixture of spices and pulverized nuts to produce a chunky crust. Since Hawaii is the home of macadamia nuts, this popular nut was often used.

I love fish and I’m very fond of macadamia nuts, so I was particularly enticed by this entrée but I was wary because I know that many chefs like to use panko (Japanese bread crumbs) and add flour to such mixtures even though it isn’t absolutely necessary and is often not mentioned in the entrée’s description on the menu. So, I found myself engaged in a very typical conversation with the waiter. It went something like this:

• Me: I’m wondering about the nut mixture used to coat the fish. Is there wheat flour or bread crumbs in it?
• Waiter: I don’t know, but I’ll check with the chef and let you know.
• Me to husband: I better choose another entrée just in case he/she comes back with bad news.
• Waiter: The chef says there is (flour or bread crumbs or both) mixed in with the nuts and spices. Sorry.
• Me: That’s fine. Thanks for checking on that for me. Instead, I’ll have the…

After I returned from this otherwise fabulous trip, I vowed to create my version of this entrée so I could have it at home whenever I wanted. I will share it here with you, but first a little background on macadamia nuts.

Macadamia Nuts
Though expensive, macadamia nuts are a treat and Hawaii is well known for this delicious nut. If macadamia nuts are too expensive or not available in your area, you can use slivered almonds instead. Despite their sometimes “bad” reputation, nuts offer important nutrients and good, healthy fat. But the real reason I was attracted to this dish was the crunchy texture that is so important to me in my gluten-free diet.

The best way to crush the macadamia nuts is to put them in a small coffee grinder or food processor and grind just until they reach a coarsely chopped stage. Don’t grind them any further or you might end up with “mush” instead of pulverized nuts. To prevent the nuts from sticking together, I grind them with a small amount of cornstarch.

Some of you may never have traveled to Hawaii. Others, like me, may not get a chance to return to Hawaii for a long time but at least we can bring a little bit of the islands to our dinner table with this tempting dish.

Macadamia-Crusted Snapper with Pineapple Salsa

Ingredients:

• 4 fish fillets (red snapper, mahi mahi, or firm-flesh fillets--about 6 ounces each)
• 4 tablespoons olive oil, divided
• 1 teaspoon ground ginger
• 1 teaspoon ground coriander
• 1 teaspoon paprika, plus some for dusting
• 1 teaspoon salt
• ½ teaspoon freshly ground pepper
• 1 cup coarsely ground macadamia nuts or almonds (ground with ¼ cup cornstarch)
• Additional salt and pepper to taste

Salsa Ingredients:

• 1 can (8 ounces) pineapple tidbits, drained
• ½ cup finely diced red bell pepper
• ½ cup chopped fresh cilantro
• ¼ cup finely diced red onion
• 1 tablespoon fresh lime juice
• 1 tablespoon rice vinegar
• 1 teaspoon olive oil
• 1 serrano chile pepper, seeded and finely diced
• ¼ teaspoon salt
• ¼ teaspoon sugar

Directions:
At least an hour before dinner, combine all of the salsa ingredients in a small serving bowl, cover, and let sit at room temperature. Preheat the oven to 400°F. Lightly grease a baking dish or sheet large enough to hold the fish fillets side by side and at least 2 inches apart. Use 1 tablespoon of the olive oil or you may line the pan with aluminum oil and lightly coat with cooking spray. Grind the nuts and cornstarch together. Evenly spread the nut mixture on a large dinner plate.

Combine remaining 3 tablespoons of the oil, ginger, coriander, and paprika. Brush each filet with this mixture; sprinkle both sides with salt and pepper. Dredge each fillet in the nuts, pressing mixture on fish with your fingers to cover it evenly on both sides. Gently transfer fish to prepared baking dish. Sprinkle with a dusting of paprika. Bake fish fillets until they are cooked through and the nut crust is golden brown, anywhere from 10 to 15 minutes or more depending on the thickness of the fish. Season with additional salt and pepper to taste. Serve immediately with 1/3 cup of Pineapple Salsa per serving. Serves 4.

You don’t have to save this nut crust for fish. It works great on chicken fillets, too. Plan ahead by grinding more nuts than you need then freezing the remainder. That way, it’s just a simple step to mix in the necessary spices or whatever else the recipe calls for.

Celiac.com 09/01/2018 - Celiac disease is a common disease triggered by gliadin exposure in genetically sensitive individuals.  It has long been known that untreated celiac disease is associated with intestinal malabsorption, but it is also associated with ongoing inflammation.  This inflammation may have adverse effects on the uptake of important nutrients.  This is probably the underlying reason for the increased risk of osteoporosis demonstrated in patients with celiac disease.  Malabsorption and ongoing inflammation in untreated celiac disease could also potentially have a negative effect on fetal development.

Several reports have indicated an adverse effect of untreated celiac disease on pregnancy outcome.  We set out to use the national registers of Sweden to:

1. Evaluate the association of untreated celiac disease and birth weight, pregnancy duration and intrauterine growth.
2. Evaluate the same association in treated celiac disease.
3. Compare the risk of the above two groups with a reference group of 2.8 million births to mothers who never had a diagnosis of celiac disease.
4. A fourth objective was to evaluate placental weight to see if lower placental weight was more frequent in women with celiac disease.

We found that untreated celiac disease (women diagnosed after pregnancy, but most likely having untreated celiac disease at time of pregnancy) was associated with a two-fold risk of low birth weight, pre-term birth, intrauterine growth retardation and cesarean section.

The low birth weight and intrauterine growth retardation may have been mediated through malabsorption, since placental weight was lowest in women with untreated celiac disease.

This study was published in Gastroenterology Aug 2005. A link to this paper can be found here: gastrojournal.org

After that we set out to evaluate the association between adverse pregnancy outcome in males with untreated and treated celiac disease.  In a previous paper, we had found an increased risk of adverse pregnancy outcome when the father had celiac disease (Ludvigsson et al, Gut, 2001).  Now, taking advantage of the large Swedish national registers (all births since 1973 and onwards are recorded), we found no increased risk of low birth weight, pre-term birth or cesarean section in infants to fathers with untreated or treated celiac disease.  This study was published in the Scandinavian Journal of Gastroenterology in Feb 2006.

Celiac.com 08/30/2018 - Celiac disease is a disorder characterized by a clinical syndrome of intestinal malabsorption and a characteristic though not specific histological lesion consisting in total, subtotal or partial small-bowel villous atrophy (predominating in the proximal segments).  A correct gluten-free diet results in clinical and histological improvement(1,2).  It has become increasingly apparent that the prevalence of celiac disease is higher than previously thought, and that this is mainly because of increasing awareness of atypical, mildly symptomatic, or silent cases(3).  Therefore, many patients have upper gastrointestinal endoscopy as an initial investigation, which provides an opportunity to perform a biopsy in the second portion of the duodenum.  

The role of endoscopy in diagnosing celiac disease
It has long been known that celiac disease can produce changes in the appearance of small intestine on barium contrast radiographs, one such change being so-called “loss” of duodenal folds.  However, over the last two decades it has been recognized that a number of changes in the duodenum clearly associated with celiac disease can be identified endoscopically.  Because it is now understood that the manifestations of celiac disease are wide and variable, and that the disease is more common than recognized in the past, the clinical significance of these endoscopic observations has been greatly amplified.  Awareness of these endoscopic features may alert the endoscopist to the presence of celiac disease and the need for duodenal biopsies in patients undergoing endoscopy for symptoms unrelated to the disease as well as those with vague, non-specific manifestations.

The endoscopic features in the duodenum that are well-established as markers for celiac disease include: loss of folds; scalloping of folds; mucosal mosaic pattern; whilst less commonly described findings include a visible vascular pattern and micronodularity in the duodenal bulb.

1.    Loss of folds
“Loss” of folds is defined as an obvious reduction in height or number of folds in the second portion when viewed with maximal air insufflation.  The sensitivity and specificity of this marker range from 73 to 88% and from 83 to 97% respectively (4,5).

2.    Scalloping of duodenal folds
Scalloping occurs when multiple grooves run over the apex of a duodenal fold.  Grooves in the mucosa between folds have also associated with celiac disease and likely a manifestation of the same process that leads to scalloping.  The sensitivity and specificity of this marker are 88% and 87% respectively (6,7).

3.    Mucosal mosaic pattern
Mucosal mosaic pattern may be recognized both in the duodenal bulb and in the second portion of the duodenum, and its assessment may be easily performed by chromoendoscopy.  Unfortunately, the sensitivity of this marker is quite low (57%) (8).

4.    Micronodularity in duodenal bulb
This marker is quite frequent in childhood and adolescent patients, but it can be also recognized in young adults 9-11.  

5.    Visible vascular pattern
This marker describes a prominence of underlying duodenal blood vessels in patients with celiac disease.  Unfortunately, this is the least sensitive endoscopic marker in all studies in which it was specifically evaluated (6,12,13).  

All these markers are helpful in recognising celiac disease.  Moreover, in some cases specific endoscopic features can be associated with specific histological damage and may be associated with the clinical form of the disease.  We found in fact that endoscopic appearance of the duodenum may be predictive of histological damage grading.  Moreover, we showed that in young patient with subclinical/silent celiac disease there is a greater probability of finding slight/mild endoscopic abnormal/mild histological damage (11).

Unfortunately, an endoscopic marker suspected for celiac disease itself is not specific for celiac disease.  For example, looking at scalloping, Shah, et.  al., described 13 cases in which scalloping of duodenal folds was not caused by celiac disease but due to other causes (HIV-related infection, tropical sprue, giardiasis, eosinophilic gastroenteritis)(14).

On the other hand, the presence of one or more endoscopic markers increases the sensitivity and specificity ranging from 87.5 to 94%  and from 99 to 100% respectively (12,15).   

There is non-existing classification of endoscopic lesions in celiac disease.  However, I think that it may be graded according to some simple considerations.  Celiac disease is considered a crianial-caudal disease which affects primarily the proximal segments (first the duodenal bulb and then the second and third duodenal portions) and then the distal segments of the small bowel (first jejeunum and then the ileum).  Therefore, we may hypothesize that endoscopic damage occurs first in the duodenal bulb and then in the distal tracts of the duodenum.  For this reason, and according to other endoscopists in Italy, I proposed the following classification in 2002(11):

• a.    Slight/mild endoscopic damage: micronodular bulb, granular mucosa of the second duodenal portion, scalloping of duodenal folds, reduction of duodenal folds;
• b.    Severe damage: “mosaic” pattern of the duodenal mucosa, visible vascular pattern, loss of duodenal folds.

The effectiveness of this grading system was confirmed in the same study.  In fact we found that  the so-called “slight-mild endoscopic damages” seen at endoscopy was associated with a mild-moderate histological damage (p<0.005), while the so-called “severe endoscopic damages” was related to severe histological damage (p<0.0005).  Unfortunately, no Consensus Conference on celiac disease has discussed this problem yet.         

New endoscopic methods
Several new endoscopic techniques have been recently developed to increase the sensitivity and specificity of endoscopy in diagnosing celiac disease.

a.    “Immersion” technique.
The “immersion” technique consists in observing duodenal mucosa using a high-resolution, high-magnifying (x2) videoendoscope that observes the villous architecture with a water film.  This approach seems to be effective in allowing the visualization of duodenal villi and the detection of total villous atrophy(16).  A recent study found that this approach is highly accurate in detecting total villous atrophy in suspected celiac cases, and it seems both accurate and cost-sparing to diagnose celiac disease in subjects with marked duodenal villous atrophy, having a sensitivity, specificity, and positive and negative predicting values of 100%17.  Moreover, this approach also seems to be effective in detecting patchy villous atrophy in celiac patients with patchy lesions (18).

b.    Zoom endoscopy
This technique provides a very impressive magnification capability of x115.  This approach may allow the macroscopic detection of unrecognised villous atrophy in patients with unsuspected celiac disease.  Badreldin, et.  al., found recently that zoom endoscopy may be valuable in assessing degree of villous atrophy, having a positive predicting value of 83% and a negative predicting value of 77% in detecting villous atrophy (19).

c.    Double-balloon endoscopy (DBE)
This technique will become probably the best endoscopy technique in investigating small bowel.  It allows high-resolution visualization, biopsies and therapeutic interventions in all segments of the GI tract.  DBE is a safe and feasible diagnostic and therapeutic tool for suspected or documented small-bowel diseases.  However, it requires a long time for small bowel exploration (about 70 minutes from the oral route and  about 90 minute from the anal route) and requires expertise personnel to obtain better results 20.  At present, the best candidates for the procedure appear to be those with obscure GI bleeding.           

d.    Wireless capsule endoscopy
Celiac disease is an inflammatory disease that involves the entire small intestine.  Even in the 1960s was documented, by using peroral biopsies, that the inflammatory atrophic process can extend a variable distance down the small intestine, not uncommonly involving the ileum(21).  These data have been recently confirmed by endoscopic studies, that found ileal inflammatory changes predicting villous atrophy in duodenal biopsy specimens(22).

Wireless capsule endoscopy is a new effective and easy method to investigate small bowel.  The M2A video capsule endoscope (Given Imaging LTd; Yokneam, Israel) is a wireless capsule (11 mmx27 mm) comprised a light source, lens, CMOS imager, battery and a wireless transmitter.  The slippery out side coating of the capsule allows easy ingestion and prevents adhesion of intestinal contents, while the capsule moves via peristalsis from mouth to anus.  The battery provides seven to eight hours of work in which the capsule photographs two images per second (between 50,000-60,000 images all together), which are transmitted to a recorder which is worn on the belt.  The recorder is downloaded into a computer and seen as a continuous video film.  Since its development additional support systems have been added, a localization system, a blood detector and a double picture viewer.  All of this is intended to assist the interpreter of the film and to shorten the reviewing period.

The full range of indications for CE became apparent with time.  The initial device was invented to address for a better diagnostic tool for small bowel pathologies (such as obscure gastrointestinal bleeding or Crohn’s disease)(23).  In light of this high specificity for the diagnosis of small bowel diseases, it is considered that capsule endoscopy may be of value in the diagnosis of celiac disease for patients with a positive endomysial or tissue transglutaminase antibody and who are unable to or unwilling to undergo EGDscopy(24).  The very important limit of this new technique in celiac disease is represented by the absence of histological-proven damage.  It is recognised that the endoscopic signs of villous atrophy are not sensitive for the lesser degrees of villous atrophy, so partial villous atrophy may be missed by this approach(13).

On the other hand, I think that the patients who appear to be ideal candidates for capsule endoscopy are those patients who fail to respond to a gluten-free diet, or who develop alarm symptoms while on a gluten-free diet.  These patients often undergo extensive radiologic, and sometimes, surgical evaluation, because of concern for the development of complications (such as lymphoma(25,26) or ulcerative jejunitis(27).  It is clear that lesions detected by capsule endoscopy in this high-risk group will require further evaluation of these abnormalities through biopsy.  Capsule endoscopy may thus be used to select patients to undergo enteroscopy(28) or, more probably in the near future, double-balloon endoscopy(29).  

The role of endoscopy in the follow-up of celiac disease
Data on small-intestinal recovery in patients with celiac disease are scarce and contradictory.  This is especially the case for adult patients, who often show incomplete histological recovery after starting GFD.  On the other hand, there are very few data about the endoscopic recovery on GFD.  We recently conducted a two-year prospective study on 42 consecutive adults with newly diagnosed celiac disease.  All the patients underwent EGDscopy and small-bowel biopsy.  A normal endoscopic appearance (absence or mucosal irregular findings, normal duodenal folds)  was found in 76.2% after two-year on a GFD.  Subdividing the patients according to age, patients aged from 15 to 60 years showed significant improvement within 12 months but faster in patients in patients <45 years, whereas the improvement in endoscopic findings in patients older than 60 years was not statistically significant even 24 months after starting GFD.  On the contrary, histological recovery was much more slower, since only younger patients (5-30 years) showed significant improvement of histology within 24 months(30).  These data showed for the first time that endoscopic recovery is faster than histological recovery after starting GFD.  

Conclusive Advice
A number of studies have demonstrated a strong correlation between the endoscopic duodenal findings and celiac disease.  Furthermore, absence of specific features suspected from celiac disease does not exclude celiac disease and specimens should always be obtained when there is a suspicion that the disease may be present.  For this reason, capsule endoscopy should be not recommended as first endoscopic step in searching celiac disease, but it may be best used to recognize endoscopic recovery and to exclude complication in celiac patients on GFD.  

The last question is: How long should we continue with endoscopic and histological follow-up? Looking at the results recently obtained from our group, my advice on follow-up could be summarized as follows: patients aged under 30 years should undergo endoscopic/histological assessment after one year; patients aged 30-45 years should be reassessed after two years; and patients aged 50 years and over should be reassessed after two years, including an immunohistological assessment to exclude refractory celiac disease.

References:

1)    Martucci S, Biagi F, Di Sabatino A, Corazza GR.  Coeliac disease.  Digest Liver Dis 2002;34 (suppl.  2): S150-S153.
2)    When is a celiac a celiac? Report of a working group of the United European Gastroenterology Week in Amsterdam, 2001.  Eur J Gastroenterol Hepatol 2001;13: 1123-8.
3)    Tursi A, Giorgetti GM, Brandimarte G, Rubino E, Lombardi D, Gasbarrini G.  Prevalence and clinical presentation of subclinical/silent coeliac disease in adults: an analysis on a 12-year observation.  Hepato-gastroenterol 2001; 39: 462-4.
4)    Brocchi E, Corazza G, Caletti G et al.  Endoscopic demonstration of loss of duodenal folds in the diagnosis of celiac disease.  N Engl J Med 1988;319: 741-4.
5)    Mc Intere AS, Mg DP, Smith JA , Amoah J, Long RG.  The endoscopic appearance of duodenal folds is predictive of untreated adult celiac disease.  Gastrointest Endosc 1992;38: 148-51.
6)    Corazza GR, Caletti GC, Lazzari R et al.  Scalloped duodenal folds in childhood celiac disease.  Gastrointest Endosc 1993; 29: 543-5.
7)    Smith AD, Graham I, Rose JD.  A prospective endoscopic study of scalloped folds and grooves in the mucosa of the duodenum as sign of villous atrophy.  Gastrointest Endosc 1998;47: 461-5.
8)    Stevens FM, McCarthy CF.  The endoscopic demonstration of coeliac disease.  Endoscopy 1976;8: 177-80.
9)    Brocchi E, Corazza GR, Brusco G, Mangia L, Gasbarrini G.  Unsuspected celiac disease diagnosed by endoscopic visualization of duodenal bulb micronodules.  Gastrointest Endosc 1996;4: 610-1.
10)    Vogelsang H, Hänel S, Steiner B, Oberhuber G.  Diagnostic duodenal bulb biopsy in celiac disease.  Endoscopy 2001;33: 336-40.
11)    Tursi A, Grandimarte G, Giorgetti GM, Gigliobianco A.  Endoscopic features of celiac disease in adults and their correlation with age, histological damage, and clinical form of the disease.  Endoscopy 2002;34: 787-92.
12)    Niveloni S, Fiorini A, Dezi R et al.  Usefulness of videoduodenoscopy and vutal dye staining as indicators of mucosal atrophy of celiac disease: assessment of interobserver agreement.  Gastrointest Endosc 1998;47: 223-9.
13)    Dickey W, Hughes D.  Disappointing sensitivity of endoscopic markers for villous atrophy in a high-risk population: inplication for celiac disease diagnosis during routine endoscopy.  Am J Gastroenterol 2001;96: 2126-8.
14)    Shah VH, Rotterdam H, Kjotler DP, Fasano A, Green PH.  All that scallops is not celiac disease.  Gastrointest Endosc 2000;51: 717-20.
15)    Dickey W, Hughes D.  Prevalence of celiac disease and its endoscopic markers among patients having routine upper gastrointestinal endoscopy.  Am J Gastroenterol 1999;94: 2182-6.
16)    Cammarota G, Martino A, Pirozzi GA et al.  Direct visualization of intestinal villi by high-resolution magnifying upper endoscopy: a validation study.  Gastrointest Endosc 2004;60: 732-8.
17)    Cammarota G, Cesaro P, Martino A et al.  High accuracy and cost-effetciveness of a biopsy-avoiding endoscopic approach in diagnosing celiac disease.  Aliment Pharmacol Ther 2006;23: 61-9.
18)    Cammarota G, Martino A, Di Caro S et al.  High-resolution magnifying upper endoscopy in a patient with patchy celiac disease.  Dig Dis Sci 2005;50: 601-4.
19)    Badreldin R, Barrett P, Wooff DA, Mansfield J, Yiannakou Y.  How good is zoom endoscopy for assessment of villous atrophy in coeliac disease? Endoscopy 2005;37: 994-8.
20)    Di Caro S, May A, Heine DG, Fini L et al.  The European experience with bouble-balloon enteroscopy: indications, methodology, safety, and clinical impact.  Gastrointest Endosc 2005;62: 545-50.
21)    MacDonald WC, Brandiborg LL, Flick AL et al.  Studies of celiac sprue.  IV.  The response of the whole length of the small bowel to a gluten-free diet.  Gastroenterology 1964;47: 573-89.
22)    Dickey W, Hughes DF.  Histology of the terminal ileum in coeliac disease.  Scand J Gastroenterol 2004;39: 665-7.
23)    Eliakim R.  Wireless capsule video endoscopy: three years experience.  World J Gastroenterol 2004;10: 1238-9.
24)    Cellier C, Green PH, Collin P et al.  The role of capsule endoscopy in coeliac disease: the way forward.  Endoscopy 2005;37: 1055-9.
25)    Green PH, Fleichauer AT, Baghat G et al.  Risk of malignancy in patients with celiac disease.  Am J Med 2003;115: 191-5.
26)    Cellier C, Delabasse E, Helmer C et al.  Refractory sprue, coeliac disease and enteropathy-associated T-cell lymphoma.  French Coeliac Disease Study Group.  Lancet 2000;356: 203-8.
27)    Green JA, Barkin JS, Gregg PA et al.  Ulcerative jejunitis in refractory celiac disease: enteroscopic visualization.  Gastrointest Endosc 1993;39: 584-5.
28)    Gay G, Delvaux M, Fassler I.  Outcome of capsule endosocpy in determining indication and route for push-and-pull enteroscopy.  Endoscopy 2006;38: 49-58.
29)    Yamamoto H, Kita H, Sunada K et al.  Clinical outcomes of double-baloon endoscopy for the diagnosis and treatment of small-intestinal diseases.  Clin Gastroenterol Hepatol 2004;2: 1010-6.
30)    Tursi A, Brandimarte G, Giorgetti GM.  Endoscopic and histological findings in the duodenum of adults with celiac disease before and after changing to a gluten-free diet: a 2-year prospective study.  Endoscopy 2006; 38: in press.

Celiac.com 07/10/2006 - Increased consumption of gluten, according to Dr. Michael Marsh, raises the risk of celiac disease symptoms¹. Although these symptoms may not indicate celiac disease, they reflect some biological realities. Grain-based foods simply do not offer the nutrients necessary to human health and they damage the human body. USDA and Canada Food Guides notwithstanding, if people eat grain-laden diets, they may develop symptoms of celiac disease (but in most cases, without the diagnostic intestinal lesion). The connection between eating disorders and celiac disease is well known and well documented^2,3,4,5. Thus, the dynamics at work in celiac disease may offer insight into the broader realm of obesity, especially among those who are eating the recommended, daily quantities of grain-derived foods, while attempting to keep their weight down by eating low-fat foods.

The primary, defining characteristic of celiac disease is gluten induced damage to the villi in the intestinal lining. Since malabsorption of vitamins and minerals are well known in the context of celiac disease, it should not be surprising that some celiac patients also demonstrate pica (Pica is an ailment characterized by eating dirt, paint, wood, and other non-food substances). Other celiac patients eat excessive quantities of food, coupled with a concurrent failure to gain weight. Yet another, perhaps larger, group of celiac patients refuse to eat (One may wonder if the latter find that eating makes them feel sick so they avoid it).

Perhaps the most neglected group is that large portion of untreated celiac patients who are obese. Dr. Dickey found that obesity is more common than being underweight among those with untreated celiac disease⁶. When I ran a Medline search under the terms "obesity" and "celiac disease" 75 citations appeared. A repeated theme in the abstracts and titles was that celiac disease is usually overlooked among obese patients. While obesity in celiac disease may be common, diagnosis appears to be uncommon. Given the facts, I certainly believe that some of the North American epidemic of obesity can be explained by undiagnosed celiac disease. However, that is only a small part of the obesity puzzle, and I suspect that celiac disease may offer a pattern for understanding much of the obesity that is sweeping this continent.

One example, a woman diagnosed by Dr. Joe Murray when he was at the University of Iowa, weighed 388 pounds at diagnosis⁷. Dr. Murray explained her situation as an over-compensation for her intestinal malabsorption. I want to suggest a two faceted, alternative explanation which may extend to a large and growing segment of the overweight and obese among the general population. As mentioned earlier, anyone consuming enough gluten will demonstrate some symptoms of celiac disease. If large scale gluten consumption damages the intestinal villi—but to a lesser degree than is usually required to diagnose celiac disease—fat absorption will be compromised. Deficiencies in essential fatty acids are a likely consequence.

The natural response to such deficiencies is to crave food despite having absorbed sufficient calories. Even when caloric intake is huge, and excess calories must be stored as body fat, the need to eat continues to be driven by the bodys craving for essential fats. Due to gluten-induced interference with fat absorption, consumption of escalating quantities of food may be necessary for adequate essential fatty acid absorption. To further compound the problem, pancreatic glucagon production will be reduced, compromising the ability of the individual to burn these stored fats, while the cells continue to demand essential fats.

Poor medical advice also contributes to the problem. The mantra of reduced fat continues to echo in the offices of health professionals despite a growing body of converse research findings. In February of this year, the results of a powerful, eight year study of almost 49,000 women showed little difference between the health of women consuming low fat diets when compared to those consuming normal diets⁸. Alarmingly, this low fat diet seems to have resulted in weight gain, a well recognized risk factor for a variety of diseases.

For some of us, this result was predictable. The likely result of a low-fat diet is an increased intake of carbohydrates while food cravings are fuelled by a deficiency of essential fatty acids. If my sense of the underlying problem (caloric excess combined with essential fatty acid deficiency due to fat malabsorption at the microvilli) is accurate, then a low fat diet is exactly the wrong prescription. Many obese persons are condemned, by such poor medical advice, to a life of ever deepening depression, autoimmune diseases, and increasing obesity.

At the end of the day, when these folks drop dead from heart attacks, strokes, or some similar disaster, the self-righteous bystanders will just know that the problem was a lack of willpower.

I watched my mom steadily gain weight for 35 years. I watched her exercise more will power beyond the capacity of most folks. Still, she could not resist her compulsive eating. I have seen her take something from the freezer and chew on it while agreeing that she had just eaten a very large meal and should feel full.

In December of 1994 I was diagnosed with celiac disease. According to the published experts in this area, my mom should also have been invited for testing. Yet, when asked for testing, her doctor refused her. Through persistence, and a pervasive faith in her son, mom finally (after months of negotiation) swayed her doctor to do the anti-gliadin antibody blood test. Despite the fact that she had been on a reduced gluten diet for the past year, her antibody levels were elevated.

She never sought a biopsy diagnosis, and the EMA and tTG were not available here in Canada at that time. However, she has been gluten-free for the past seven years or so. She dropped a considerable amount of weight.

Her weakness was never will power. She was battling an instinct so basic that few of us could have resisted. That, I think, is the story behind much of North American obesity. The widespread, excessive consumption of gluten at every meal, in addition to the low-fat religion that has been promulgated throughout the land, is resulting in intestinal damage and a widespread deficiency in essential fats is among North Americans.

Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered at www.celiac.com. Rons Web page is: www.DangerousGrains.com

References: