Celiac.com 04/19/2019 - Once you’re diagnosed with celiac disease, it takes just that first trip to the grocery store to get sticker shock from the prices of gluten-free products versus their wheat counterparts.  Consuming food is a necessity but paying a lot of money for that food isn’t.  Food is one of the few monthly expenses where you have 100% control over both selection and the amount of money to be spent. The good news is that there are all kinds of ways to save on your grocery bill.

Planning is a vital step

Take inventory of what you have on hand and think of ways to use up these foods, especially the perishable ones, in the meals you plan for the next week.  Four percent of fresh produce bought by U.S. households is thrown out each year because it was hidden or forgotten in the refrigerator and started to spoil.  Simply by looking through your refrigerator frequently and finding a way to use up the perishables, you can save an average of four percent of your grocery bill.  

While you’re in the planning stage, look online and through the newspaper to find out what the nearby grocery stores have on sale and build meals around those items.  Don’t rely on memory—write out a grocery list and then stick to buying just those items.  According to Personal Finance:

• “Shoppers making a ‘quick trip’ to the store to pick up a few specific items usually purchase 54 percent more than they planned.”
• “Forty-seven percent of shoppers go to the store three or four times each week.”
• “Consumers graze at the grocery store, with impulse buys making up between 50.8 and 67.7 percent of total purchase.”

Imagine how much you’ll save if you do zero impulse buying

The fewer trips you make to the store the fewer times you’ll be tempted to pick up nonessential items.  Save time by creating an on-going shopping list.  On a piece of paper, write down department headings (produce, meats, dairy, paper products, personal products, etc.); make copies of this then post one each week on the refrigerator so family members can add items under the different headings as needed.  

Cutting food waste can be done, but it takes vigilance on your part

When you freeze foods, use a marker to write the date the package was frozen.  Food kept in the freezer too long will develop freezer burn that ruins the taste and quality of the food so use the older items first.  Freeze things in individual servings.  This may sound like a useless step if you have a large family, but there will be times when only three people are home for dinner instead of four or if you’re all going out to dinner but your son has a terrible cold and can’t come along; then you can thaw and reheat just one frozen packet so he has a good dinner. 

Buying in bulk isn’t always better

It’s a challenge deciding if buying in bulk will save you money if you don’t really need that quantity.  If you end up throwing part of the product away, that’s the same as throwing your money away.  If you’re buying paper products and you have room to store a large amount, then bulk buying makes sense.  And don’t assume that bulk pricing is always less than buying smaller quantities.  Sometimes it isn’t.  Do the math before making the purchase.  

Check out what’s on sale but be cautious

Just because a food is advertised in a weekly circular doesn’t mean the price has been reduced.  

Buy what’s in season

You can pay $4.50 for an acorn squash in April, or you can wait until fall and buy it for fifty cents.  Harvest time always offers fantastic savings on produce.  

Use coupons

You can actually cut the cost of your grocery bill by fifty percent just by using coupons.  Don’t fall in love with a specific brand of anything.  If you need laundry soap and you can’t find a coupon for your favorite brand, but a different brand that offers a coupon.  When you make your shopping list, put a star by anything that’s on sale or for which you have a coupon.  Now look at the list and pick out the items without a star.  Go online and type the item name into your browser adding the word coupon (Example:  laundry soap coupon).  With the exception of produce and meats, you can usually find coupons online for most of your purchases.  If you can’t find a coupon, buy the store brand or generic brand.

Check the Internet

You can often save by buying your gluten-free items online.  Again, comparison shop including any shipping costs.  If only large quantities or whole cases are being sold, see if someone in your support group or another celiac will split the case with you.

Forego store loyalty

Many stores offer loss leaders, foods that are selling at a tremendous discount, to lure you into their store.  Go in, buy those particular items, then leave and go somewhere else to do the rest of your shopping.  No single store will have everything you need on special in any given week so shopping at two or three different stores will save you the most money. Check out the prices for paper products and cleaning supplies at dollar stores and big box discount stores; the savings can be significant.

Don’t waste money on packaging

Fresh deli meat will cost less than packaged lunch meat.  Buying one larger container of yogurt costs less than buying several single-serving containers.  Get a large jar of applesauce, a large can of peaches, and a large box of cereal instead of the individual-serving sizes.  

Stretch the expensive foods

Meat is expensive so find ways to use less of it.  If you’re making meatloaf, add an extra egg, oatmeal (uncontaminated), chopped tomatoes, and shredded carrots to get more servings out of a pound of ground beef.  Do the same for hamburgers.  Cook meals that use a lot of vegetables and beans and just a little meat, chicken or fish, such as stews, chili, tacos, and tuna noodle casserole.  Mexican, Italian and Asian dishes are great for this because they’re made up of inexpensive items such as beans, noodles or pasta, and fresh or frozen veggies. 

Fill up on healthy, less expensive foods.  Rice and potatoes are natural carbohydrates, low in price, and give you that satisfied full feeling at mealtime.  Brown rice holds forever in a cupboard and a half cup of raw rice will feed two people once it’s cooked.  Beans are one of nature’s healthiest (and least expensive) food options—fill up on them.  Add them to everything to stretch food further.  You can add beans to salads, soups, stews, rice dishes, casseroles, vegetable dishes, pasta sauce, tortillas and tacos… and the list goes on.

Check out gluten-free bakeries

If you’re lucky enough to have a gluten-free bakery near you, ask if you can get a significant discount on day-old bread.  Gluten-free baked goods have a very short shelf life, but you can pick up several loaves to freeze for when you want to make French toast, bread pudding, stuffing, croutons, or breadcrumbs.

Consider gardening carefully

While it may seem cost-conscious to grow your own vegetables, it’s time to do the math again.  Figure out what you’re going to spend in seeds, water, fertilizer, gardening gloves, perhaps a trellis or tomato cages, and any expenses incurred when you have your own garden, and then compare that cost to what you’ll pay when you buy those same vegetables on sale and in season at a grocery store or farmer’s market.

Don’t rule out prepared foods

While it usually costs less to bake your own cookies and prepare your own meals, gluten-free companies often offer irresistible savings coupons especially when they’re introducing a new product.  Take advantage of these sales.

Only cook what you need

We tend to cook too much sometimes, especially when it comes to pasta.  Gluten-free pasta is expensive so only cook small portions and toss it with a filling sauce that contains sautéed veggies and/or beans to make it stretch further.  

Obesity has reached epidemic proportions and one of the main causes is overeating. We eat ‘till we’re full when we should stop eating when we’re no longer hungry.  There’s a big difference between the two amounts.  If you serve smaller portions, it’s not only better for your health but you’ll be spending less in groceries.

Eliminate sodas

They’re unhealthy and they’re expensive. Ice water or iced tea can be every bit as refreshing and thirst-quenching and will cost you much less.  

Use more of the less expensive gluten-free products

Gluten-free bread is more expensive per slice than corn tortillas, so make a breakfast burrito with scrambled eggs and salsa instead of toast.  Make sandwiches on a rice flour tortilla instead of bread. Instead of using costly pizza shells, make pizzas on rice tortillas and heat them in the microwave. Bought cookies are pricey; make brown rice pudding for dessert instead.  Add your own raisins and cinnamon to plain oatmeal instead of buying the more costly flavored packets.  Skip the convenient gluten-free frozen dinners and make your own from leftovers. Don’t buy (or make) gluten-free graham crackers for pie crusts; crush leftover dried-out cookies that you have on hand, add a little butter, and make your own crust.

The old rules of shopping don’t apply in this new economy, but if you make a few changes, you’ll always walk away from the table full and happy.

Impossible Gluten-Free Pie Recipe

Ingredients:

• 2 cups leftover meat or chicken, diced
• 1-1/2 cups gluten-free gravy or condensed cream of mushroom soup
• 2 cups leftover mixed vegetables
• 1 cup gluten-free Bisquick 
• 1/2 cup milk
• 1 egg

Directions:
Preheat oven to 400 degrees. Mix the meat, gravy or soup, and vegetables in and ungreased 9-inch pie plate. Stir together the remaining ingredients with a fork until blended then spoon over the meat and veggie mixture. Bake about 30 minutes or until the top is golden brown.

Celiac.com 04/13/2019 - The word microbiota is a fancy medical word.  It means the vast numbers of bacteria that inhabit the digestive track. These bugs, most of which were once  thought to be only a nuisance or worse, are now known to be a very important part of the overall health of the gut, indeed, of the entire body. So what does this have to do with celiacs and the gluten intolerant?

Wheat

For many thousands of years wheat has been a major part of the human diet. It was easy to grow, cultivate and domesticate. It was quickly found to be highly nutritious with lots of calories, to have most of the amino acids the body needs to make protein, many vitamins and minerals, and last but not least, a considerable amount of fiber to keep the bowels regular. Just as important, wheat could be baked in many ways and stored for later use. So, wheat became the backbone of the diet for much of the human race. It was the perfect food. And, alas, it was too perfect to last for the celiac patient and the gluten intolerant.

Celiac and Gluten

It was only 60 years ago that the cause of celiac disease was uncovered. In the late 1930s a Dutch physician, began to treat celiac children with a wheat free diet. During WW II when there was famine and no wheat available in Holland, many of these sickly children became even more remarkably and miraculously well.  They then became sick once again when wheat became available after the war. It was quickly found that the gluten protein in wheat was the culprit. An abnormal antibody in the blood was discovered. The tissue lining the small bowel was found to be badly damaged when wheat and gluten were eaten. But there was one additional thing in wheat that has more recently been discovered.  Prebiotics!

The Prebiotics—Oligofructose and Inulin

These 2 food fibers are prebiotics. A prebiotic is not a probiotic. A probiotic is a live bacteria usually found in yogurt, other dairy products and pills. For a fiber to be called a prebiotic it must be tested by research and found to produce distinct health benefits in the gut and, indeed, throughout the body. They occur when these specific fibers are consumed which, in turn, causes the vigorous growth of certain beneficial bacteria in the gut. It is these healthy bacteria that produce the health benefits. These unique food fibers are found in many plants throughout the world. In plants consumed by humans they are present not only in wheat and barley but also in onions, garlic, yams, leeks, asparagus, bananas, chicory root, Jerusalem artichoke, and even in dandelions. However, it is only wheat and barley that contain gluten. All the others are gluten-free. In the 1990s it was found that wheat supplied 70-80 % of the prebiotics in the American diet. However, this information was just recently rediscovered (1).

The Health Benefits of Prebiotics

This has been a remarkable story. In just over 20 years a huge amount of medical research has uncovered a dramatic array of prebiotic induced health benefits in both animals and humans. This data has just been recently reviewed and highlighted in an extensive, state-of-the-science review on prebiotics (2). The key findings in this 63 page review are that when prebiotics beneficially change the bacterial makeup of the gut, certain health benefits occur. The following occur as measured by medical research:

• Increased calcium absorption and stronger bone density
• Enhanced immunity as measured by research techniques
• Better colon digestive and bacterial balance
• Improved regularity, bulking and stool softness
• Improvement in leaky, permeable bowel with reduced toxin absorption
• Enhanced appetite control through hormone regulation
• Reduced intestinal infection

The following are tentatively considered to occur.

• Reduced risk of obesity and type 2 diabetes
• Reduced risk and/or improvement of intestinal inflammation such as Crohns or ulcerative colitis
• Reduced risk of colon cancer

These are remarkable findings. Were a drug developed that produced these health benefits, it would be a worldwide sensation. Yet, these benefits are available to most people if they include a significant amount of these plant fibers in their diet and/or take a supplement.

The Diabolical Celiac/Gluten Dilemma 

We can now study the bacterial composition of the gut with remarkable new, genetic techniques. What has been found in the celiac person and also in anyone who follows a gluten-free diet is that the bacterial makeup of the gut deteriorates significantly. These adverse changes seem to be associated with the reduction of prebiotics in the diet. It is also likely that this change in the bacterial makeup in some people can lead to digestive symptoms. So, what might be the answer? Certainly, increasing the consumption of these prebiotic-rich but gluten-free foods is a positive first step. The goal should be to consume up to 8 grams of the oligofructose and inulin prebiotics each day. A prebiotic supplement might also be useful in order to reach this goal. The bottom line is that for most of us, a gluten-free diet by itself is not enough. The second part of the dietary gluten-free equation is to replace the prebiotics lost when wheat is removed from the diet. This can be done by ingesting enough prebiotic-rich but gluten-free foods and/or with prebiotic supplements. 

References:
1. Jackson FW (2010) Effects of a gluten-free diet on the gut microbiota and immune function in healthy adult human subjects-comment by Jackson. Br J Nutr Sept; 104(5):773 Epub 2010 May 14
2. Roberfroid M, Gibson GR, Hoyles L et al (2010) Prebiotic effects: metabolic and health benefits. Br J Nutr Aug; 104 Suppl 2: S1-63.

Celiac.com 04/12/2019 - In this 4-part Series, we’re going to look at the world of gluten sensitivity, what the current science tells us, the frustrations gluten sensitive and celiac patients often experience, and how to use the science in getting healthier. 

• Part 1: Why the Tests are Often Wrong
• Part 2: Why Don’t I Feel Great on a gluten-free diet: Cross-Reactive foods
• Part 3: Why Don’t I Feel Great on a gluten-free diet: the Intestinal Milieu
• Part 4: Why Don’t I Feel Great on a gluten-free diet: Invaders in the House

Many of us believe that the toxic peptides of gluten found in wheat, rye and barley may detrimentally affect any tissue in the body and are not restricted to the intestines. As a matter-of-fact, one of the ‘mantras’ of the Gluten Sensitivity Network comes from an 8-year old article: “That gluten sensitivity is regarded as principally a disease of the small bowel is a historical misconception.(1)” There is a key word in this statement which I suspect emphasizes the Author’s message and sets the tone for this article (and this network movement). That key word is ‘principally’.  Is Gluten sensitivity ‘principally’ a disease of the small intestine? Point-blank answer-no, it is not. For every Gluten sensitive patient with the symptoms of an enteropathy (classic celiac disease), there are 8 more with no GI symptoms(2, 3). 

And the importance of recognizing this? Unfortunately, too many doctors will tell their patients that if the intestinal symptoms are not severe, or if there is no advanced intestinal damage (total villous atrophy), then the patient does not need to be vigilant in avoiding gluten exposure at all costs(4). Many patients are advised to follow the World Health Organization or Food and Agricultural Organization Codex Alimentarius gluten-free diet, which allow up to 0.3% of gluten per 100 g of protein in foods, whereas others follow a strict GFD with no detectable gluten. However, trace amounts of gluten may be responsible for persistent symptoms in some patients with celiac disease. Up to 75% of patients with persistent symptoms despite a World Health Organization or Food and Agricultural Organization Codex Alimentarius gluten-free diet will improve when put on a ‘‘no detectable gluten’’ diet(5).

We know that for gluten-sensitive patients, eating gluten will cause inflammation in the intestines, and often in other parts of the body(6, 7, 8, 9).  The importance of ‘quieting down’ the inflammatory cascade from gluten exposure? Mortality in celiac patients is highest (6-fold higher) in those not adherent to a gluten-free diet. Non-adherence to a gluten-free diet was defined as eating gluten once-per-month(10). Vigilance is paramount. You can’t be a little pregnant. There is no convincing evidence that you can have a little gluten if you have gluten sensitivity.

The ‘conundrum of gluten sensitivity’ is when patients know they have a problem with wheat, their doctors run the standard blood profile, and one of two things happens:

1. -IgA anti-transglutaminase or anti-endomysial antibodies come back negative(11), or; 
2. -IgA anti-transglutaminase or anti-endomysial antibodies  come back negative and  anti-gliadin, or anti-deamidated gliadin antibodies come back positive and the doctor tells the patient “it’s okay to eat wheat because the tissue antibodies are negative”. The patient is left in a state of confusion. They don’t WANT to give up wheat. After all, they believe it’s a staple of life. And their doctor says it’s okay to eat it. Yet they know they don’t feel as well when they eat it. So many will rationalize “Oh well, it must be the stress of my life making me feel bad”, and they order their bagel. That’s the conundrum. Where’s the problem? The problem is the test.

Gluten sensitivity is a systemic autoimmune disease with diverse manifestations(12). Celiac disease, or gluten-sensitive enteropathy, is only one aspect of a range of possible manifestations of gluten sensitivity. And yet, this enteropathy, ‘one of the most common lifelong disorders in both the U.S. and Europe(13), receives the lion’s share of focus to the point of ignoring other manifestations. Auto-immune disease, the 3rd leading cause of morbidity and mortality in the industrialized world(14), is ten times more common in a gluten sensitive enteropathy than in the general population(15). The correlation is undeniable. The exact mechanisms of how this correlation manifests is being investigated intensively. What we can say, with a good deal of research behind us, is that the toxic peptides of gluten may act as a trigger in the development of the auto-immune mechanism (the immune system attacking our own tissues). Traditionally, doctors do not recognize this connection and wait for the accumulated damage from the immune system attacking our tissue (our thyroid, or our brains, or our skin, or…), they wait until the damage is extensive enough that there are obvious symptoms, and then we receive a diagnosis of an auto-immune disease (celiac disease, Hashimoto’s thyroiditis, type 1 diabetes, systemic lupus, inflammatory bowel disease, inflammatory skin diseases, ….)(16). Thus, the burden on society imposed by gluten sensitivity is difficult to overestimate. Earlier identification might result in earlier treatment, better quality of life and an improved prognosis for these patients(17).

The diagnosis of gluten sensitivity has been proposed to include not just intestinal damage (celiac disease), but also gluten-reactive patients without intestinal lesions. From the skin (dermatitis herpetiformis, psoriatic arthritis, alopecia areata, dermatomyositis, cutaneous vasculitis,), to the muscles (inflammatory myopathies), to the brain (gluten ataxia, altered neurotransmitter production, schizophrenia, anxiety, depression, attention deficit disorders,…) to the nerves (peripheral neuralgias, carpal tunnel syndrome, idiopathic neuropathies,…),  and beyond. Pathology in response to gluten exposure can occur in multiple systems without evidence of intestinal damage(18-27). 

Now, what about this conundrum?

The tests are negative, yet the person feels better when they do not eat gluten. Many studies have validated the sensitivity and specificity using anti-endomysial and/or anti-transglutaminase antibody testing to identify celiac disease(28, 29). This means that the science says these tests are very, very accurate. Then how is there a conundrum? Here’s the problem: the definition of celiac disease requires total villous atrophy(30). Not partial villous atrophy; not increased inflammation without any visible atrophy. The definition of celiac disease requires total villous atrophy. Thus, when researchers look at populations who have celiac disease confirmed by biopsy, and look to see how accurate the blood tests are, they come up with percentages above 95%, because they’re only including people who have total villous atrophy in their study group-because that’s the definition of celiac disease. If we were to expand the definition of celiac disease to include those with partial villous atrophy, or include those who currently show only the mechanism that wears down the villi  (increased intraepithelial lymphocytes), then the sensitivity and specificity of anti-endomysial or anti-transglutaminase goes down, in some studies dramatically down, to as low as 27-32%(31, 32, 33, 34). 

So do we want to base our health guidance and decisions on blood tests that are limited to identifying celiac disease at its end stage of intestinal deterioration (total villous atrophy)(35, 36)? Or would we want to include testing that has a much bigger picture in mind and identifies gluten sensitivity inside and outside the intestines and at earlier stages?

If we recognize the fact that gluten sensitivity may manifest as celiac disease, or it may manifest outside of the intestines(37), one of the ways of expanding our diagnostic range is to focus on whether or not our immune system is saying that gluten is a problem. We may know where the problem is manifesting, or we may not. But if our immune system is saying “We’ve got a problem here”, it is likely worth listening to. 

As a comparison, if your car is running fine on the highway at 60 miles per hour, do you listen when the immune system of the car (the dashboard gauges) says “we’ve got a problem here”, and the hot light has lit up, or do we say “the car’s running fine-I don’t see or feel any problem”, and keep driving? I think most would agree that is not a very wise move. The same is true for your body. You may ‘feel’ a problem; you may not. We’ll talk more about that in a future article. For now, the point I want to make is that we will benefit from ‘listening’ to what our immune system is saying to us. We just have to be able to hear what it’s trying to say.

The problem is accurate communication

The current blood test that every laboratory offers in looking for an immune reaction to the gluten fraction of wheat is elevated antibodies to gliadin or deamidated gliadin - every laboratory. And there are many studies that have shown that looking for elevated antibodies to gliadin is not as accurate in identifying celiac disease as looking for elevated antibodies to transglutaminase or endomysial antibodies. Why? Because sometimes the antibodies to gliadin are positive and the biopsy shows there is no celiac disease. And sometimes the gliadin antibodies are negative and the biopsy shows there is celiac disease. Thus, the consensus in the scientific community is that looking for antibodies to wheat (gliadin) is not sensitive enough when looking for celiac disease. You can’t rely on it. 

Now that doesn’t make much sense, does it? If the gluten peptide is the problem, why can’t we measure the immune reaction to it when other gauges on the dashboard are hot? Two reasons:

1. Researchers tell us it is “inappropriate” to compare gliadin antibodies against transglutaminase or endomysial antibodies because gluten sensitivity can exist without villous atrophy. Thus the gliadin antibodies may be elevated (and often are) without recognizable celiac disease. It’s showing us a bigger problem than just Celiac disease. They’re not ‘false positives’. It’s the immune system saying “we’ve got a problem here” that is not currently manifesting in the intestines-it is likely manifesting somewhere else, such as in the brain or the nervous system(38).
2. Identifying antibodies just against the fraction of gluten called gliadin is not thorough enough in looking for an immune reaction to gluten(39).

Amino acids are the building blocks of protein. When we eat protein, any protein, it’s the job of the digestive system to break down that protein into 1, 2, or at most 3 amino acid peptides that are easily absorbed into the blood stream through the ‘cheesecloth’ of the intestines. When someone has gluten sensitivity, the gluten molecules in wheat, barley and rye are not digested into small enough molecules to easily fit through the cheesecloth, be absorbed into the blood stream, and they remain in larger peptides, sometimes very large peptides. These large peptides, called macromolecules, trigger the immune system to say “these are not good for me(40, 41)”. An exposure to a large peptide on a rare occasion would not likely have initially been a problem. But with pancakes for breakfast, a sandwich for lunch, pasta for dinner, toast for breakfast, a sandwich for lunch, croutons on the salad at dinner, day in and day out, eventually you’ve got a hot light on the dashboard that is reaching the critical stage(42). Then ‘boom’ your engine overheats and you begin to notice symptoms-perhaps in the intestines, perhaps in the joints, perhaps in the skin, perhaps in the skull (depression, anxiety, headaches), perhaps fatigue,…..

So let’s get back to the large peptides left in the intestines due to an inability to digest the gluten molecule. We know there are many peptides of gluten result from poor digestion(43). One study identified over 60 putative peptides of gluten(44). Yet the current blood tests only test for one - gliadin. Studies have said that gliadin is the primary toxic peptide. But, only about 50% of celiac patients have antibodies to the gliadin peptide of gluten(39). The rest of the celiacs don’t. They have antibodies to other peptides of gluten(45). This is the reason for the conundrum-you test for it, the test only looks for antibodies to gliadin, the test comes back negative, and yet you ‘know’ you feel better off of gluten. It’s the test! In that example, the person does not react to the gliadin peptide-they are likely to be reacting to a different peptide of gluten.

Why don’t laboratories test for other peptides of gluten?

Good question. I do not know the answer to that. Some of the studies on this go back to the mid 1990’s. Probably a supply and demand issue for commercial laboratories.

Well, no longer.

There is a new blood test, looking at 12 different peptides of gluten-not just Gliadin. You can go to www.cyrexlabs.com or to my web site www.theDr.com to read more about this test. Looking at antibodies to 12 different peptides of gluten (including gliadin) will certainly increase the detection rate of the immune system saying “we’ve got a problem here with gluten”. We know celiac disease is due to sensitivity to the peptides of gluten found in wheat, barley and rye, many of the peptides in gluten-not just to gliadin. And now, another diagnostic tool has been added to your doctor’s repertoire assisting in accurately identifying gluten sensitivity with or without the serious end-stage of tissue destruction-total villous atrophy.

And my personal prayer is that as a result of this expanded test looking for a reaction to gluten, we no longer miss those with earlier stages of celiac disease and gluten sensitivity thus being able to calm down the ‘fire in the belly’, the hot light on the dashboard, before the engine blows up. Before the diagnosis of attention deficit hyperactivity disorder, before the diagnosis of autoimmune thyroid disease, before the diagnosis of type 1 diabetes, before the diagnosis of migraines, before the loss of a pregnancy,…. and doctors will have the tools to truly guide their patients in increasing their health - tuning the engine before it blows up with a diagnosable disease. So our bodies can carry us through life purring instead of rumbling along.

References:
1.    Hadjavassilios, M., Gluten sensitivity as a Neurological illness, J Neurol Neurosurg Psychiatry 2002;72:560–563 
2.    van Heel D., West J, Recent Advances in Coeliac Disease, Gut 2006;55:1037–1046
3.    Fasano A, Catassi C., Current Approaches to Diagnosis and Treatment of Celiac disease: An Evolving Spectrum Gastroenterology 2001;120:636-651 
4.    Goddard CJ., Gillett H R., Complications of coeliac disease: are all patients at risk? Postgrad. Med. J. 2006;82;705-712
5.    Green PHR, Stavropoulos SN, Panagi SG, et al. Characteristics of adult celiac disease in the USA: results of a national survey. Am J Gasroenterol 2001;96:126–31.
6.    Olesen M, Eriksson S, Bohr J, Jarnerot G, Tysk C. Microscopic colitis: a common diarrhoeal disease. An epidemiological study in Orebro, Sweden, 1993-1998. Gut, 2004; 53:346-350.
7.    Gillet HR, Freeman HJ. Prevalence of celiac disease in collagenous and lymphocytic colitis. Can J Gastroenterol, 2000; 14: 919-921.
8.    Koskela RM, Niemelä SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scand J Gastroenterol, 2004;39: 837-845.
9.    Dickey W, Celiac disease and the Colon, PRACTICAL GASTROENTEROLOGY • SEPTEMBER 2008
10.    Corrao G, Corrazza GR, Bagnardi V, et al. Mortality in patients with coeliac disease and their relatives: a cohort study. Lancet 2001;358:356–61.
11.    Hill I Salem W, Dirks M, Liptak G, Colletti R , Fasano A, Guandalini S, Hoffenberg E, Horvath K, Murray J, Pivor M, Salem W, Seidman E, Guideline for the Diagnosis and Treatment of Celiac disease in Children: Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, J Pediatr Gastroenterol Nutr, Vol. 40, No. 1, January 2005
12.    Hadjavassilios, M, Gluten sensitivity: from Gut to Brain. Lancet Neurol 2010; 9: 318–30
13.    Fasano, A, Celiac disease-How to handle a Clinical Chameleon, NEJM 348;25 June 19,2003
14.    Arnson Y, Amital H, and Shoenfeld Y, Vitamin D and autoimmunity: new aetiological and therapeutic considerations, J of Immunology, 2005, 175: 4119–4126.
15.    Alaedini A, Okamoto H, Briani, C, Wollenberg K, Shill H, Bushara K, Sander H,  Green P, Hallett M, Latov N, Immune Cross-Reactivity in Celiac disease: Anti-Gliadin Antibodies Bind to Neuronal Synapsin I, The Journal of Immunology, 2007, 178: 6590–6595.
16.    Bland J., Understanding the Origins and Applying Advanced Nutritional Strategies for Autoimmune Disease, Metagenics Seminar Series, 2006
17.    Green P, Alaedini A, Sander HW, Brannagan III TH, Latov N, Chin R, Mechanisms underlying celiac disease and its Neurologic Manifestations Cell. Mol. Life Sci. 62 (2005) 791–799
18.    Marietta E, Black K, Camilleri M, Krause P, Rogers RS 3rd, David C, Pittelkow MR, Murray JA., A new model for dermatitis herpetiformis that uses HLA-DQ8 transgenic NOD mice, J Clin Invest. 2004 Oct;114(8):1090-7
19.    Lindqvist U, Rudsander A, Boström A, Nilsson B, Michaëlsson G., IgA antibodies to gliadin and coeliac disease in psoriatic arthritis, Rheumatology (Oxford). 2002 Jan;41(1):31-7.
20.    Humbert P, Pelletier F, Dreno B, Puzenat E, Aubin F, Gluten intolerance and skin diseases, Eur J Dermatol 2006; 16 (1): 4-11
21.    Selva-O’Callaghan A, Casellas F, de Torres I, Palou E, Grau-Junyent JM, Vilardell-Tarrés M., CELIAC DISEASE AND ANTIBODIES ASSOCIATED WITH CELIAC DISEASE IN PATIENTS WITH INFLAMMATORY MYOPATHY, Muscle Nerve. 2007 Jan;35(1):49-54.
22.    Hadjivassiliou M, Grünewald R, Sharrack B, Sanders D, Lobo A, Williamson C, Woodroofe N, Wood N, Davies-Jones A., Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics, Brain. 2003 Mar;126(Pt 3):685-91.
23.    Hadjivassiliou M, Aeschlimann D, Grünewald RA, Sanders DS, Sharrack B, Woodroofe N, GAD antibody-associated neurological illness and its relationship to gluten sensitivity, Acta Neurol Scand. 2010 Apr 15
24.    Eaton W, Mortensen PB, Agerbo E, Byrne M, Mors O, Ewald H., Coeliac disease and schizophrenia: population based case control study with linkage of Danish national registers, BMJ. 2004 Feb 21;328(7437):438-9
25.    Hadjivassiliou M, Grünewald RA, Chattopadhyay AK, Davies­Jones GAB, Gibson A, Jarratt JA, et al. Clinical, radiological, neurophysiological and neuropathological characteristics of gluten ataxia. Lancet 1998;352:1582­5.
26.    J Neurol Neurosurg Psychiatry. 2006 Nov;77(11):1262-6., Hadjivassiliou M, Grünewald RA, Kandler RH, Chattopadhyay AK, Jarratt JA, Sanders DS, Sharrack B, Wharton SB, Davies-Jones GA, Neuropathy associated with gluten sensitivity.
27.    Gluten sensitivity: from gut to brain., Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D, Lancet Neurol. 2010 Mar;9(3):318-30
28.    Hopper A., et.al., Pre-endoscopy serological testing for coeliac disease:evaluation of a clinical decision tool, BMJ. 2007 Apr 7;334(7596):729
29.    Hill ID., What are the sensitivity and specificity of serologic tests for celiac disease? Do sensitivity and specificity vary in different populations? Gastroenterology. 2005 Apr;128(4 Suppl 1):S25-32
30.    Memeo L, Jhang J, Hibshoosh H, Green PH, Rotterdam H, Bhagat G., Duodenal intraepithelial lymphocytosis with normal villous architecture: common occurrence in H. pylori gastritis, Mod Pathol. 2005 Aug;18(8):1134-44
31.    Abrams JA, Diamond B, Rotterdam H, Green PH. Seronegative celiac disease: increased prevalence with lesser degrees of villous atrophy, Dig Dis Sci. 2004 Apr;49(4):546-50
32.    Tursi A., Seronegative Coeliac Disease: a Clinical Challenge. BMJ 26 April, 2005
33.    Rostami, K., Unforgiving Master of Non-Specificity and Disguise, BMJ 27, April 2005
34.    Lebwold, Green P., Screening for Celiac disease. N Engl J Med Oct.23 2003,1673-4 
35.    Freeman HJ., Pearls and pitfalls in the diagnosis of adult celiac disease. Can J Gastroenterol 2008;22(3):273-280.
36.    Bonamico M., Serologic and Genetic Markers of Celiac disease: A Sequential Study in the Screening of First Degree Relatives, Journal of Pediatric Gastroenterology and Nutrition 42:150–154
37.    Fasano A., Catassi C., Current Approaches to Diagnosis and Treatment of Celiac disease: An Evolving Spectrum, GASTROENTEROLOGY 2001;120:636–651
38.    Hadjavassiliou M., Grunewald R., The Neurology of Gluten sensitivity:Science vs. Conviction  Practical Neurology, 2004, 4, 124–126
39.    Camarca, A., et.al., Intestinal T Cell Responses to Gluten Peptides Are Largely Heterogeneous: Implications for a Peptide-Based Therapy in Celiac disease, J. Immunol. 2009;182;4158-4166
40.    Meresse B., , Ripoche J., Heyman M., Cerf-Bensussan N., Celiac disease: from oral tolerance to intestinal inflammation, autoimmunity and lymphomagenesis, Nature Vol 2 No 1, JANUARY 2009 
41.    Bethune M.,Parallels Between Pathogens and Gluten Peptides in Celiac Sprue, Plos Pathogens Feb 2008 Vol 4: 2;e34 
42.    Ehrhardt G., et.al. Discriminating gene expression profiles of memory B cell subpopulations JEM VOL. 205, August 4, 2008
43.    Martucci S., Corazza G., Spreading and Focusing of Gluten Epitopes in Celiac disease GASTROENTEROLOGY Vol. 122, No. 7, 2002
44.    Pastore L., et.al., Orally Based Diagnosis of Celiac disease: Current Perspectives, J Dent Res 87(12):1100-1107, 2008
45.    Vader W., et.al., The Gluten Response in Children With Celiac disease Is Directed Toward Multiple Gliadin and Glutenin Peptides, GASTROENTEROLOGY 2002;122:1729–1737

Celiac.com 03/29/2019 - What are we looking for when we ask for testing for celiac disease? The primary objective is usually to discover whether a given set of troubling symptoms are the result of eating gluten. With asymtomatic family members, the objective is likely to avoid developing the many health problems that are in the offing for those with untreated celiac disease. But maybe there is another reason to test for celiac disease. Perhaps some people could achieve optimum health— a better and longer life—through eliminating gluten from their diets. Two relatively new developments in the field of celiac disease research may open the path to testing aimed at optimal health. These discoveries may offer a better understanding of the dynamics of celiac disease and others who are genetically susceptible to gluten’s negative impact on human health. In 2009, Dr. Ivano Bertini and colleagues reported their discovery of a metabonomic signature of celiac disease (1). Metabonomics is a field of study involving an examination of blood and urine looking for signs of multiple metabolic changes caused by a biological irritant or perturbation. These signs are formed by the products of food digestion, cellular assimilation of these nutrients, and the by-products of cellular conversion of  food products to energy, as well as the enzymes produced to facilitate these conversions. These metabolites are identified, quantified, and the patterns they form are determined through a process of nuclear magnetic resonance and subsequent statistical analysis of these findings.  

Bertini et al discovered that those with untreated celiac disease show a pattern of these various  substances in both their blood and urine (1). This offers a new, holistic approach to the study and understanding of celiac disease. Although, for diagnostic purposes, it is not as accurate as serum antibody tests. This is partly because it does not do as well at distinguishing between latent and active celiac disease. However, this investigative approach does explain some of the variations in the many manifestations of celiac disease, while it transcends many of the controversies that currently surround appropriate treatment of celiac disease, potential celiac disease, latent celiac disease, and asymptomatic celiac disease. It may even offer insight into some elements of non-celiac gluten sensitivity. 

I have previously described some of the problems with the diagnosis of celiac disease on the basis of intestinal biopsy. In short, these problems include improper sample orientation or harvesting damage done during the endoscopic procedure. Sometimes an inadequate number of biopsies (in the past a single sample was often considered adequate to exclude celiac disease) impedes accurate diagnosis or exclusion. Sampling errors can also cause problems due to patchy villous atrophy in the intestine. There are still some pathologists who do not use the Marsh system, or one of its derivatives, or refuse to count intra-epithelial lymphocytes. They also inhibit accurate diagnosis of this common disease. Sometimes, just getting a referral to see a gastroenterologist can also pose a diagnostic problem. General practitioners can serve as gate-keepers who will not refer patients to gastroenterologists for a variety of reasons. If patients are demonstrating symptoms of celiac disease but are overweight or even of normal weight, or if the patient is demonstrating signs and symptoms of celiac disease with which the practitioner is unfamiliar, they are often refused a referral. These same practitioners will also resist ordering serological antibody testing, despite requests from their patients, citing similar reasons.  When patients have experienced improvements after a trial of a gluten free diet, and now want a diagnosis, they will likely be disappointed. Whether under the supervision of specialists or general practitioners, gluten challenges are particularly difficult as nobody can predict the duration or quantity of gluten that should be consumed to ensure an accurate test.   

The problems with serum antibody tests are at least equally perplexing. They will often miss milder cases of celiac disease and sometimes fail to identify serious cases, both of which might have been caught if an endoscopic biopsy had been done. Without a concurrent measurement of total IgA, those with IgA deficiency will also be overlooked. IgA deficiency has been reported to constitute about 14% of celiac patients (2). False positive serological tests can also pose a diagnostic problem. Some reports contend that these false positive antibody tests constitute potential or latent celiac disease, while others report them in the context of other bowel diseases, arthritis, and other autoimmune diseases. Still others insist that a gluten free diet should only be recommended to people who have celiac disease with demonstrable villous atrophy. 

To further confound this issue, some of these antibody tests require the technician to make subtle color distinctions while others are impugned because intestinal parasites and other autoimmune diseases will also cause production of these antibodies, and for any of a number of other reasons. Further, no antibody tests produce results that are completely congruent with intestinal biopsies, so they carry the added problem of being dismissed by many practitioners who recognize celiac disease only on the basis of intestinal biopsies. To further confound this situation, the cyclic nature of celiac disease may also interfere with diagnosis on the basis of either intestinal biopsies or blood tests. This is because a series of intestinal biopsies may appear normal, or blood tests may produce normal results, at one time, yet subsequent testing will reveal celiac disease. 

Testing for the metabonomic signature of celiac disease, on the other hand, identifies specific metabolite patterns in the urine and blood, and may someday circumvent every one of these problems. The metabonomic signature may prove to be unsurpassed as a tool for increasing our understanding of celiac disease. This investigative process has already reflected three important components of  untreated celiac disease: malabsorption; changes to cellular energy metabolism, and; altered gut microflora/intestinal permeability. 

While some of this information has been found by other means, this research has produced some new insights into impaired glycolysis at the cellular level, in the context of active celiac disease. This leads to reduced pyruvate and lactate with concurrent increases in blood glucose levels. This compromises our ability to make full use of one of our two main sources of cellular energy. Because of fat malabsorption, which is characteristic of celiac disease, the other major source of cellular nutrients is also compromised. Ketone bodies, a by-product of cellular use of fat, also become an important source of brain fuel in cases of active celiac disease.  Thus, we now know a little more about the lethargy and malaise that often accompanies celiac disease. Our cells are starving for energy and we are incurring much of the same damage that is seen in poorly controlled diabetes, due to chronically elevated blood glucose levels, while some brain functions may be spared through utilizing ketone bodies.  

Such features of this metabonomic signature are abolished after a year of gluten avoidance.  In subsequent research reported in December of 2010, metabonomic testing has shown similar metabolite patterns in latent or potential celiac disease, which also normalize after a year of following a gluten free diet (3). This is powerful evidence that those with latent or potential celiac disease can benefit as much from the gluten free diet as those who already have villous atrophy. It also opens the door for understanding the dynamics whereby some celiac patients can be overweight while others are underweight but both suffer malnutrition with respect to some micro-nutrients. And it clarifies the importance and therapeutic value of a gluten free diet for those who might otherwise be told that they have potential or latent celiac disease and therefore don’t need the diet.

Susan, a friend of mine in Arizona who has celiac symptoms and a suggestive family history, was recently told by her gastro that “we don’t believe in gluten sensitivity where there is no villous atrophy”.  Bertini and colleagues comment on their findings with respect to patients such as Susan saying: “They already experience some subtle alteration of the enterocytes (at the microscopic functional level but not at the macroscopic level) and metabolically appear similar to overt celiac disease also without any histological evidence of intestinal damage.” Yet their blood and urine carries a metabonomic signature that clearly demonstrates they would benefit from a gluten-free diet. So despite her negative biopsy, Susan really should follow a gluten-free diet. Bertini and colleagues have demonstrated the benefits through metabolic research.    

Metabonomics is an exciting new field of research that is poised to reveal hidden facets of many ailments, but it may be particularly helpful to improving our understandings of intestinal ailments and a variety of psychiatric illnesses where we are already aware of altered urinary peptide profiles. Perhaps we will soon see support for the therapeutic use of the gluten free diet in many intestinal, autoimmune, and psychiatric illnesses because of this unique approach to understanding the exquisitely complex machinations of our bodies in sickness and in health.  

Sources: 
1. Bertini I, Calabrò A, De Carli V, Luchinat C, Nepi S, Porfirio B, Renzi D, Saccenti E, Tenori L. The metabonomic signature of celiac disease. J Proteome Res. 2009 Jan;8(1):170-7.
2. Bahari A, Karimi M, Sanei-Moghaddam I, Firouzi F, Hashemi M. Prevalence of celiac disease among blood donors in Sistan and Balouchestan Province, Southeastern Iran. Arch Iran Med. 2010 Jul;13(4):301-5.
3. Bernini P, Bertini I, Calabrò A, la Marca G, Lami G, Luchinat C, Renzi D, Tenori L. Are Patients with Potential Celiac Disease Really Potential? The Answer of Metabonomics.  J Proteome Res. 2010 Dec 13.

Celiac.com 03/28/2019 - You could say that I was pretty spoiled when it came to medical care while growing up. At 12 years old I was diagnosed with juvenile diabetes on my first visit to Children’s Hospital in Boston. Three years later, I was diagnosed with celiac disease at the same hospital in a single visit (blood tests and an endoscopy confirmed the diagnosis, but there was a presumptive celiac disease diagnosis made in less than an hour). My experience seems to contrast the norm: according to the University of Chicago’s Celiac Disease Center, the average child visits eight pediatricians before being accurately diagnosed with celiac disease.  

During my college years, I deftly managed both conditions with relative ease. I didn’t let my pair of autoimmune diseases stop me from traveling to Italy, Brazil, and Chile and living overseas in Israel and Jordan. I became very good at following a gluten-free diet across different cultures, cuisines, and languages. Overall, I became content with the state of my celiac disease. But that all changed after I graduated from college—the student health center was no longer an option and I was forced to find a doctor on my own for the first time. 

My first attempt was a somewhat frightening, but ultimately enlightening, experience. After meeting with a physician for what felt like five minutes, he informed me that he was interested in taking some general lab tests, and that he wanted me to schedule a follow-up appointment. “Standard stuff,” I thought to myself. Since I hadn’t seen a doctor relating to my celiac disease since my diagnosis, I asked the physician, “Are there any tests that I should get for my celiac condition? Aren’t I at risk for certain nutritional deficiencies? Are there any supplements I should be taking?” The physician responded with a puzzled look and blurted out, “I’m not sure what you’re talking about.”

I left that appointment feeling confused and upset. Was I wrong? I could have sworn a doctor told me at some point to take at least a multivitamin. My ignorance of celiac disease was profound; I thought I was doing a pretty good job of managing it. Until this point in time, it really only affected my lifestyle in two ways—it was always Jack and Diet Coke instead of beer, and meat and veggies instead of pasta and sandwiches.

After a basic Internet search, I discovered that it was the doctor who was wrong. There are follow-up tests that are appropriate for someone with celiac disease—especially for someone who hasn’t been seen by a specialist for several years (in my case, nearly a decade). He was also misinformed about supplement use for celiac disease patients, as there is a general consensus that people with celiac disease should take a gluten-free multivitamin.

While frustrating, that doctor’s visit turned out to be a life-changing experience. It was at that moment that I decided to take my health into my own hands. Until that point in time, all I knew about celiac disease was that I had to follow a gluten-free diet. I had an Earth-shattering paradigm shift about how celiac disease impacted my life. 

I immediately immersed myself in celiac disease information by scouring the articles on celiac.com (one of the most popular sources of educational material on celiac disease). I was surprised to find a wealth of information about the ways that celiac disease affects overall health. I went on to order and read the books Cereal Killers by Scott Adams and Dr. Ron Hoggan and Celiac Disease by Dr. Peter Green. Both books provide a great overview of celiac disease and its various manifestations. They also helped me understand the difference between gluten intolerance and celiac disease. Most importantly, they gave me more information on how to take extra steps to manage my celiac disease beyond the gluten-free diet. These books informed me about the most common celiac-induced nutrient deficiencies and touched on supplementation as well.

As I plunged deeper into the online world of celiac disease I stumbled upon Gluten-Free Faces, a social media site created just for people with celiac disease. This website is a phenomenal resource that helps people connect with others with celiac disease in your area. Members exchange information on restaurants and recipes, join common interest groups, and share tips on managing celiac disease. In my case, I was lucky to find Elizabeth Smith, a certified nutritionist and creator of www.manageceliac.com. Elizabeth was an immense help. She easily answered all of the questions I had about celiac disease, nutritional deficiencies, and supplementation.

During this time, I also had the pleasure of meeting Brian Dean, a registered dietitian with a Masters degree in nutrition. Brian was a tremendous resource in helping me understand the impact of celiac-induced malabsorption and the nutrients that I may be deficient in due to the absence of the major cereal grains from my diet.

After researching the issue extensively and consulting regularly with Elizabeth and Brian, it became obvious that there were steps beyond a gluten-free diet that people with celiac disease should take to improve their health. More specifically, those with celiac disease should add essential nutrients to their diet in order to optimize their health and augment their gluten-free diet. These supplements fall into five major categories, summarized below.

Full Spectrum Multivitamin

Above all else, it is imperative that people with celiac disease take a multivitamin. One of the primary manifestations of celiac disease is nutrient malabsorption. Intestinal villi become damaged during the immunological response to gluten ingestion, blunting nutrient absorption. Even after following a gluten-free diet normal absorption may never fully resume. In fact, a study done by Hallert et al showed that more than half of celiac patients who had been following a gluten-free diet for over 10 years still showed a higher total plasma homocysteine level than the general population, indicating B vitamin deficiencies(1). A celiac-specific multivitamin must contain the fat-soluble vitamins (A, D, E and K) and B-complex vitamins. Most importantly, it must include the anti-anemics of folic acid, vitamin B-12, and iron since anemia is one of the most common complications in people with celiac disease(2). 

Bone Density Support 

Another potential complication in both adults and children with celiac disease is an increased risk of low bone density. A recent study showed that 40% of newly diagnosed patients with celiac disease have osteopenia (reduced bone mass, but not severe enough to be classified as osteoporosis) and 26% have osteoporosis(3). This phenomenon occurs for a number of reasons. Firstly, calcium —the most critical bone-building nutrient— is not properly absorbed in people with celiac disease. Further, a significant portion of people with celiac disease are also lactose intolerant, limiting their ability to ingest calcium-rich dairy products.

However, calcium alone is not enough for optimal bone health. Vitamin D supplementation is critical due to its role in calcium absorption and utilization. It has been shown that Vitamin D increases calcium absorption by as much as 80%(4).  Another critical nutrient that should be included in any bone density-enhancing supplement is magnesium. Magnesium enhances calcium supplementation, as it’s used by the parathyroid gland to regulate calcium metabolism. Without magnesium, calcium is excreted from the body and not retained to perform its essential functions. Several studies have shown that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium(5). 

Intestinal Healing / Strenghtening Nutrient

Intestinal damage is a hallmark sign of celiac disease. It’s well understood that villus atrophy caused by the autoimmune-mediated response to gluten is the underlying cause of poor nutrient status commonly seen in the celiac disease population. However, a gluten-free diet is insufficient for intestinal repair. Ciacci et al reports that more than half of diagnosed and treated celiac disease patients have clinically damaged intestines, as determined by biopsy. In addition, 23% of cases were determined to have severe intestinal damage(6). Furthermore, in a recent study conducted by the Mayo Clinic, it was found that only 37% of subjects showed mucosal recovery after two years on a gluten-free diet. After five years, this number increased to just 66%(7). Fortunately, there are a number of nutrients that can be supplemented to promote the healing of the intestinal lining. These nutrients include zinc, glutamine, and citrus bioflavonoids, among others.

Probiotics

Dr. Alessio Fasano of the University of Maryland’s Celiac Disease Center believes that probiotics may one day provide a cure for celiac disease(8). While this technology does not yet exist, probiotics have already been used to treat many illnesses and diseases pertaining to the human digestive system including irritable bowel diseases, intestinal infections, and celiac disease(9).

Celiac disease patients are vulnerable to dysbiosis, an imbalance of bacterial strains in the gut. In a study of gut microflora in patients both with and without celiac disease, researchers determined that patients with celiac disease have a much higher total and gram negative bacteria count. Bacteroides and E. coli were significantly more abundant in celiac disease patients with active disease, while those with inactive disease and those without celiac disease exhibited a much higher ratio of probiotic bacteria(10). In a literature review, Salminen et al determined that probiotics are clinically effective treatments for disorders of the gut stemming from dysbiosis(11).

In a recent study by Lindfors et al it was concluded that the live B. lactis bacteria may directly counteract the harmful effects of gluten(12). A 2010 study published by De Palma et al found that the use of probiotics significantly reduced intestinal inflammation of celiac disease affected cells in vitro(13).

Enzymes

Pancreatic exocrine insufficiency (reduced pancreatic enzyme secretion) is a consequence of many diseases of the pancreas, as well as extrapancreatic diseases like celiac disease(14). Pancreatic enzymes are essential in the digestive process(15). Supplementation of these enzymes aid in the breakdown of fats, proteins, and carbohydrates. The benefit of pancreatic enzyme supplementation is clinically significant for people who have compromised digestion, such as celiac disease patients(16).

Chronic diarrhea is a common symptom of celiac disease patients(17). A study done by Leeds et al examined the effect of pancreatic enzyme supplementation in celiac disease patients with chronic diarrhea. The authors concluded that supplementation of pancreatic enzymes significantly reduced the frequency of diarrhea(15).

Pancreatic enzymes are beneficial to patients with celiac disease because they are among the most potent digestive aids available. They help break down food, allowing for further absorption of nutrients. Also, they have anti-inflammatory properties that provide significant benefits to the digestive tract(18). 

Conclusion

Following a strict gluten-free diet is of utmost importance for people with celiac disease. However, there are additional steps that people with celiac disease should take to optimize their health. Since no medications are currently available, the best alternative is supplementation. It is my hope that others will be able to benefit from this ongoing research and that they will decide to take their health back into their own hands.

References
1.    Hallert C et al Evidence of poor vitamin status in celiac patients on a gluten-free diet for 10 years. Alimentary Pharmacology Therapeutics. 2002;16:1333-1339.
2.    Nelson DA. Gluten-sensitive enteropathy (celiac disease): more common than you think. American Family Physician. 2002;66:2259-2266.
3.    See J and Murray JA. Gluten-free diet: the medical and nutrition management of celiac disease. Nutrition in Clinical Practice. 2006;21:1-15.
4.    Adams S and Hoggan R. Cereal killers: celiac disease and the gluten-free a to z. Waterworks and Celiac.com. 2010.
5.    NIH. Magnesium. Office of Dietary Supplements. 2009. http://ods.od.nih.gov/factsheets/magnesium.asp
6.    Ciacci C, Cirillo M, Cavallaro R, Mazzacca G. Long-term follow-up of celiac adults on gluten-free diet: prevalence and correlates of intestinal damage. Digestion. 2002;66:178-85.
7.    Rubio-Tapia A et al Mucosal recovery and mortality in adults with celiac disease after treatment with a gluten-free diet. American Journal of Gastroenterology. 2010;105:1412-1420.
8.    Fasano A. Surprises from Celiac Disease. Scientific American. 2009;301(2):54-61. 
9.    Mennigen R and Bruewer M. Effect of probiotics on intestinal barrier function. Annals of the New York Academy of Sciences. 2009;1165:183-189.
10.    Nadal I et al Imbalance in the composition of the duodenal microbiota of children with celiac disease. Journal of Meicald Microbiology. 2007;56:1669-1674.
11.    Saavedra JN. Clinical applications of probiotic agents. American Journal of Clinical Nutrition. 2001;73:S1147––S1151.
12.    Lindfors K, Blomqvist T, et al Live probiotic bifidobacterium lactis bacteria inhibit the toxic effects induced by wheat gliadin in epithelial cell culture. Clinical and Experimental Immunology. 2008;152:552-558.
13.    De Palma G, Cinova J, et al Pivotal advance: bifidobacteria and gram-negative bacteria differentially influence immune responses in proinflammatory milieu of celiac disease. Journal of Leukocyte Biology. 2010;87:765-778.
14.    Dominguez-Munoz JE. Pancreatic enzyme therapy for pancreatic exocrine insufficiency. Current Gastroenterology Reports. 2007;9:116-122.
15.    Malterre T. Digestive and nutritional considerations in celiac disease: could supplementation help? Alternative Medicine Review. 2009;14:247-257.
16.    Roxas M. The role of enzyme supplementation in digestive disorders. Alternative Medicine Review. 2008;13:307-314.
17.    U.S. Department of Health and Human Services. Celiac disease. National Digestive Diseases Information Clearinghouse. September 2008.
18.    Britton RS, Leicester KL, Bacon BR. Iron toxicity and chelation therapy. International Journal of Hematology. 2002 Oct;76(3):219-228.
 

Celiac.com 05/16/2011 - Nearly 75% of the 24 million Americans suffering from autoimmune disease are women, according to the American Autoimmune Related Diseases Association (AARDA).  Women appear to mount larger inflammatory responses than men when their immune systems are triggered, thereby increasing their risk of autoimmunity.  The fact that sex hormones are involved is indicated by the fact that many autoimmune diseases fluctuate with hormonal changes such as those that occur during pregnancy, during the menstrual cycle, or when using oral contraceptives. A history of pregnancy also appears to increase the risk for autoimmune disease.

The sex hormone that is commonly low in such women is Dehydroepiandrosterone (DHEA). This is a natural steroid and is produced by the adrenal glands, the reproductive organs and the brain.  DHEA is used by the body to make the male and female hormones, testosterone and estrogen respectively, and is known to have anti-inflammatory effects. It has been proposed that a DHEA deficiency is a contributing factor in autoimmune diseases.  Last year a study was done to look at precisely that effect.  The study’s conclusions have been supported by other, similar research and I think you’ll find it quite interesting.
The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 6 2044-2051(2009) published an article entitled “Low Serum Levels of Sex Steroids Are Associated with Disease Characteristics in Primary Sjogren’s Syndrome; Supplementation with Dehydroepiandrosterone Restores the Concentrations”. The authors investigated whether there was a relationship between steroid levels and the disease characteristics of Sjogren’s.

They based their study on the known data that DHEA not only declines with aging but is reduced in Sjogren’s, an autoimmune disease. The study was populated by 23 post-menopausal women with primary Sjogren’s syndrome and subnormal levels of DHEA. The investigation was a controlled, double blind crossover study, conducted over a 9 month period, where DHEA was assessed by sophisticated laboratory measurements and typical symptoms of Sjogren’s such as dry mouth and eyes and salivary flow rates were similarly assessed.

Results revealed a strong correlation between low DHEA and Sjogren’s symptoms.  DHEA and its sex hormone metabolites (testosterone and estrogen) were found to increase with DHEA supplementation but not with the placebo. Symptoms such as dry eyes were seen to improve as estrogen levels

The researchers concluded that the disease manifestations of primary Sjogren’s syndrome were associated with low sex hormone levels and the supplementation of DHEA allowed the body to transform into androgens, testosterone and estrogen, with testosterone production predominating.

Please allow me to add some personal interpretation. For the most part I agree with the premise and applaud the results. The facts that autoimmune disease occurs more often in women, that women frequently have low DHEA, and that androgens have anti-inflammatory effects that can benefit autoimmune disease are all true.

But should we simply give such women DHEA and call it a day? I don’t think so.  I propose that we do three things: First, evaluate hormonal levels in women regularly; Second, address WHY their hormonal levels are imbalanced;  And third, when supplementing with hormones such as DHEA, ensure that the delivery system is one that mimics what the body does naturally.

Remember that autoimmune disease can begin many years before the first symptoms become manifest. Therefore evaluating hormonal levels in our younger women is a good idea.  When I find DHEA levels that are low, my first order of business is to assess why.  Frequently it is due to a phenomenon known as “pregnenelone steal” that occurs when the adrenal glands are under stress.  It is a common occurrence and one of the fantastic abilities of the human body to shift from one pathway to another when under stress.  The “steal” pathway diverts the body away from making sex hormones and instead it makes more “stress” hormones.  So while adding some DHEA into the mix might very well help, does it make sense to find out WHY it’s being diverted away from making sex hormones?  I hope so because it’s the very foundation of the medicine that we practice—functional medicine.

Once you understand the root cause of the deficiency you can take steps to truly remedy it rather than simply covering it up by taking DHEA.  Not to keep hitting you over the head with this concept, but supplementing with DHEA as your sole treatment misses the underlying cause since the body is designed to make adequate quantities of DHEA.

A common reason for the diversion or “steal” pathway to become activated is adrenal stress from poor absorption of nutrients, unstable blood sugar and the presence of infections—all problems we see with the gluten intolerant patient! While I’m not implying that every autoimmune patient has a gluten intolerance, it certainly warrants screening all of them because of its high prevalence.
As we travel down the road to optimal health through avoiding any food the body isn’t tolerating well, improving the integrity of the small intestine and normalizing adrenal function, there are certainly times when hormonal supplementation is beneficial. I don’t recommend the oral route because the first place the hormone travels is to the liver and this can be burdensome to that organ.  When the body makes hormones naturally it delivers them straight to the bloodstream.  In an effort to mimic that delivery system we use a buccal route (placed between cheek and gum in the mouth) that does a good job in bringing the hormone directly to the bloodstream and bypassing the liver and digestive tract.

Autoimmune diseases comprise the third leading cause of death in our country and research strongly suggests that its rapid increase is due to environmental factors, especially those that weaken the small intestine. I am committed to earlier diagnosis while the disease is still remediable, as well as overall reduction of incidence through addressing digestive health.

I hope you find this informative.  Please share this information with those who have autoimmune disease themselves as well as in their family.

Celiac.com 01/12/2011 - When Americans shop for caffeine-free tea or soda, the process is a simple one. First, they find their brand of choice, scan the labels for “decaffeinated,” then toss the product into their shopping baskets. Unfortunately, it’s not that simple to find gluten-free versions of foods. Although proposals for gluten-free labeling laws are in the works, currently there is no official definition in this country for “gluten-free,” meaning that gluten-free shoppers can’t rely on a gluten-free label to tell them whether a food product is gluten-free. 

According to Living Without, neither of the two major food government agencies, the U.S. Department of Agriculture, which regulates egg, meat, and poultry products, nor the FDA, which regulates packaged and other foods, have a specific definition for “gluten free.” Currently, the FDA’s standard for gluten-free labeling is that the label be “truthful and not misleading,” so if a food product is designated “free” of an ingredient, it shouldn’t have that ingredient in it. 

Whereas certain products can claim to be “free” of substances such as caffeine, a fact which can be confirmed with testing, the analytic technology for testing for zero gluten doesn’t exist yet. Gluten is tested in parts per million (ppm), and currently the smallest detectable amount is 20 ppm. According to Living Without, while celiac experts seem to agree that this is a safe gluten level, other countries define “gluten-free” as containing below 20 ppm of gluten. This means that the current FDA guideline isn’t very useful when it comes to gluten-free labeling. 

The American Celiac Disease Alliance has published on its website, AmericanCeliac.org, a question-and-answer series from the FDA on the current gluten-free labeling guideline proposals, which were developed in 2006 in accordance with the Food Allergen Labeling and Consumer Protection Act (FALCPA) of 2004. Due to the limitations in the current analytic technology, the current proposals require that a product contain less than 20 ppm of gluten. 

According to Living Without, “With the number of products making unregulated gluten-free claims on the rise, the marketplace can be potentially dangerous for consumers with gluten sensitivity and wheat allergy.” Before a labeling regulation can be put into effect, however, the FDA needs to make another draft of the proposal available to the public, then gather and consider the commentary it generates. Following this, a notice regarding the safety assessment must be published. 

“The FDA will likely publish the notice on the safety assessment soon,” Celiac.com reports, but there is no indication as to just when they will issue the final rule. With “gluten-free” labeling on the rise, it seems more crucial than ever to get these regulations passed with a clear definition for “gluten free.”  

With even the tiniest amount of gluten having the capacity to make celiac patients ill, reading labels when shopping for gluten-free foods is a fundamental skill to be acquired from the very start of a gluten-free diet. Until there is a standard definition for “gluten-free” and a reliable set of FDA guidelines governing voluntary gluten-free labeling, celiacs need to be especially vigilant when hunting for gluten-free foods. This watchfulness begins with the vital understanding that a “gluten-free” label doesn’t guarantee a product is gluten-free. 

Resources:
• American Celiac Disease Alliance: Gluten-Free Labeling Proposed Rule
• Celiac.com: FDA Set to Adopt New Gluten-Free Labeling Standards In-Line with New Codex Alimentarius Standards
• Diet.com: Contamination of Naturally Gluten-Free Grains 
• “GF Product CLAIMS: Can You Trust Them?” Living Without: April/May 2010.