Celiac.com 12/25/2020 - In Spring 2006, Journal of Gluten Sensitivity Newsletter published an article titled “To HAIT And Back” about my encounter with gluten-induced autoimmune thyroiditis.  At the time I wrote that piece, I was confident that the elimination of gluten and proper level of thyroid hormone supplementation had me on a track back to full health.  

However, little did I know that my illness consisted of two syndromes.  Every gluten-induced illness, no matter which of the body’s systems it affects, is accompanied by some degree of intestinal destruction.  This is true even in cases of “silent” gluten intolerance/ celiac disease, where there are no obvious digestive symptoms.  In fact, my health problems were layered: in addition to thyroid destruction, I also had significant, silent intestinal destruction.  In addition to the autoimmune thyroid issue, a second issue of malnutrition had to be corrected before my health would return to a truly high level.  

As 2005 drew to a close, I realized that, although I was feeling generally much better, my health was not perfect.  I was willing, at that point, to attribute this to what Ridha Arem M.D had said in his book, Thyroid Solution: a return to the euthyroid state may not immediately eliminate all symptoms.  For that reason, I used a small dose of Mirtazapine to help me feel better.  I was able to maintain a fairly level state into spring 2006.  

By late spring 2006, however, my sleep had begun to deteriorate again in spite of the assistance provided by Mirtazapine and other prescription drugs.  In May, I tried acupuncture a few times, and bought a light-box, but still could not get relief.  By the time summer rolled around, I was back in the office of the naturopath who had originally convinced me to go gluten-free in June, 2003 due to gliadin antibodies.  

An adrenal test showed that my adrenal function had gone down to almost nothing.  A continual downward trend in adrenal function was shown by tests in 2002, 2004, and 2006.  The naturopath contended that I needed to go back on Cortef (hydrocortisone) and DHEA to prop up my adrenals.  But that did not provide much symptom relief.  

By September, I was feeling really bad.  The naturopath and her assistant decided that I should be tested for heavy metals.  The test came back positive: significantly elevated level of lead, and somewhat elevated level of mercury.  

Shortly thereafter, I started chelation therapy with the chelating agent DMSA.  This continued for eleven 2-week rounds, into Feb.  2007.  Although I had periods where the chelation seemed to be making me feel better, the result was not as successful as I expected.  Three months after the chelation ended, a follow-up test (non-provoked) showed an undetectable lead level, so it seems unlikely that I have a large amount of lead stored in bone.  

In spring 2007 I was back in my thyroid doctor’s office, and we discussed other treatment alternatives.  Who in the area was likely to come up with new avenues of investigation? The result was a referral to see a “holistic” M.D.  in March 2007.  

Improvement thereafter was rapid.  On my second visit to the “holistic” M.D., he recommended that I do a urine test for the stress disorder pyroluria.  The results came back positive, although not strongly so.  He recommended starting treatment anyway, with a high-dose vitamin and mineral preparation.  This preparation contains vitamins B6/P5P, niacin, and pantothenic acid, along with zinc, manganese, and magnesium.  I was skeptical, but had no serious objection to trying something that was highly unlikely to be toxic.  

The result was that I felt almost completely well within three weeks.  However, I started feeling worse after about five weeks.  Because of my long experience with drugs, I suspected that the very high dose of “pyroluria formula” I was taking might be too high.  Cutting back the dose brought me to a state in which I felt clear, calm, collected, and slept well.  Because my read-out on the pyroluria test was in the gray zone between no diagnosis and firm diagnosis, it seems sensible that I would not require a mega-dose.  I was later to determine that my negative response to large amounts of the preparation was probably due to the high levels of pantothenic acid it contains, and eventually began supplementing the formula with plain B-6 and zinc.  

To augment my treatment by the “holistic” M.D., I shortly thereafter began seeing a Certified Nutritionist he recommended.  On the very first visit, the CN looked over my case history and made a couple recommendations.  The first was to add a supplement regimen designed to heal gluten enteropathy.  That regimen included large doses of ground flax-seed, Metagenics’ Glutagenics (glutamine/licorice/aloe), probiotics, and minerals.  The second recommendation was to do a trial elimination of dairy products, based on her previous observation that people with gluten enteropathy, often cannot digest dairy foods.  

Going dairy-free turned out to be a positive step.  Within a few weeks, I noted that my digestion was working much better.  Based on this result, I was ready to follow more of the CN’s advice.  At our second visit, she recommended changes to my supplementation plan.  She also noted that I am one of a few patients she and the “holistic” M.D.  are monitoring to see if pyroluria improves with intestinal healing.  The theory is that, when “pyroluria” is actually due to intestinal damage, the pyroluria will recede if the intestine can be healed.  

These recommendations proved to be good ones.  Within about six months, I noticed that I could skip supplement doses without negative effects.  I also noticed that my previous sensitivity to dairy foods had disappeared.  By the end of 2007, I was finally able to reach the correct, therapeutic dose of thyroxine that would give me a TSH just above 1.0.  This ended 17 years of hypothyroidism.  

Today, I religiously take 118mcg of T4 each night between bedtime and arising.  For me, thyroxine acts almost as a sleeping pill.  And as before, I am religiously avoiding all traces of gluten grains in my diet, as I have for more than 4 years.  This latter bout of illness has taught me an interesting medical fact that I hope I’ll never have to use again: the (relatively) inexpensive test for pyroluria, is an excellent way to diagnose malnutrition caused by destruction of the intestine.  

Summary
In retrospect, the most important things I learned from this last 2 years of illness, on top of the previous 15 years, were: 

• Every gluten-induced illness is going to be accompanied by some degree of intestinal destruction.  If you have gluten problems but no obvious digestive symptoms, you probably have the silent form of gluten intolerance/celiac.  
• It is possible to heal gluten-induced destruction, but it can take a very long time.  And, you probably cannot do it yourself; you will need a RD or CN who is knowledgeable about gluten-induced destruction, to help you along.  
• Most M.D’s don’t know how to diagnose malnutrition.  In fact, most of them are completely unaware of pyroluria.  However, the pyroluria test appears to be a fairly reliable way of diagnosing intestinal destruction leading to malnutrition.  Of course, genetic pyroluria is a real disorder, but the utility of the test as a diagnostic tool for intestinal destruction, in people who do not have a past history of genetic pyroluria, cannot be denied.  
• The co-existence of HAIT and “pyroluria” (malnutrition) in my case, suggests a hypothesis as to why “Hashimoto’s Anxiety Syndrome”/”Hashimoto’s Encephalopathy” occurs in some people, but not others.  Obviously, HAIT by itself causes some anxiety, since ridding myself of HAIT antibodies reduced anxiety related to administration of thyroid hormone.  It seems a reasonable hypothesis that any of several biochemical syndromes that are known to cause anxiety, could add anxiety to that caused by HAIT, greatly amplifying overall anxiety.  Among the many symptoms of “pyroluria” (in my case, malnutrition), whose functional deficiency of B6 and zinc disproportionately affects the neurological system, are anxiety and atypical/unusual reaction to drugs and hormones.  
• It is known that high oxidative stress can create food allergies (per William Walsh PhD of the Pfeiffer Treatment Center).  Since pyroluria (i.e. malnutrition) causes oxidative stress, it is a (unproven at this point) theory that my food allergies may have been worsened by co-existing malnutrition.  

Celiac.com 12/25/2020 - When you think about it, most cultures have some kind of wrap or tortilla.  The Mexicans and Brazilians offer corn tortillas, Thailand has a rice tortilla, China has wheat tortillas for Moo Shu, the French have crepes and Socca made from chickpea flour.  Ethiopians have teff tortillas.  Nepalese have chappatis made from amaranth flour.  Thank heaven, here in America there are gluten-free tortillas we can buy off-the-shelf.  Candy’s Corn tortillas and Food for Life rice tortillas are gluten-free staple foods in my kitchen, but there is nothing more comforting than a homemade tortilla.  The gluten-free world needs its own tortilla!  Let’s call our tortilla the “Alternative” tortilla, to signify a gluten-free safe-to-eat tortilla.  This may catch on—imagine going into Chipotle and saying, “I’ll have mine on the “Alternative”…

While exhibiting at gluten-free conferences this past year numerous people asked me if I could offer a recipe for a tortilla.  Some seemed a bit intimidated about making a tortilla, so I hope this article will diminish all fears and equip you with tortilla techniques to help you feel empowered not only to make the recipe provided below, but to expand, experiment and customize your own recipes.  

Tortilla Ratio

If you’d rather eat a bug than cook, making tortillas is for you!  The standard process is simple.  Mix together liquid, flour and salt into a ball.  Roll it or press it into a round, flat tortilla and cook it.  The ratio is simple too:

• 2 cups flour
• 1 cup liquid
• 3 Tablespoons oil

It’s just a little different for gluten-free.  Since we don’t have gluten—an elastic-like protein to hold everything together, we add xanthan gum.  Optionally, if you want a more puffy tortilla, you can add baking powder.  

With gluten free baking in general, it’s best to use a combination of flours, but since tortillas are “flat bread” most gluten-free flours will work fine by themselves.  On the other hand, using several different flours boosts taste and nutrition.  I prefer to make mine with mostly whole grains such as sorghum, brown rice, amaranth, quinoa, buckwheat, millet or teff flour. 

If you know you are going to need 2 cups of flour, think of one as the stabilizer and the others as enhancers.  The stabilizer should represent 50% of the flour in the recipe.  Sorghum and rice flour are the two most common stabilizer flours.  Sorghum flour yields a smooth, light texture whereas rice flour is coarser.  I love the texture of baked items made with both.  The other flours you choose can make a dramatic difference in the outcome.  Enhancer flours make up the other 50% and include teff, amaranth, nut meal, bean flour, starchy flours or quinoa.  These can be mixed and matched—25% of one, 25% of another.

Alternative Flours

Sorghum flour is the workhorse of gluten-free baking.  I think of it as the primary flour for most baked goods and build around it.  

Brown Rice Flour is the other workhorse / stabilizer flour.  It is considered a whole grain.  Some manufacturers grind whole grain rice flour more finely.  For example, Authentic Food’s brown rice flour yields an item with a smoother texture than Bob’s Red Mill’s brown rice flour.  Both are good, depending on the outcome you desire.  

Teff is considered one of the highest protein grains.  It is high in fiber and carbohydrates.  Considering that the world’s best marathon runners come from Ethopia and their staple grain is teff, athletes would be well-advised to incorporate teff into their diets.   

Amaranth and Quinoa flour can be dry-toasted in a pan which adds a nutty taste to the tortilla.  Just add the flour to a sauce pan and turn the heat on medium/high.  Keep the flour moving until it turns brown.  Cool and use in the recipe.  

Buckwheat, in spite of its name is not derived from wheat.  It adds a distinctive taste and light texture to baked goods.  

Tapioca Flour is made from my favorite root—the yuca root or cassava plant.  It enhances elasticity when added to the flour mix.  

Potato Flour is very starchy and will make the final product lighter.  

Nut Meal adds texture and protein.  Nuts can be ground coarsely or finely depending on your taste.  Some easy-to-find nut meals include almond meal and hazelnut meal.  If you have a food processor, you can grind your own.  Just don’t add oil or liquid, or you’ll end up with nut butter! (If this happens, add salt and enjoy it on a tortilla!)  

Corn Flour comes in several different varieties.  Masa Harina is corn processed with lime, ground finely and commonly used for tortillas.  A more coarse grind is corn meal, and the most coarsely ground is polenta.  I wouldn’t recommend using polenta for corn tortillas because the texture is too coarse, but cornmeal works well.  

Bean Flours add lots of protein and make the final product a bit lighter.  Try garbanzo, fava, navy or pinto bean flour in your tortillas.   

Liquids

Most people use water when making tortillas, and that is perfectly fine—but you could be creative with the liquid too and make some interesting compliments to your food.  For example, if you plan to stuff them with roasted vegetables, consider using vegetable juice for the liquid.  Herb teas or broths are other liquids to consider.  

Tortilla Techniques

Most traditional tortilla recipes call for lard or saturated fat.  Substituting oil means the preparation is a little different.  Use warm water, and mix the water and the oil together separately.  Then combine the water/oil mixture with the flour and salt.  Then, with a whisk, incorporate the water and flour mixtures.  Oiling your hands before forming the balls keeps the moisture in the dry, gluten-free dough.  Let the dough balls rest a few minutes.  This yields a lighter product.  A tortilla press is a true kitchen marvel.  Corn tortillas are usually pressed in a tortilla press, and wheat flour-based tortillas are usually rolled with a rolling pin.  That is because the gluten in wheat flour is more resistant to pressing.  Gluten-free flour tortillas work well in a tortilla press.  If you have one, place plastic wrap on the top and bottom plates of the press.  Place the ball off center toward the hinge and press until the dough reaches the outside of the press.  Transport the dough on the plastic wrap to the griddle.  If you use a rolling pin, oil it before rolling out the dough.  It is preferable to cook tortillas on a cast iron tortilla griddle because they hold the heat, but any frying pan will work too.  Press the tortilla while it is cooking with a pancake turner.  Flip it once and cook the other side.  

My upcoming book Delicious Delightful Delicacies—GFCF BAKING Cookbook, is a baking primer covering all types of baked goods including many easy-to make tortillas, packed with flavor.  Tortillas can be stuffed with savory beans, fresh or roasted vegetables and topped with fresh chopped salsa or eaten plain as a snack.  Making fresh tortillas is something your whole family can enjoy doing together.  

Alternative Flour Tortillas

Reprinted from Delicious Delightful Delicacies, by Jean Duane.

Ingredients:

• 1 cup brown rice flour
• ½ cup sorghum flour
• ½ cup tapioca flour
• 2 tsp.  xanthan gum
• 1 tsp.  salt
• 1 cup warm water
• 3 TBS sunflower or olive oil

Directions:
Whisk together the flours, baking power, salt and xanthan gum.  Separately mix water, and oil together, then add to the flour mixture.  Mix with hands or a pastry whisk until incorporated.  Oil hands and form dough into 8 “golf balls”.  

Place plastic wrap over the bottom of a tortilla press and put a ball of dough on the plastic wrap.  Place another piece of plastic wrap on top of the dough, and slowly press the tortilla with the press until it is flattened.  (Or, roll the dough out on waxed paper with an oiled rolling pin.)

Heat an oiled cast iron pan or griddle and place the tortilla on it.  Press it while it is cooking.  When browned, turn and cook the other side.  Place in a tortilla warmer until ready to serve.  

Celiac.com 12/18/2020 - This understanding of viruses is actually the culmination of my study—and the reason why my book has not been written—yet.  I have been waiting for the “punch line” and this is it—how we actually reap what we sow in our physical lives.

All it takes is a brief review of virology and what these little guys do in nature—which is vital to the creation and its moment-by-moment operation—and then we can see the truth about why it has all gone wrong.  Am I over-dramatizing?  I don’t think so.

Simply put, viruses were made to adapt.  They also are integral in the variation we see in nature.  The other essential piece of information you need is how they incorporate their genetic information into ours.  Once again, it is a scientific FACT that we have more viral information in our double stranded DNA than we do genes.  Wow—does that answer a lot!

So, do the genes that code for your eye color or the fact that you have two rams, two legs, one liver, and one nose suddenly mutate and give you a “genetic” disease?  No, it is the viruses embedded in that DNA that do this.  They have been there for generations and new ones are added with each generation.  The acquisition of viruses was meant for good—to help us to adapt to our ever-changing environment.  So, we should really thank someone who gives you a virus, shouldn’t we?  If we were optimally healthy, we would acquire the guy and get on with our healthy lives.

BUT, because of what we have done to ourselves, the environment, and the animals that harbor many of these viruses, some of the viruses have become “virulent”.  Yes, they have been FORCED into adapting into something stronger because of what we have done.  Once again, we reap what we sow.

Then, as we become more and more unhealthy while continuing to challenge our viral inhabitants with lectins, chemicals, pollution and “carcinogens”, we reach critical mass.  Our immune system IS the governor of this situation and is constantly trying to control this situation.  We have all heard it said that we are fighting cancer at every moment of every day.  Yep.  So, what happens when we “assassinate our governor” by doing what we do?  Yes, the poor nutrition, malabsorption syndromes caused by the “big 4” food intolerances, the lack of sleep, the chemicals, and more are ALL bullets that were firing away at our governor.  Once again, we reap what we sow.

With an ineffective, bullet-riddled governor and the continuation of the virus-challenging process, we lose our grip while the viruses are forced to adapt into something more powerful just to survive (which again is what they were charged with from the beginning—to adapt at all costs—even to our detriment if it came to that).

Think of them as little robots.  Well hey—look at them.  Most of them LOOK like little robots.  Have you seen them?  They have a head that looks like the geodesic dome of the Epcot center.  They have legs like a lunar lander and are very mechanical looking.  So, the analogy is most accurate.  Are they living or not?  A great debate rages on about this.  I think they have to be, just not by the standards that we normally use for “living”.  Think of them as androids.  Yeah, that’s it.

And yes, once backed into a corner, they play their ultimate card—to induce a tumor that protects them and the cells in which they reside—a fortress that walls itself off from these continued challenges.  I used to think they were trying to escape the immune system—now I know better.

And, does a single tumor in a lung lobe or lymph node kill anyone?  Hmmm—how about the drugs and radiation designed to kill that tumor?  Hmmm—again.  Oh oh.  And what’s more, what does a virus get forced into doing if its new cocoon is threatened?  MOVE, right?  Yes, that is called metastasis.  So simple, so clear—right?

Question: Would cancer resolve IF we did enough right by stopping what we are doing that is driving these viruses crazy?  We know we can prevent cancer by doing these things, right (Unfortunately, it is more appropriately put that we can accelerate cancer by doing enough bad things)?

But could we take a person who has cancer (or any chronic viral disease), move them to a pristine location, feed them perfectly, give them unpolluted water, and alter their lifestyle so that they sleep well and get plenty of exercise and have that cancer or condition resolve?  I believe the answer is a resounding YES, YES, YES.  There is plenty of evidence of this.  We hear stories of people curing themselves of cancer, MS, and other serious conditions and dismiss them because we simply don’t believe that we can recover from such things.  What an attitude, eh?  Where did that come from anyway?  When did we lose faith in this miraculous body?  And when did we start the process of literally handcuffing its attempts to heal itself by taking all of this symptomatic medication (e.g., NSAIDS to reduce fevers caused by viruses)?  I know when and it fits like a glove into man’s history.

I no longer put any limitations on what this body can do, only one what WE can do for our body.  Does that pristine environment exist?  Can we eat perfectly with what we have done to our food supply?  The good news is that we don’t necessarily have to be perfect.  The absolute worst of the worst do, unfortunately.  But everything I have learned about medicine in the past six years screams at me that we are made to recover.  We just start too late and rarely do enough—right?  But once we see that disease is a “spectrum disorder”, with its victims ranging from the “best of the best” to the “worst of the worst”, we can easily see why some people get better with “holistic” treatment and others do not.  Have those that don’t done enough right?

So, what IS the cure for cancer?  Does the answer lie in the laboratory?  Is it hidden in the jungles of South America?  OR does it lie within us all?  I think we all really know the answer to this one now, don’t we?  And once again—how cool is that?

Celiac.com 12/12/2020 - Italia—the land of superb food.  When you think of Italian food, chances are that the first thing that comes to mind is pasta.  Do you know that rice and corn pasta can be every bit as luscious as wheat pasta when cooked properly?  (The secret is not to overcook it.) So indulge in the scents and tastes of Italy’s best known delicacy.

Rice is a popular ingredient in Italy, especially risotto.  Risotto is made with medium-grain Arborio, Vialone or Carnaroli rice.  Cooked, the rounded grains are firm and creamy due to their high starch content.  To make risotto, cook the rice briefly in butter or olive oil until evenly coated and the rice starts to turn translucent, then add broth, one ladle at a time.  One popular dish is Risotto a la Milanese, made with chicken or beef stock and saffron; it is traditionally served with osso buco (a stew made from veal bones).  

Cannelloni beans (white kidney beans), or fagiole, taste a lot like Great Northern beans and are the pride of the Tuscany region.  The beans are boiled, then sautéed in olive oil with sage and tomatoes.

Italian cooking is impossible without herbs, preferably fresh herbs.  Basil is a staple and is used in salads, on meats, and definitely in tomato sauce.  The best way to prolong the life of fresh herbs is to wash them, wrap them in a paper towel to soak up excess moisture, then store them in a plastic bag in the refrigerator.  Other “musts” for Italian foods are fresh parsley, oregano, rosemary, sage and thyme...and then there is glorious garlic!

The purple carciofi (artichoke), has little resemblance to the artichokes we find in the produce sections of American grocery stores.  In Italy, artichokes are cooked in every conceivable way, including braising, stuffing, stewing, frying, broiling and grilling.  If you have never cleaned an artichoke, the first time may be a bit daunting.  First, fill a large bowl ¾ full with water and add the juice of one fresh lemon.  With a sharp knife, trim off all but one inch of the stem.  Break off and discard the older, tough, outside leaves.  Cut off the top 1/3 of the artichoke and discard.  The easiest way to remove the choke is to cut the artichoke in half and scrape out the fuzzy center and prickly leaves, rinse, then place in lemon water until ready to use.  Roast these delicacies in tomato sauce, or prepare au gratin, or pan-fry—but do make them and enjoy their succulent taste.

Filling or stuffing vegetables is an accomplished art for Italians.  Some fillings are as simple as removing the center of a vegetable, chopping the centers and mixing them with herbs and spices and some cheese, placing the filling back in the shells then baking.  But more frequently the vegetable is stuffed with a meat, pasta or rice filling.  Add a side salad and a slice of gluten-free bread and you have a complete meal.  Stuffed peppers are a regular stand-by, as are stuffed onions, eggplant, and zucchini.  The large yellow zucchini flowers are often stuffed with ricotta or shredded potatoes that have been sautéed in a spicy tomato sauce.

Italy invented the antipasti (or ‘antipasto’ as we call it).  The purpose of this array of sampler foods is to stimulate your senses before your meal, wake up your appetite.  A typical antipasti platter in Italy includes an endless choice of vegetables (roasted, grilled, marinated and fried), cold meats (usually prosciutto and salami), olives and wedges of aged Parmesan, mozzarella or goat cheese, along with platters of seafood salad, and perhaps steamed muscles and clams.  

Italy also lays claim to fame for cornmeal polenta.  Polenta can be creamy, served soft with a scoop of sauce, or firm and served as a side dish to grilled or roasted meats, or stirred into soups and stews to thicken and add flavor.  Whatever way you choose to eat polenta, the basic principles of preparation remain the same:   Bring 4 ½ cups of water to a boil in a medium saucepan.  Add 1 tablespoon salt and reduce the heat to medium low.  As soon as the water begins to simmer, start pouring in 1 cup cornmeal in a thin stream, very slowly while stirring constantly with a wooden spoon to prevent lumps.  Once all the cornmeal has been added, keep the water at a simmer and stir frequently.  It should take about 20 minutes to fully cook the polenta.  When fully cooked, the polenta should pull away from the sides of the pot easily.  Once your polenta is cooked, you can serve it soft or firm, baked, fried or grilled.  You can top it with butter or marinara sauce, or add cheese, browned crumbled sausage or shredded veggies to the cornmeal mixture.  

But what is Italian food without pasta?  The gluten-free pastas need a bit more watching while the pot is boiling to prevent them from falling apart, but with the right sauce...  magnifiquo!   While marinara sauce may be the first sauce to come to mind, aglio olio (garlic oil sauce) is also an Italian favorite.  All kinds of things are folded into the pasta or spooned on top:  pesto sauce, sausage and peppers, shrimp and tomatoes, ham and beans, or sun dried tomatoes and olives.  

Using a spoon as a loading zone for the pasta strands is and American, not Italian, tradition.  In Italy, they just swirl the strands onto their forks which often results in a larger yield than the mouth can accommodate.  So what is the perfect method for gathering the pasta in a dish?  Gather only three or four strands on your fork before twirling.

Formal entertaining in Italy is done by serving multiple courses of small amounts of food.  Prior to the first course being served, the antipasti (appetizer) platter is presented for consumption.  This is followed by a first course of either soup or pasta.  The second course is an entrée of either meat or fish with a side of vegetables.  The final course at an Italian table is the salad, which seems both to refresh the diner after a heavy meal as well as cleanse the palate before the dessert course.

The dessert course is usually served in two stages.  Stage number one consists of ice cold fresh fruit often served with nuts.  Then comes the final offering of something sweet like tiramisu, biscotti or an ice.  Espresso coffee is served throughout the meal and dessert.  

Nutty Biscotti by Connie Sarros

This recipe is from the new book I co-authored with Danna Korn: “Gluten-free Cooking for Dummies” (a sequel to Danna’s “Living Gluten-free for Dummies” book). 

Biscotti are perfect to keep on hand.  They will hold several days in a plastic self-seal bag or in a covered plastic container.  After the second baking, these ‘sticks’ will harden a bit, so be sure not to over bake them.  If you want to live life on the wild side, soak some dried cranberries in Kaluha, and then fold them into the batter.

*My flour mixture already contains xanthan gum.  If you are using a different flour mixture, add 1 ½ teaspoons xanthan gum to the dry ingredients.

Ingredients:

• ¾ cup blanched slivered almonds
• 3 tablespoons butter, softened
• 2/3 cup sugar
• 2 eggs
• 1 teaspoon vanilla
• ¼ teaspoon almond flavoring
• 1 ½ cups gluten-free flour mixture*
• 1 ½ teaspoon baking powder
• 1 teaspoon baking soda
• 1 teaspoon gluten-free instant coffee granules
• 1/8 teaspoon salt
• ½ teaspoon cinnamon
• ½ cup gluten-free miniature semisweet chocolate chips 
• 4 ounces semisweet chocolate
• 1 teaspoon corn oil

Directions:
Preheat oven to 350F degrees.

In a small skillet, sauté almonds in 1 tablespoon butter until golden, stirring frequently.  Remove from heat and let cool.  Line a baking sheet with wax paper (or parchment paper).  Set aside.  In a medium mixing bowl, whip together 2 tablespoons butter, sugar, and eggs on high speed until mixture is thick and fluffy (about 5 minutes).  Add vanilla and almond flavorings.

In a small bowl, whisk together flour mixture, baking powder, baking soda, coffee granules, salt, and cinnamon.  Add flour mixture to egg mixture, beating just until thoroughly combined.  Fold in chocolate chips and almonds.

Transfer dough to wax paper (or parchment) lined baking pan.  With damp hands, form dough into a log about 14 inches long and 2 inches high (Dough will be somewhat sticky to work with but don’t add more flour or your biscotti will turn out dry).

Bake for 25 minutes or until just beginning to brown on the outside and firm to the touch.
Remove from oven and let cool for 10 minutes.

Gently slice log into ½-inch slices.  Stand slices upright on a cookie sheet.  Bake for 20 minutes until firm (but NOT rock hard) and golden.  Remove from oven and cool.  Cut semisweet chocolate into small pieces and place in a medium skillet with the oil.  Heat very slowly, stirring often, until chocolate has melted.  (If heat is too high, chocolate will burn.)  Remove pan from heat and dip bottoms of biscotti in chocolate to coat.  Set each piece on its side on a piece of wax paper to dry.  Yield:  18 slices.

Celiac.com 12/08/2020 - Are you confused about genetic testing for celiac disease? Do you want to know what tests you should request and which laboratory to use?  Have you already had celiac DQ genetic testing but are not sure what the results mean or what your risk is of developing celiac disease or gluten sensitivity? These are the questions I will answer in the next few pages.  

What is HLA DQ celiac genetic testing?

To understand celiac DQ genetics and the risk estimates you must also understand how the DQ types are determined and some basic terminology.  Each of us has 46 chromosomes, 23 pairs received from our parents.  We all have two copies of chromosome 6, one from each parent.  Homozygous is when a person has two copies of the same gene, one from each parent.  Our white blood cells (leukocytes) have proteins called human leukocyte antigens or HLA proteins that are inherited from our parents.  The genetic code that determines our HLA patterns resides on chromosome 6.  

We all have two DQ patterns, one from each of parents, such that we are all DQx/DQx, where x is a number between 1 and 9.  I am DQ2/DQ7 and my wife is DQ2/DQ5.  We are both therefore heterozygous for DQ2.  That is, we have only one copy of DQ2.  Scott Adams, the founder of celiac.com is DQ8/DQ8.  He is homozygous for DQ8.  There are several HLA patterns.  Some are proteins that reside within cells and others are on the outer surface of cells, and are called class II.  The class II HLA proteins have very important immune functions.  There are several class II HLA protein types but DQ have been found to be important in celiac disease, specifically DQ2 and DQ8.  

What does it mean to be homozygous or heterozygous for celiac genes?

Homozygous means that you have two copies e.g.  DQ2/DQ2, DQ8/DQ8 whereas heterozygous means you have one copy of DQ2 or DQ8.  Some people have one copy of DQ2 and one of DQ8 (DQ2/DQ8) and they have a greater risk for celiac disease than someone with only one copy of either DQ2 or DQ8 but not as great a risk as someone with two copies of DQ2 (DQ2/DQ2).  Since DQ2 is associated with a greater risk of celiac disease than DQ8, then one copy of DQ2 plus a DQ8 (DQ2/DQ8) indicates a higher risk than having two copies of DQ8 (DQ8/DQ8).  Hopefully, I have not lost you yet but if I have please continue to read on because the information that follows will still be helpful to you.  

What is this alpha and beta subunit typing and why is it important?

HLA DQ typing consists of two subunits of the DQ molecule, an alpha and beta subunit.  So, both DQ types that indicate a risk of celiac disease, DQ2 and DQ8, are made up of two protein subunits designated alpha and beta.  They determine the complex letter and number combinations reported.  For example, the full DQ2 molecule is typically HLA DQA1*05xx DQB1*02xx.  The A1 is the alpha unit and the B1 is the beta subunit.  

The beta subunit is the most important component of the DQ molecule, but the alpha subunit has also been shown to carry an increased risk for celiac disease.  Unfortunately, since testing for both is more complicated and expensive it is not always done.  

Also, some think that since the beta subunit carries most of the risk and the alpha unit only minor risk, testing for only the beta subunit is adequate.  Several clinical laboratories have chosen this approach.  They only test for, and report on, DQ2 and DQ8 based on beta subunit types, so their results typically look like this: HLA DQB1*02 detected, DQ2 positive, etc.  This is the policy of the laboratory at Bonfils, who also does testing for Quest Diagnostics and Enterolab as well as many hospitals.  However, the alpha subunit of DQ2 also carries some risk for celiac disease.  

What if you are positive for the beta subunit of DQ2 or DQ8 by testing from Bonfils, Enterolab or Quest?

If the beta subunit is present then Bonfils, Enterolab and Quest tests will report DQ2 and/or DQ8 positive.  Sometimes the report will just report DQ2 negative and DQ8 negative, especially when a hospital is reporting the results obtained from Bonfils.  However, when the beta subunit is not present and they report DQ2 negative and/or DQ8 negative, it is still possible that an alpha subunit could be present.  Results reported in this manner are, in my opinion, potentially misleading.  I believe they can lead a doctor to assume that an individual is not at increased risk for, or cannot have celiac disease, when this may or may not be true.  Unfortunately, the patient in such circumstances may be told that they can not have celiac disease, yet they may not only be at risk for the disease, they may well have it while being told it is impossible or extremely improbable.  

What does Prometheus do and how do they report their results?

Prometheus, like Kimball and LabCorp, includes alpha and beta subunit typing.  In the past they did not indicate whether there was one or two copies of DQ2 or DQ8 if someone was positive.  If a patient was DQ2 and DQ8 positive then these labs reported their full genetic DQ type.  However, if one or the other was negative, their exact genotype was not reported.  Recently, not only has Prometheus started reporting the full DQ2 and DQ8 genotype, but they are now reporting whether someone is homozygous or heterozygous as well.  They are also reporting the relative risk for celiac disease based on the pattern shown by testing.  However, they are still not reporting the other DQ types.  

What is the advantage of the new Prometheus reporting?

Since Prometheus results now include a calculation of the individual’s risk of celiac disease, compared with the general population, the patient can see how high their risk of celiac disease is, as well as being able to estimate the risk for their parents and their children.  

As you can see, the risk of celiac disease has a wide range of possibilities, which depend on the individual’s DQ results.  This risk can be below 0.1% if you do not have any portion of the high-risk genes DQ2 and DQ8.  On the other hand, the risk may be very high (more than 31 times the risk of the general population) if you have two copies of the full complement of DQ2 molecule.  Again, I would like to point out that if you have DQ2/DQ2, DQ2/DQ8, or DQ8/DQ8, then both of your parents and all of your children have to have at least one copy of an at-risk celiac gene.  Your child’s complete type will depend on the DQ contribution from their other parent.  

What other laboratories do both alpha and beta subunit testing?

Kimball Genetics and LabCorp also report both alpha and beta subunit results but the advantage of their testing is that they report the other specific DQ types detected.  Gluten sensitivity is found in all DQ types except DQ4.  Other DQ types, particularly DQ1, DQ5, are associated with a risk of gluten related neurological and skin problems.  Microscopic colitis, food allergies and oral allergy syndrome reactions are also found in association with other DQ types.  Though Enterolab does report other DQ types, including these markers of risk for gluten sensitivity, they do not test for, or report, alpha subunits since their DQ testing is done by Bonfils.  Based on the limited data I have accumulated so far, DQ2 and DQ8 also seem to carry a risk of mastocytic enterocolitis.  

What if you do not have DQ2 or DQ8? 

According to data accumulated, but as of February 2008, not yet published by Dr. Ken Fine, unless you are DQ4/DQ4 you are still at risk for being sensitive to or intolerant of gluten.  According to Fine’s fecal gliadin antibody data all DQ types except for DQ4 carry a risk of gluten sensitivity.  My clinical experience supports this claim.  The presence of one copy of DQ1, DQ3, DQ5, DQ6, DQ7, or DQ9, even with one DQ4, is associated with a risk for elevated stool gliadin antibody and symptoms of gluten sensitivity that responds to a gluten free diet.  

What if your genetic testing was done by Enterolab, Quest, Bonfils or a hospital that utilized Bonfils, and it indicated that you were DQ2 and DQ8 negative?  

Since Bonfils does not test for the alpha subunit and they perform the testing for Enerolab and Quest, you may not be completely negative for DQ2 or DQ8.  You do not have the beta subunits associated with the highest risk for celiac disease.  For example, you could be “half-DQ2” positive and still be genetically at risk for the autoimmune form of gluten sensitivity that we know as celiac disease, along with all of its risks.  

What if you have not yet had celiac DQ genetic testing?  

I recommend that everyone have the testing.  I realize that most insurance companies and doctors, including some celiac experts, would disagree with me.  However, the value of DQ testing is that it can provide a great deal of information about your risk, especially if you have testing done for both alpha and beta subunits.  I recommend that you have testing done by Kimball Genetics, LabCorp or Prometheus if you have not yet had genetic testing done.  If your insurance or budget does not allow for this more expensive testing, but does cover testing by Quest or Bonfils or you can afford the $159 that Enterolab charges, then I still recommend that you get DQ testing using one of these laboratories.  You just need to be aware of the limitations of the results as I have reviewed them here.

What are the advantages of DQ testing through Kimball Genetics? 

Kimball can perform testing on either blood or mouth swab samples.  The tests can be ordered without a doctor’s order.  You can purchase testing on mouth swab sample for $345.  The advantages of Kimball’s tests include alpha and beta subunit testing and full DQ typing to determine if you carry the other gluten sensitive DQ patterns besides DQ2 and DQ8.

What about LabCorp? 

LabCorp also provides both alpha and beta subunit testing and they report the other DQ types.  They only provide testing on blood samples, a doctor must order the testing, and preauthorization is required.  

Do health insurance companies cover celiac DQ genetic testing?

Many but not all health insurance companies cover HLA DQ testing and almost all require preauthorization.  The ICD9 diagnostic codes that typically are honored are V18.5 genetic predisposition for gastrointestinal disease; V84.8, genetic predisposition for other diseases; and 579.0, celiac disease.  

Why are the genetics so difficult to understand and why are so many doctors either unaware of the testing or reluctant to order the tests?

I write and speak about DQ genetic testing frequently, and try to get testing for as many of my patients as possible.  However, many insurance companies will not cover the cost of these tests.  Most primary care doctors and even some GI doctors are completely unaware of the existence of a genetic test for celiac disease.  The testing is difficult to understand and the reporting by some labs is very confusing and even misleading.  

I realize that understanding the DQ genetics is difficult for the average layperson.  Most scientists and doctors don’t understand this information, so don’t despair if you are having difficulty following this or understanding your results, and don’t be surprised if your doctor does not understand them either.  However, you do not need to completely understand the complexities of HLA typing to locate your DQ types on figure 1 and determine your risk of celiac disease, non-celiac gluten sensitivity, etc.  

Then what do you need to know or remember about celiac DQ genetics? 

Hopefully, you now understand enough to know that you should consider having celiac DQ testing, if possible, especially if you have symptoms, laboratory tests, or an intestinal biopsy that is suggestive of celiac disease.  You should also know that the testing can be done on blood or mouth swabs, and many insurance companies will cover the testing but most require preauthorization.  You should also be aware that the testing is available without a doctor’s order, if you are willing to pay for it, and that some tests are better than others.  I also hope you understand that the tests can help you determine your risk for celiac disease or if you are at risk for non-celiac gluten sensitivity.  You should also know that your results, especially when combined with those of one or more family members, may help you determine, to some degree, the risks for your parents and your children.  You should also know what laboratories offer testing, what test codes your doctor should use to order the tests, and that the absence of DQ2 or DQ8 does not exclude risk of gluten sensitivity or intolerance.  Depending on what laboratory conducts your DQ testing, your results also may fail to exclude your risk of celiac disease.  

What if I am still confused or I don’t know how to interpret my genetic results or my previous evaluation for celiac disease?

If you are still confused by your test results or want more a personalized review of your results, symptoms or diagnostic tests I recommend that you see a physician who is an expert in celiac disease and understands these tests.  I also offer on-line consultation for a reasonable fee through a secure consultation site, medem.com.  You simply register (registration is free) for secure on-line communication and request a consultation.  The consultation fee is $50, and some insurance companies will cover on-line communication.  I also see many patients from outside of Colorado Springs for consultation if you are willing to travel here.  

Celiac.com 11/28/2020 - Non-celiacs show Interleukin 15 production when challenged with gliadin peptides. A recent study by a team of Spanish researchers puts the world on notice that gluten may trigger adverse reactions in both celiacs and non-celiacs alike.  The research team was made up of Doctors E.  Arranz, D. Bernardo, L. Fernandez-Salazar, J.  A.  Garrote and their colleague S.  Riestra, all based in Spain.  

According to the current medical wisdom, innate immunity to gluten plays a critical role in the development of celiac disease.  This innate immune response is caused by a reaction to the ‘toxic’ gluten peptides that are mediated by a chemical in the white blood cells called interleukin 15, which stimulates these cells to react against foreign proteins like the 19-mer.  The reaction is independent of genetic HLA markers associated with celiac disease.  This causes epithelial stress and triggers the intraepithelial lymphocytes to turn into natural killer (NK)-like cells, which then causes enterocyte cells to die resulting in a compromised permeability of the cells lining of the gut…and, violà, celiac disease! 

It is by breaching this intestinal lining that peptides such as the 33-mer, come into contact with the lamina propria, which triggers general immune reactions.  

The specific response in celiac disease has been pretty well documented, but until recently, no one had described any differential factors between people with celiac disease and those without.  

Since the toxic 19-mer triggers its damaging effects independent of the celiac associated HLA markers, researchers wondered whether the innate immune response was common in people with and those without celiac disease.  They wondered whether the adaptive response is found only in those susceptible to celiac disease.  

The gliadin-challenged patients with celiac disease who were on a GFD, showed increased nitrite levels, which those without celiac disease did not show.  Only patients with celiac disease showed modifications to what are called adaptive mediators (STAT1, STAT3, IFNc).  

The samples of those celiac patients on a gluten-free diet showed interferon levels that were 80 times higher than those without celiac disease, along with a slightly higher production of nitrites.  

This appears to be the first time that researchers have described an interleukin 15-mediated innate response to gliadin and gliadin peptides in people without celiac disease, as well as the first time they have described an IL15-mediated innate response to the ‘non-toxic’ deaminated immuno-dominant 33-mer peptide.  

What this all means is that, for the first time, scientists have documented harmful effects of gluten on people without celiac disease.  This hypothesis seems to be born out by the fact that all individuals who took part in the study, both those with and those without celiac disease, showed an innate immune response to gluten, though only those with celiac disease showed an adaptive immune response to gluten.  

Clearly, before doctors can draw any hard and fast conclusions, they will need to do more studies on larger groups.  

The research team also suggests that people with celiac disease have a lower threshold for triggering an adaptive TH1 response than do non-celiacs.  

The reason for the differences in threshold levels between celiacs and non-celiacs might be the result of higher levels of immune reactions in celiac patients compared to those without celiac disease.  That’s one possibility.  

The difference in threshold levels might also have to do with some kind of defect in permeability of the gut membrane in those with celiac disease, or a greater immune sensitivity to equivalent quantities of toxic gliadin fractions which might come from a higher density of interleukin 15 receptors in patients with celiac disease.  

Source: Gut 2007;56:889–890

Celiac.com 11/21/2020 - A light snow is falling and the air carries a December chill.  I am reminded of my brother's death on a similar day eleven short years ago.  During the preceding year, doctors refused to test my brother for celiac disease following his diagnosis with lymphoma.  Their stated reasons were that celiac disease is too rare to be considered, he showed none of the classic signs of celiac disease, and his lymphoma, a separate and more serious illness, needed to be addressed first.  One physician even stated that the gluten-free diet was nutritionally inadequate and it would deprive my brother of the meal-time pleasures of a regular diet "during the time he has left." Celiac disease, I was told, could be investigated after the lymphoma was resolved.  Concurrent and subsequent discussion revealed that my brother's death was the resolution they expected.  At that time, only a small pocket of researchers, along with a group of informed physicians (and others) who managed to stay current with the medical literature regarding celiac disease, were aware that it can be a large underlying contributor to lymphoma and other cancers, and institution of a gluten-free diet can provide some important benefits to those battling cancers in the context of celiac disease.  

Aside from the obvious objections to claiming that Jack would enjoy food—any food—during multiple courses of chemo and radiation therapy is suspect, and that it might have been valuable to forestall prophesying his death until after these treatments were at least begun, a number of larger objections arise out of these physicians' confident disregard for the medical and scientific literature.  The pervasive attitude was one that trivialized celiac disease and dismissed any other form of gluten sensitivity.  Fortunately, an emerging paradigm is supplanting these outdated prejudices and the last decade has witnessed huge gains in physicians' and public awareness of celiac disease.

Students of celiac disease, dermatitis herpetiformis, and gluten syndrome (non-celiac gluten sensitivity) know that gluten induced illness is far from rare and can manifest in an enormously wide range of signs and symptoms.  Turn-of-the-century publication of multi-center research has established that celiac disease, far from being rare, is found in about one percent of the U.S.  population.  Most of these individuals also lacked the classic signs and symptoms of celiac disease.  Further, the rate of gluten syndrome is at least ten times that of celiac disease, and gluten antibodies are very frequently found among those with neurological disease.  The research team headed by Marios Hadjivassiliou at the Royal Hallamshire Hospital in Sheffield, England has shown that more than half of patients suffering from neurological ailments of unknown origin are gluten sensitive.  (Most neurological diseases are of unknown origin.) Another group working at the University of Alberta, led by B. Yacyshyn, reported leaky gut in twenty five percent of a group of twenty multiple sclerosis patients, so gluten is an important suspect in at least some cases of one neurological disease that is fairly well characterized.  Another report of just two patients shows that a gluten-free diet can abolish islet cell antibodies that destroy insulin producing cells in the pancreas.  These antibodies are the basis of type I diabetes.  Other reports show that obesity can be induced by gluten and mediated by a gluten-free diet.  Still others report amelioration of psychiatric illnesses, behavioral abnormalities, and/or learning disabilities as the result of a gluten-free diet.  Most students of the gluten syndrome are learning about this wide range of signs, symptoms, and associated illnesses.  Many of us have experienced improved general health along with subtle improvements across a range of modalities and perceptions.  Many of us suspect that these changes exceeded what could be expected to arise from improved general health.  When learning about the protean manifestations of gluten induced illness, those suspicions are affirmed.  

It is through sharing this learning that celiac disease and gluten syndrome have begun a shift from the fringes of our culture to widespread, mainstream awareness of gluten induced illness in all its manifestations.  Much of the research community involved in celiac disease has led the way.  Increasingly informed (largely through the Internet) patients and their support groups have moved awareness of celiac disease from obscurity to mainstream in little over a decade.  Recognition of gluten syndrome lags far behind celiac disease, but is increasing rapidly.  The final, large step in this process of enlightenment is to assist those struggling, straggling, overworked general practitioners get up to speed on this most common illness.  These are the individuals who continue to ignore the literature on this topic.  They confidently dismiss the possibility of celiac disease or gluten syndrome on the basis of an out-dated, often prejudiced, largely erroneous understanding of gluten-induced illness as it was taught during their training.  

The sadness of my brother's passing has abated to the point where I can now think and talk about it without the sense of emptiness and loss that comes of knowing that I won't see him again—and without the anger and frustration borne of the widespread medical ignorance at the general practitioner level.  Today, I can freely share my brother's painful, final journey in the hope that it will hasten the abolition of the medical ignorance and arrogance that helped speed his untimely death.  I still struggle with the memory that my brother's doctors complained to Jack about my badgering them to test him for celiac disease.  They complained to a dying man about my annoying letters, while they ignored my repeated pleas that he be tested for celiac disease.  I am still chagrined by their dismissal of research showing a substantial genetic component in celiac disease, knowing full well that I, his brother, had previously been diagnosed with celiac disease.

During the eleven years since my brother's death, an emerging awareness of gluten mediated illness has blossomed throughout the industrialized world and has reached tentacles into the third world.  Although knowledge of the health hazards of gluten is spreading world-wide, recognition of gluten's threat to human health is still an emerging paradigm.  Another decade of dedicated effort on the part of support groups, researchers, and others, should have celiac disease appearing frequently in the differential diagnosis for an enormously wide range of signs and symptoms, with gluten syndrome following on its heels.  And perhaps a gluten-free, dairy-free diet will soon be standard fare for most cancer patients, freeing their immune systems to battle malignancies rather than gluten.

Celiac.com 11/06/2020 - Discussion of Celiac Disease and gluten intolerance often centers on symptoms, gluten-containing foods to avoid, and medical treatments.  But did you ever wonder why gluten negatively affects us?  And did you ever think that there just might be a single cause for a multitude of modern diseases?

A Very Brief Human Dietary History

Thanks to modern archeology, we know that humans have inhabited this big blue ball for more than two million years—and we know both the types of foods consumed by our ancestors and the means used to obtain them.  For the overwhelming majority of that time, our subsistence method has been that of the hunter gatherer.  Only within the last ten thousand years, at most, have humans consumed the gluten-containing products of agriculture, transitioning from what is sometimes called the Paleolithic, or hunter gatherer, period to the Neolithic, or farming and ranching, period (That’s ten thousand years if your genes happen to be from the Fertile Crescent in the Middle East.  That number shrinks to about one or two thousand if you are of northern European descent—and even much less than that if your genes are from African, the Americas, or another origin that has recently shifted to Neolithic food production and consumption).

So what does this mean?

It means that humans have been consuming agriculture-derived foods at most for one half of one per cent of our time here on earth.  It means that grains (gluten-containing or not) aren’t natural food for human beings and that, not surprisingly, there are negative health consequences for consuming, in volume, anything outside our natural range of foods.

But wouldn’t humans have consumed wild grains, at least in times of scarcity?

First, the idea that hunter gatherers frequently experienced scarcity is exaggerated.  The idea is based on studies of modern hunter gatherers who have been forced to the fringes of habitable land by modernity.  More recent evidence shows that our ancestors did not live that way.  In fact, science has not only shown a general abundance of food among pre-modern hunter gatherers, it has also revealed that, in contrast to our own, these people lived lives of comparative leisure.   

Second, all grains are tiny grass seeds that require quite a bit of labor in order to extract minimal energy.  Wild grains were even smaller and less energy dense than today’s grains.  Given the abundance of game, fruit, nuts, and other food sources during the Paleolithic, it would take a lot of work for relatively little reward, even if these wild grains were considered a desirable food.  One would have to be rather desperate to even try to rely upon grains as a primary food source.  (This may be exactly what happened 10,000 years ago, perhaps due to widespread population growth or famine, leading our ancestors to abandon the Garden of Eden and pick up the plow).

But haven’t we evolved since the adoption of agriculture to tolerate gluten-containing grains?

Well, obviously the subscribers to this newsletter haven’t!  While it’s clear that celiacs and the gluten intolerant should abstain entirely from consuming gluten-containing foods, frankly the concept that any human ought to consume any grain in any form, gluten-containing or not, is debatable.  No doubt some adaptation has occurred for those populations who have been exposed to the products of agriculture long enough—but who knows how long it would take to develop full tolerance?  And at what price in terms of numbers of years and numbers of human lives?  It may be true that some grains such as rice may be less harmful to human health, but it is clear both that human adaptation to cereals has been partial at best, and the best diet for all human beings is still one that most closely mimics what we’ve been eating for millennia, the hunter gatherer or “paleo” diet.

So what did our ancestral diet look like?

While humans have consumed a remarkably wide range of foods as hunter gatherers, there are some constants.  First, although it may make some of our vegetarian friends uncomfortable, humans have always been omnivores and therefore meat eaters.  Science has shown that the enlargement of the human brain was consequent with increased carnivory.  And while there is some debate as to which vegetables (and how much) were consumed by our ancestors, it is clear that until very recently we never consumed modern staples such as corn (which is really a grain not a vegetable) or legumes (including peanuts!).  There is also considerable debate about whether tubers are paleo since they require cooking, which came on the scene relatively late.  But very few Paleolithic dietary experts will deny that leafy green vegetables are a safe and healthy bet.  Fruits were, by and large, only consumed in season and, unlike most modern examples, were always high in fiber and low in sugar.  True nuts were also available only in season.  

Now comes a shocker: Dairy was very rarely consumed if ever before the Neolithic revolution.  As paleo author Ray Audette put it, you try milking a wild-eyed wildebeest!  Milk is something that was only sourced directly from the mother’s breast for the first few years of life—more than sufficient calcium was obtained from the diet.

The paleo diet

We all know that gluten is the direct cause of celiac and gluten intolerance.  We know that we can avoid symptoms by simply avoiding foods and other gluten containing products.  But using light shed by modern anthropological discoveries of the natural, ancestral human diet, we can now apply the paleo template and see why gluten affects us as it does.  It’s not difficult to see that our newfangled Neolithic diets are causing not just celiac disease and gluten intolerance, but potentially a host of other diseases caused by dietary divergence from our evolutionary past.

Resources:

• Books: The Paleo Diet by Dr.  Loren Cordain; Neanderthin by Ray Audette; Protein Power Lifeplan by Drs.  Michael and Mary Dan Eades (a very poorly titled but strong book that deserves to be read cover to cover, especially the chapter on gluten intolerance entitled “The Leaky Gut Syndrome”);
• The Rosedale Diet by Dr.  Ron Rosedale; Dangerous Grains by James Braly and Ron Hoggan
• Published Research: Cordain, L., Cereal Grains: Humanity’s Double Edged Sword, World Rev Nutr Diet.  1999;84:19-73.

Celiac.com 10/31/2020 - Since this article was originally published in 2008, the tTG test has become the standard for celiac disease screening, while a newer test called "Deamidated Gliadin Peptide (DGP)" is now considered the best for CD, and the company 2G Pharma is unfortunately no longer in business.

Do you know someone who might benefit from a celiac blood test? Maybe they are too shy to assert themselves.  Or maybe they’ve been turned down flat by a physician who is not current with the medical literature on celiac disease.  As many of us know, asking for celiac testing is sometimes like hitting a brick wall.  Stories abound of incorrect diagnoses, cavalier indifference, dismissal, denial, frustration, illness, often leading to a pervasive sense of futility.  Each of these stories is punctuated by pain, illness, heartache, and sometimes, death.  For the lucky ones, a health care professional who is well versed in celiac disease sometimes furnished the answer.  Others found their own way to a gluten free diet.  Until now, most have not been so lucky.

However, the brick wall is starting to crumble.  A powerful force is poised to bring new hope to that unlucky, unhappy, unhealthy majority of untreated, undiagnosed group with celiac disease.  2G Pharma Inc.  is now offering an at-home test for IgA tissue transglutaminase antibodies (tTG) called the Biocard celiac test.  Although currently only available in Canada, it can be ordered over the Internet for only $50.  Although  not yet approved by Health Canada, the newer version also tests for IgA deficiency, and will thus be more accurate than the celiac testing offered by many conventional laboratories (because they often fail to consider IgA deficiency).  

Few physicians would deny the extreme likelihood of celiac disease in the context of positive tTG test results.  If the test shows IgA deficiency (when approved) although it is not as reliable an indicator of celiac disease, it would also be well accepted as indicating the need for further investigation for celiac disease.  So this new test is offering something very special, and for a very small price.  

Those of us who are familiar with celiac disease know that if it goes untreated it can pose a wide range of challenges.  Untreated celiacs can appear healthy.  Or they can manifest just a single sign or symptom such as isolated iron deficiency or osteoporosis, or rheumatoid arthritis or cancer or thyroid disease or a brain disorder or a fertility problem.  On the other hand, untreated celiacs can also show a confusing array of signs, symptoms, and associated autoimmune disease.  Still others will report concerns and symptoms that seem more like psychological complaints than physical manifestations of a diet-driven autoimmune disease.  For instance, we now know that there are more overweight and obese individuals with untreated celiac disease than there are underweight celiacs.  That is what they mean when researchers talk about the protean manifestations of celiac disease.  

Whatever the symptom, sign, or ailment, it can stand alone as the sole indicator, or it can be one of a constellation of problems that are due to, or associated with, an underlying case of undiagnosed celiac disease.  Yet few physicians will make the connection.  Until now, most cases of celiac disease will never be diagnosed because medical professionals are taught to look for a consistent complex of signs and symptoms.  Most believe that untreated celiac patients are gaunt, wasted, sickly, and have protruding bellies.  While this may have been true in the past we now know that celiac disease is difficult, often impossible, to identify on the basis of symptoms.  Objective testing is often the only way that celiac disease can be diagnosed.  

Thus, this new test will identify the vast majority of untreated celiac patients.  And the test is easily defended against those who might look askance at home testing.  Korponay-Szabo et.  al.  report in Alimentary Pharmacology and Therapeutics that this test is 97% specific and 97% sensitive (1).  Test sensitivity is determined by how many celiacs are identified by a positive test.  Only 3% of those with celiac disease failed to be identified by this test.  However, the one celiac patient that was missed in this research project suffered from IgA deficiency, which is much more common in the context of celiac disease than in the general population.  Further, because the newer form of this test would have identified this deficiency, it is very likely that the patient would be further investigated for celiac disease.  Thus, the test could be argued to have been 100% sensitive in their study.  The same group reported that the test is 97% specific.  That means that the test will show positive in cases of celiac disease as well as in 3% of patients who do not have celiac diseae.  Several other groups of researchers report that many of those who test positive for tTG often go on to develop celiac disease within a few months or years.  

Crovella et.  al., report in Digestive and Liver Disease, similar results but with one important exception.  When this test was used among a group of impoverished individuals who were infected with filariasis its specificity weakened substantially.  People who were infected with this parasite showed positive tTG test results despite the absence of celiac disease.  Thus, despite 100% specificity among Brazilian urbanites, the test was only 76% specific when used to screen impoverished suburban Brazilians.  Thus, although this test is less than ideal in some third world settings among those with filariasis infections, it is clearly a powerful tool for identifying celiac disease in the industrialized world.  

Closer to home, 2G Pharma Inc.  is rolling out this new test in Canada, as I write this column.  I suggested to Janet Monk that there might be a little cross-border shopping.  Her company has chosen to take the high road and avoid the risk of contravening U.S.  import/export laws.  Sadly, many crooks and charlatans feel perfectly happy to send drugs and other dangerous substances into the US.  Yet this young company, offering a simple (but powerful) blood test that could save the US medical system billions of dollars annually, is forced to await appropriate approvals before sending their product into the US.  Bear in mind that it is not a drug.  It is an at-home test for a dangerous disease that goes undiagnosed in 97% of cases in the U.S.  (3) and because of all the associated ailments, takes an enormous toll on at least three million Americans (4).  

I would love to see this product available in the U.S., if only to stem the enormous risk of illness and lurking cancers that have been shown to reduce on a gluten free diet among those with celiac disease.  

If you live in Canada, you can order or encourage others to order the test.  If you live elsewhere, perhaps there is something you can do to make this test available in the U.S.  If nothing else, you can order and make use of the test when you visit Canada.  In the meantime, this grand new test is poised and ready help diagnose the millions of Americans who will otherwise go untested and undiagnosed.  I am confident that some alternative can be implemented to harness this test and get it working for Americans and Canadians alike.  

Sources: 

1. Korponay-Szabó IR, Raivio T, Laurila K, Opre J, Király R, Kovács JB, Kaukinen K, Fésüs L, Mäki M.Coeliac disease case finding and diet monitoring by point-of-care testing.  Aliment Pharmacol Ther.  2005 Oct 15;22(8):729-37.
2. Crovella S, Brandao L, Guimaraes R, Filho JL, Arraes LC, Ventura A, Not T.Speeding up coeliac disease diagnosis in the developing countries.  Dig Liver Dis.  2007 Oct;39(10):900-2.  Epub 2007 Aug 13.
3. Green PH.Where are all those patients with Celiac disease? Am J Gastroenterol.  2007 Jul;102(7):1461-3.
4. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K.  Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study.  Arch Intern Med.  2003 Feb 10;163(3):286-92.