Celiac.com 03/06/2020 - Celiac disease has an incidence of about 1% in the general population. It is an automimmune disease triggered by a proline-rich protein, gliadin, when it enters the small intestine and leaks into the wall of the small intestine (therefore the name leaky gut). Humans cannot break down proline-rich proteins. In healthy persons, gliadin passes through the gastrointestinal tract and is excreted in stool and urine without consequences. Celiac patients, build antibodies in the small intestine and these antibodies travel through the blood stream in all areas of the body. In some patients, there are no apparent symptoms or they can be very mild, while in others the symptoms are quite severe and are even associated with an increased risk of a certain type of intestinal cancer. 

Researchers have identified that the body breaks down some of the components of gliadin, but the human body cannot break down and digest the components that contain the amino acid proline. There are two such segments of the gliadin molecule that are causing an inflammatory reaction and they are called 33-mer and 26-mer peptides, because they contain a 33 and respectively a 26 amino acid sequence.

In an effort to prevent the gliadin molecule from leaking into the wall of the small intestine, a variety of methods have been tried. These include, closing the junctions through which gliadin leaks, encapsulating the gliadin molecule, and enzymatic degradation of the inflammatory segments of the gliadin molecule.  

The smallest protein chain that can cause an inflammatory reaction is 9 amino acids long, and the goal would be to break down the gliadin molecule in segments of 8 or less amino acids. This has to happen before the gliadin molecule enters the small intestine and leak into the wall of the intestine. 

The most commonly sold over-the counter enzymes are in the DPP-IV group, and while they are in fact very effective in breaking down gliadin's smaller segments, they cannot break down the proline rich areas in segments of less than 9 amino acids, and are therefore not effective in preventing an inflammatory reaction. 

The three enzymes that have shown promising results are ALV003, an enzyme combination of 2 enzymes that is currently undergoing FDA testing, AN-PEP, produced by DSM, and enzyme that was originally used to make cold brewed beer clear, and a product called KumaMax, purchased by Takeda Pharmaceuticals. At this time only AN-PEP is available in various concentrations on the market. It has been particularly effective at breaking down gluten at a low pH commonly found in the stomach, and a study has shown that AN-PEP is even more effective if combined with a food grade acid. The tests were done in healthy volunteers and under laboratory conditions and several groups of researchers came to the same conclusions that AN-PEP is very effective in cleaving the gliadin molecule. The tests are considered pertinent even if healthy volunteers were selected because enzymes work in the stomach and not systemically and in that respect, there is no difference between a celiac patient and a healthy individual.  

Until a few years ago, gluten-sensitivity was considered to have the same cause as celiac disease, namely the gliadin molecule and in order to avoid regulator issues, these enzymes were recommended only for gluten sensitivity but not for celiac disease. Recent work suggests that these enzymes are in fact not as effective for gluten sensitivity because the culprit of most gluten sensitivities might not be the gliadin molecule. 

Enzymes Do Not Change the Nature of Celiac Disease and Do Not Treat or Cure It

Existing data is very encouraging and clearly proves that AN-PEP enzymes greatly reduce the concentration of gliadin and can possibly even make it undetectable. It is important to note, that these enzymes do not change the nature of celiac disease and therefore do not treat or cure it. They can only break down the molecule that is triggering a reaction and therefore help maintain a gluten-free diet when contaminants are present. Essentially, there are two ways to maintain a gluten-free diet. One way is to avoid any contaminants in the food but most authorities agree that this is almost unattainable. The second way, is to break down the contaminants before they can cause damage. The underlying immune-deficiency is not changed and adherence to a gluten-free diet can not be neglected. Clinicians are reluctant to recommend enzymes for gluten contamination and certainly not for intentional consumption without regulatory approval. 

The big challenge is that short term gluten challenge studies have been inconclusive because they did not prove an advantage over a placebo. In order to obtain conclusive results, patients who have been on a gluten-free diet for months or even for years before they develop symptoms or antibodies, and therefore a study to prove conclusively an advantage over a placebo, is very difficult to conduct and might take years. Given this challenge, it is unlikely that an enzyme will ever go through the FDA process. As long as enzymes are not recommended to treat or cure a disease, they do not have to be FDA approved but are regulated by the FDA and have to be registered as dietary ingredients. 

Enzymes Could Lead to Being Less Careful and Cause a Higher Risk of Gluten Exposure

There is the concern that enzymes could lead to being less careful and therefore causing a higher risk of gluten exposure, and this is a valid argument, but the ethical question then arises whether this is enough reason to withhold the additional benefit of safety to those who are careful.

A recent study suggests that there is a method to measure the impact of gluten with a blood test of interleukin-2 within a few hours of gluten ingestion, and the results could make a gluten-challenge study shorter and safer and could help investigate enzymes or other methods that support a gluten-free diet.

Another very promising application for enzymes is to treat gluten-containing food products and break down the immunogenic components of gliadin. These foods could not be labeled as gluten-free but only as gluten-removed. It is currently accepted that alcoholic drinks such as vodka or whiskey that are made from gluten containing grains are considered safe because of the distillation process that removes all gluten-proteins from the final product. Current laboratory tests are very accurate in determining if a product does or does not contain gluten. Currently an enzymatically treated product is not considered at the same level of safety as when gluten (gliadin molecule) is completely removed from a food product. However, at least theoretically, there should be no difference between a product that is made from non-gluten containing ingredients and a product that has been treated in a way that the finished product has no detectable gluten molecules. 

In conclusion, evidence is very strong that enzymes could be recommended for the breakdown of contaminants in support of a gluten-free diet, but not to replace a gluten-free diet. This does greatly enhance the quality of life for celiac patients when eating outside of a completely controlled environment, which is not attainable for most people. 

Join the forum discussion on on enzymes discussed in this article.

Studies on AN-PEP:

• Extra-Intestinal Manifestation of Celiac Disease in Children. Nutrients 2018, 10(6), 755; doi:10.3390/nu10060755
• Efficient degradation of gluten by a prolyl endoprotease in a gastrointestinal model
• Enzymatic gluten detoxification: the proof of the pudding is in the eating!
• Highly efficient gluten degradation with a newly identified prolyl endoprotease: implications for celiac disease
• Degradation of gluten in wheat bran and bread drink by means of a proline-specific peptidase

References:

• Hausch, F., Shan, L., Santiago, N. A., Gray, G. M. & Khosla, C. Intestinal digestive resistance of immunodominant gliadin peptides. Am. J. Physiol. Gastrointest. Liver Physiol. 283, G996–G1003 (2002)
• Shan, L. et al. Structural basis for gluten intolerance in celiac sprue. Science 297, 2275–2279 (2002)
• Greco, L. et al. Safety for patients with celiac disease of baked goods made of wheat flour hydrolyzed during food processing. Clin. Gastroenterol. Hepatol. 9, 24–29 (2011)
• Stoven, S., Murray, J. A. & Marietta, E. Celiac disease: advances in treatment via gluten modification. Clin. Gastroenterol. Hepatol. 10, 859–862 (2012)
• Gass, J. & Khosla, C. Prolyl endopeptidases. Cell. Mol. Life Sci. 64, 345–355 (2007)
• Mitea, C. et al. Efficient degradation of gluten by a prolyl endoprotease in a gastrointestinal model: implications for coeliac disease. Gut 57, 25–32 (2008)
• Shan, L., Marti, T., Sollid, L. M., Gray, G. M. & Khosla, C. Comparative biochemical analysis of three bacterial prolyl endopeptidases: implications for coeliac sprue. Biochem. J. 383, 311–318 (2004)
• Edens, L. et al. Extracellular prolyl endoprotease from Aspergillus niger and its use in the debittering of protein hydrolysates. J. Agric. Food Chem. 53, 7950–7957 (2005)
• Marti, T. et al. Prolyl endopeptidase-mediated destruction of T cell epitopes in whole gluten: chemical and immunological characterization. J. Pharmacol. Exp. Ther. 312, 19–26 (2005)
• Stepniak, D. et al. Highly efficient gluten degradation with a newly identified prolyl endoprotease: implications for celiac disease. Am. J. Physiol. Gastrointest. Liver Physiol. 291, G621–G629 (2006)
• Pyle, G. G. et al. Effect of pretreatment of food gluten with prolyl endopeptidase on gluten induced malabsorption in celiac sprue. Clin. Gastroenterol. Hepatol. 3, 687–694 (2005)
• Gass, J., Vora, H., Bethune, M. T., Gray, G. M. & Khosla, C. Effect of barley endoprotease EPB2 on gluten digestion in the intact rat. J. Pharmacol. Exp. Ther. 318, 1178–1186 (2006)
• Bethune, M. T. et al. A non-human primate model for gluten sensitivity. PLoS ONE 3, e1614 (2008). 29. Siegel, M. et al. Rational design of combination enzyme therapy for celiac sprue. Chem. Biol. 13, 649–658 (2006)
• Gass, J., Bethune, M. T., Siegel, M., Spencer, A. & Khosla, C. Combination enzyme therapy for gastric digestion of dietary gluten in patients with celiac sprue. Gastroenterology 133, 472–480 (2007)
• Siegel, M. et al. Safety, tolerability, and activity of ALV003: results from two phase 1 single, escalating-dose clinical trials. Dig. Dis. Sci. 57, 440–450 (2012)
• Tye-Din, J. A. et al. The effects of ALV003 predigestion of gluten on immune response and symptoms in celiac disease in vivo. Clin. Immunol. 134, 289–295 (2010)
• Lähdeaho, M. L. et al. ALV003, a novel glutanase, attenuates gluten-induced small intestinal mucosal injury in coeliac disease patients: a randomized controlled phase 2a clinical trial. Gut Suppl. 60, A12 (2011)
• Janssen, G. et al. Ineffective degradation of immunogenic gluten epitopes by currently available digestive enzyme supplements. PLos One 10, e0128065 (2015).
• Stenman, S. et al. Enzymatic detoxification of gluten by germinating wheat proteases: implications for new treatment of celiac disease. Ann. Med. 41, 390–400 (2009)
• Stenman, S. et al. Degradation of coeliac disease-inducing rye secalin by germinating cereal enzymes: diminishing toxic effects in intestinal epithelial cells. Clin. Exp. Immunol. 161, 242–249 (2010)
• Laparra, J. M. & Sanz, Y. Bifidobacteria inhibit the inflammatory response induced by gliadins in intestinal epithelial cells via modifications of toxic peptide generation during digestion. J. Cell. Biochem. 109, 801–807 (2010)
• De Angelis, M. et al. VSL#3 probiotic preparation has the capacity to hydrolyze gliadin polypeptides responsible for celiac sprue. Biochim. Biophys. Acta 1762, 80–93 (2006)
• Julia König et al. Is an enzyme supplement for celiac disease finally on the cards?
• Pages 531-533 | Received 01 Feb 2018, Accepted 02 May 2018, Accepted author version posted online: 06 May 2018, Published online: 11 May 2018
• Pinier, M. et al. Polymeric binders suppress gliadin-induced toxicity in the intestinal epithelium. Gastroenterology 136, 288–298 (2009)
• Pinier, M. et al. The copolymer P(HEMAcoSS) binds gluten and reduces immune response in gluten-sensitized mice and human tissues. Gastroenterology 142, 316–325 (2012)
• Smecuol, E. et al. Gastrointestinal permeability in celiac disease. Gastroenterology 112, 1129–1136 (1997)
• Tripathi, A. et al. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin2. Proc. Natl Acad. Sci. 106, 16799–16804 (2009)
• Lammers, K. M. et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology 135, 194–204 e193 (2008)
• Di Pierro, M. et al. Zonula occludens toxin structure-function analysis. Identification of the fragment biologically active on tight junctions and of the zonulin receptor binding domain. J. Biol. Chem. 276, 19160–19165 (2001)
• Leffler, D. A. et al. A randomized, double-blind study of larazotide acetate to prevent the activation of celiac disease during gluten challenge. Am. J. Gastroenterol. 107, 1554–1562 (2012)
• Kelly, C. P. et al. Larazotide acetate in patients with coeliac disease undergoing a gluten challenge: a randomised placebo-controlled study. Aliment. Pharmacol. Ther. 37, 252–262 (2013)
• Katharina Anne et al. Novel approaches for enzymatic gluten degradation to create high-quality gluten-free products https://doi.org/10.1016/j.foodres.2016.11.021

Celiac.com 02/29/2020 - It has been a long and winding road, and around each curve something new has been discovered. I have learned more than I ever thought there was to know about celiac disease. I am forever grateful for having received a celiac diagnosis because it was on that day that I began my journey back to health.

On my first day of diagnosis I set out to find out as much as possible about this seemingly rare, but obviously complicated disease. My diagnosis answered a lot of questions for me, yet I was also struck by how many new questions arose.

What was the trigger for celiac disease, of course gluten played a part, but what in my past history put me over the edge? What had changed? Did the doctors know so little about the trigger for celiac disease that it was only now becoming clinically identifiable?

My last article was an attempt to explain how genetics and environment intersect in celiac disease, but I may have gotten part of it wrong, in part because the International Journal of Celiac Disease (IJCD) got it wrong (at least in my case they did).

After the IJCD cited Pellagra in celiacs at a 58% percent rate, I piled on the bandwagon. Quoting “The two diseases can be connected in two aspects. 58% of pellagra patients were shown to have malabsorption and many had intestinal pathology on biopsies.” But we were both wrong I now believe—hold onto that 58% thought, as it will come up later—and I think it's important in helping to confirm my new theory.

So where did my pellagra position go wrong? I chose the capstone, pellagra, and not the cornerstone, which may actually be thiamine (B1), and this is easier to do than you might imagine. These diseases have diffuse symptom’s common in their pathogenesis, and only testing can confirm my high suspicion that I may have had undiagnosed, or misdiagnosed, beriberi. Beriberi is is caused by low thiamine (B1).

I recently came across research that is 30+ years old that establishes, in mammal’s at least, a trigger for thinning villi titled “Effect of dietary thiamin deficiency on intestinal functions in rats.” To quote from the research “The activities of brush border sucrase, lactase, maltase, alkaline phosphatase, and leucine aminopeptidase were reduced by 42 to 66% in thiamine deficiency, compared to pair-fed controls. Kinetic studies with sucrase and alkaline phosphatase evinced that a decrease in Vmax (61 and 64%, respectively) with no change in Km (33.8 and 4.3 mM, respectively) was responsible for observed impairment in the enzyme activities in thiamine deficiency.”

This research leads me to believe that the lactose intolerance so common in those with celiac disease may actually be triggered by thiamine deficiency.

I had many of the symptom’s of beriberi, but since I was not in a concentration camp or was not an alcoholic the clinical suspicion was not high enough to have me tested for a thiamine deficiency, despite thiamine and other B vitamins deficiencies that are common in celiac disease.

Unfortunately even going on a gluten-free diet does not always correct B vitamin deficiencies, and thiamine, niacin and riboflavin deficiencies have been excluded from most celiac disease studies. One study entitled  “Evidence of poor vitamin status in Celiac patients on a gluten-free diet for 10 years" shows that such deficiencies can continue long after diagnosis.

Another study entitled “Vitamin and Mineral Deficiencies Are Highly Prevalent in Newly Diagnosed Celiac Disease Patients” says: “Almost all celiac disease-patients (87%) had at least one value below the lower limit of reference.” Testing for certain vitamin deficiencies is standard care following a celiac disease diagnosis, however levels of thiamine (B1), niacin (B3) and riboflavin (B2) are not usually part of a standard screening.

It is my hope from reading this that you are alerted to possible B vitamin deficiencies so that you can ask your doctor to have your levels checked, especially if you have been recently diagnosed, or are still struggling with diffuse symptoms years later, for example fatigue, muscle cramps, tingling in your feet and hands, burning feet syndrome, worse at night, etc.

You may still be low in thiamine, riboflavin and/or niacin, and doctors often overlook screening for these deficiencies in celiac disease.

Celiac Disease is a Genetic Disease with an Environmental Trigger

This is where B vitamins come in, as they help us make energy and regulate our environment at the cellular level. It is a 50/50 equation of stress vs. environment combined with genetics, and this can be a hard concept to understand because many people believe that it's all due to DNA.

Research from December 2019 entitled “DNA Has Relatively Little Say in Disease Risk (Usually)” says: “In fact, for such (most) diseases, the genetic contribution to disease risk is just 5–10%. There are diseases, however, for which the genetic contribution is about 40–50%. These diseases include Crohn’s disease, celiac disease, and macular degeneration.”

B Vitamins, Especially Thiamine (B1), Could be the Missing Pieces to the Puzzle

Via the Parasympathetic Nervous System (PNS) the neurotransmitter "acetylcholine" regulates our organ functions throughout the body, and could be why both undiagnosed celiac disease and beriberi affect so many organs in the body. Without enough thiamine our body can’t synthesize enough acetylcholine to regulate it’s organs, which may cause the body to go into high alert mode and trigger a runaway auto-immune reaction like celiac disease. Another study shows a connection with the microvilli that line organs and how they can trigger auto-immune reactions throughout the body.

What about that 58% I mentioned earlier? It happens to be the same rate that Japanese sailors developed beriberi, which is what you would expect to find when someone relies on too many carbs, including too much rice or wheat in their diets. It's possible that when the carb happens to be wheat this deficiency could trigger celiac disease, a disease that was discovered by Willem-Karel Dicke in the post WWII Netherlands, or present itself as beriberi when one only eats rice.

It took 20 years and countless deaths before the Japanese army discovered what the Japanese navy had learned 20 years earlier, and this article on the “Barley Baron” supports why there is a strong need to enrich gluten-free bread with B vitamins, exactly as regular wheat bread is enriched. According to this article, "(w)e now know that beriberi stems from a lack of vitamin B1, which the body requires for metabolizing carbohydrates and maintaining neurological functions. Without it, a person succumbs to nerve damage and eventually death."

So, perhaps a thiamine deficiency is one of the overall environmental triggers of celiac disease in those who have the genetic disposition? Could beriberi trigger celiac disease in susceptible individuals? Hopefully more research will be done to determine this, but in the meantime, get your thiamine levels checked!

Additional Resources:

• https://www.ncbi.nlm.nih.gov/pubmed/23379830 
• https://www.ncbi.nlm.nih.gov/pubmed/29982183 
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4863043/ 

Celiac.com 02/21/2020 - It seems fiber is important, especially for those suffering from celiac disease. Who knew? A study published in the March 2018 issue of Clinical Gastroenterology determined that increased fiber intake helped with ongoing celiac symptoms among sero-negative patients, and those with healed small intestine mucosa.

The study looked at 47 confirmed celiac disease patients, of which 22 were not suffering from ongoing celiac symptoms, while 25 had ongoing symptoms. Both groups had healed intestinal mucosa and negative blood tests for celiac disease. They also tested a whole bunch of other technical biomarkers such as "CD3 + and γδ + intraepithelial lymphocytes (IELs), CD25 + and FOXP3 + regulatory T cells, and CD117 + mast cells, and the expression of tight junction proteins claudin-3 and occludin, heat shock protein 60, interleukin 15, and Toll-like receptor 2 and 4 were evaluated in duodenal biopsies." I have no idea what these are or why they are important, but they looked at them. My guess is that they are related to the autoimmune and/or inflammatory processes.

The asymptomatic patients ate more fiber and had a larger number of CD3 intraephithelial lymphocytes (IELs). According to the study, "There may be a correlation between the number of CD3 IELs and intestinal inflammation."

The big take away for me on this is that we should eat more fiber. The gluten-free diet is notoriously low in fiber. Some good sources of fiber are beans, greens, coconut, corn, broccoli, sweet potatoes, and brown rice. 

Beans can cause unfortunate gas and bloating which can be mistaken for celiac symptoms. Soaking beans overnight before cooking and using the Beano enzymes are good ways to counteract this. I find I can eat beans one day, but struggle if I try to eat them two days in a row. Leafy greens, again two days in a row throws my body into a fit. Maybe alternating days of beans and greens might help!

Also, there is no shame in a gluten-free fiber supplement. I find psyllium husk fiber supplements to be exceptionally hard on my system. I use flax seeds when I need to. Here is a great article on how to choose a good fiber supplement for yourself.

Anyway, if you are experiencing ongoing celiac symptoms, try a fiber supplement for a few weeks. Many people will tell you to eliminate diary, all grains, or a low FODMAP diet. This might be simpler and easier to implement than any of those and might provide relief. I would say this is worth a try!

Celiac.com 02/13/2020 - I made a rare visit to a cousin a year or so after I was diagnosed with celiac disease. As the youngest child in a large extended family, my cousin was closer to my mother's age than mine. He took my mother and me on a beautiful ride around Kansas City. I sat in the back seat as they reminisced about their younger lives while passing the places where they experienced them. It came time for lunch and he wanted to take us to a favorite BBQ place in the heart of Independence, MO. I hesitated at his suggestion, and he said, "You aren't one of those vegemanaterians, are you?" The coy word he used, and his tone suggested his disapproval of anything out of the ordinary. (In fact, at that time I was a gluten-free vegan!) I said, "I'll find something." During lunch, I picked at French fries, pretty sure they were cooked in a dedicated fryer. My mother and cousin exuberantly scarfed the BBQ. My cousin told us about another cousin I hadn't seen in over 40 years that I apparently look like and reminded him of. He said, "Cousin Sandra is weird. She used to bring her own food to our family dinners." 

He was referring to a time, fifty years ago. Back then, members of the extended family met at my grandmother's house every Sunday to share their views on politics and happenings in the world. It was a close-knit family. Dinner consisted of the main dish (usually pressure cooked ham, green beans, onions, potatoes, bread, and cake for dessert) made by my grandmother, and side dishes brought by my aunts. I was no older than five, and have hazy recollections of these dinners, other than the warmth of family and the familiar smells of home cooking. To be included meant to eat, drink, smoke (it seemed they all did it back then) and converse around that big dining room table. I can imagine that someone daring to bring their own food, spreading it out on their placemat and eating it, while all those other dishes were being passed, might not go over well. 

As I reflect on my cousin Sandra, it occurs to me that she may have had celiac disease. That was in the early 1960's when it was virtually unheard of in the United States. Why else would she have had to bring her own food to those cherished dinners? A diagnosis prohibiting food of any kind would have been alien and unfathomable to anyone in my family. These are people who lived through the depression after all, where popcorn was the fare for breakfast, lunch, and dinner, if they even had that! Waving away any food, especially foods made by loving hands would have been viewed as an arrogant rejection of their abundance and love. 

Perhaps she had a mental illness that made her "weird," or maybe she made unreasonable demands on the family, but I think the most likely reason is that she was just trying to protect her health. Considering how my cousin put it, she was weird only because she brought her own food to the family dinners. In his eyes, she became the "weird one," ousted by the family because of her audacity to bring her own food to the dinner party. Family lore according to my mother goes on to say that: "She ultimately divorced our family." Can you do that?

It's a sad story, isn't it? But I think about it from time to time. I wondered if Sandra was so maligned because the family decided her special needs were so odd that they ostracized her, and she ultimately rejected them. Does that mean that anyone in the younger generation who may have inherited the same disease runs the risk of being shunned? I'd like to think we're more enlightened now, but thankfully, I'll never know. I do recall that my mother shushed family when they talked about their illnesses around me, fearing I'd imitate them, I suppose. Her attitude was that you made yourself well, or you made yourself sick, and I think she was careful to protect me from hearing about other people's illnesses so I didn't get the idea that I may have them too. She had a Pollyannaish perspective, and thought everyone in her family was perfect, no matter what. That made it very challenging for me to convince her that something wasn't perfect with me when I was finally diagnosed with celiac disease. In fact, I think she thought I brought it on myself. (I was in my mid-forties when properly diagnosed.) These were her "truths" and likely the "truths" of the collective family.

Most of those people around that dinner table fifty years ago have passed on, I imagine happily gathered "around that table in the sky." In Sandra's case, family members didn't understand her dietary restrictions, agreeing she was "weird" and rejecting her for her special needs. She was stereotyped as a prima-donna. Cumulative family lore develops through repeated acts of storytelling formulating familial ideologies that perpetuate collective "truths." These stories form the group's opinion on given topics. Sometimes these "truths" evolve from just participating in the same activities together, and developing a way of doing things that everyone agrees on, as described with the Sunday dinners above. In their lively discussions, my extended family debated "truths" about politics, news stories, and current events. Similarly, they had a collective opinion about how each other should act while sitting around that table. When someone altered the established norms, like Cousin Sandra, she disturbed rituals, and rocked the family's agreed-upon "truths." Her rejection of the foods required the family to rewrite their collective story. This is rarely done on a conscious level, but rather it is done as groupthink. The unspoken "truth" was: you do what we do, eat what we eat, and even smoke what we smoke in order to fit in. Buck that system, and suffer the consequences. 

In Cousin Sandra's case, the group determined her choices were a rejection of the others. She refuted the established but unspoken ideology (or taken for granted truths). As a result, she was rejected and mocked. From their view, if she didn't participate, she self-selected alienation. Before rejecting her, they likely cajoled her to participate, suggesting a little won't hurt you, or come on, just a bite. In fact, I can "see" my grandmother holding up a fork with a bite on it, saying, wouldn't you like just a taste? These urgings are attempts to include rather than exclude. What they really are saying is: you don't want to be rejected by the family by refusing our norms… come on, just have a little so you can stay a part of our group. That is actually a compassionate message. But we don't "hear" it that way when the food being offered to us is poison, and when we feel our needs are not being honored or understood. 

"Man is by nature a political animal with an innate tendency to form into groups" (Aristotle). Cousin Sandra was a victim of groupthink. Groupthink is a process described originally by Janis (1972) where those empowered in a group share a common belief, whether it is true or not, and then put pressure on those who do not comply with those truths. Those not going along with the group's ways of thinking are censored, ignored, or ultimately culled unless they comply. Those who share the group's opinion are unified members of the group. Groupthink evolves through the process of familial storytelling where "truths" are formed and solidified, sometimes becoming self-censored, and self-serving (Janis, 1972). Ideologies are assimilated through conversation that conveys a story that intertwines cultural influences with long-held beliefs (Fisher, 1989). Narrators balance truth with motivations in a cohesive story with significant meaning (White, 1980) and seek reinforcement or agreement from outside culture, religion, and political influential forces (McAdams, Reynolds, Lewis, Patten, & Bowman, 2011). This story telling process to formulate "truths" is integral to family traditions, making meaning of shared life, "doing family" (Langellier, & Peterson, 2018, p. 1), and teaching family values (Koenig Kellas & Kranstuber Horstman, 2015). It is in our initial home where we learn fundamentals for what and how to eat, how to cook, how to participate in food-related rituals), as well as gender roles and power structure biases around food (de Certeau, et al., 1998; Pecchoni, Overton, & Thompson, 2008). Groupthink is a way of encouraging belonging to the group or family and creates power structures of "us" and "them." I don't think anyone in my family ever intended to bully Cousin Sandra out of the group, It just happened because of their rigid policies on how we ought to act perpetuating the ideology: Think like us, and belong. I doubt anyone ever talked openly about it because they lacked the tools and skill to broach a constructive conversation.

Food is so integral to our social existence that forsaking the foods made by loving hands implies a repudiation of those hands, and the people who share it. Breaking bread around the dinner table is a way that people bond. Not taking that bread, or accepting that cup of tea, or eating what everyone else eats, is viewed as a silent form of rejection. This is why having gluten sensitivities causes so many social issues, and is one of the topics in my book. People I surveyed and interviewed told me many stories like the one above. As I reflected on what people said, I realized that the root of the problem is that we do not have language to talk about these things. If we could say, "I'm not rejecting any of you by not sharing your food. I have a disease that prevents me from eating it, and I still want to sit at this table and be a part of the conversation." We just don't seem to be able to have these candid conversations. But by identifying these flawed social norms, we can work to change them, so people rejecting food served around the extended family dinner table can be included, loved, and un-judged for their choices. The first step is to identify these long held "truths," put words to them, and discuss them openly, rather than living with unstated dysfunctional consensual rules that cause people who defy them to be alienated. 

Let's discuss.

1. What long held "truths" does your family live by?
2. Please describe a time when you felt excluded because you didn't eat the foods everyone else was eating around the table. How did you handle it? How did the others at the table handle it?
3. What would you tell Cousin Sandra if you could talk to her? 
4. How does your family form "truths?" What happens when someone rocks the "truth" boat in your family? How do you collective reform your opinions/"truths?"

References:

• de Certeau, M., Giard, L., & Mayol, P. (1998). The practice of everyday life, Vol. 2. Minneapolis, MN: University of Minnesota Press.
• Fisher, W. R. (1989). Human communication as narration: toward a philosophy of reason, value, and action. Columbia, SC: University of South Carolina Press.
• Janis, I. L. (1972). Victims of groupthink. Boston: Houghton Mifflin.
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Celiac.com 02/07/2020 - Gluten sensitivity during pregnancy can profoundly impact fetal brain development. Gluten is a protein found in wheat, rye, and barley. 

Many people who have a gluten intolerance may also have other food sensitivities to common antigens like corn, soy, dairy, and sugar. Many times, without a histamine response like hives, people can be blissfully unaware of their food sensitivity. 

Studies have shown gluten sensitivity destroys brain and nervous tissue more than any other tissue in the body, and is linked to a number of other neurological disorders. (Read my blog Gluten Intolerance Testing for more information about this.)

Eating Gluten During Pregnancy May Potentially Put Your Child At Risk

Beginning before birth, the left and right hemispheres of the brain develop in stages according to a very sophisticated schedule. Each hemisphere depends on the other to meet its developmental goals within a precise window of time. While in-utero and in early childhood, viruses, infection, and inflammation (such as that from a gluten sensitivity), can throw a wrench in this intricate timing and hinder proper brain development. This sets the stage for a wide range of neurological disorders, attention-deficit/hyperactivity disorder (ADHD), autism, Tourette's syndrome, depression, anxiety, and other childhood brain disorders. 

Childhood mental disorders now affect one in five children, and the rates are increasing.

Wheat Can impact Brain Function

There are at least 13 different ways I know of that a gluten sensitivity can impact the brain. Let's look at a couple of the big ones.

One mechanism is that there can be elevated antibodies to wheat and the cerebellum and GAD-65. Your cerebellum controls your muscle movements. After years of your body attacking this brain tissue, the brain may shrink.

People with GAD-65 antibodies indicate a high trigger for anxiety and ADHD.

Another common mechanism is hypoperfusion, a lack of blood flow going to the brain. 73% of people with a sensitivity to wheat have hypoperfusion. Just like your cells need hydration, your brain needs to be saturated.

So many people go undiagnosed with a gluten-related disorder for years. Imagine what we are doing to our children (and ourselves) when we eat that bowl of cereal or toast before school or work. We are not able to function optimally. This is why "brain fog" is the most common symptom for people with a sensitivity to wheat.

In 2006, a study looked at 132 people with symptoms of ADHD who had a wheat sensitivity. When they put them on a gluten-free diet, the researchers reported markedly  significant improvement in all behavioral markers within six months.  

Gluten sensitivity may also more than double your child's risk of developing schizophrenia later in life.  

The first study to reveal food sensitivity was linked to a greater risk for psychosis, autism and other brain disorders in the child. Researchers looked at blood samples of nearly 800 individuals born in Sweden between 1975 and 1985. 

What did they find? People with schizophrenia had high levels of gluten antibodies in their blood at birth - meaning a gluten sensitivity was passed from mother to child.

You Might Have an Undiagnosed Gluten Sensitivity

Awareness is growing as rates of celiac disease, an intestinal autoimmune disease caused by gluten, have quadrupled in the last 50 years. 

The numbers could be much higher. In fact, it's estimated that 95 percent of those with celiac disease go undiagnosed. 
Researchers also estimate the numbers of people with gluten sensitivity — a non-celiac inflammatory reaction to gluten — range from 10 to 30 percent of the population. 

During Pregnancy, Mom's Gluten Sensitivity May Affect Her Baby's Brain 

If you look at the current explosion in inflammatory disorders today, the rise of these brain-based disorders is less of a mystery. Immune-activated mothers are giving birth to immune-activated babies. 

If you can, don't wait until pregnancy to look into food sensitivities. Every woman needs to consider a screen for gluten sensitivity. Look for anti-gliadin antibodies and, if that test comes back positive, go on a gluten-free diet. 

We don't know at which point during pregnancy a mother's gluten sensitivity impacts the fetal brain, but we do know the baby's brain and nervous system begin developing in the first trimester. Although the association between a mother's gluten sensitivity and the baby's increased risk of psychosis as an adult is not yet fully understood, it makes sense to err on the side of caution. 

"During My Pregnancy, I Didn't Get Nauseous. I Must Not Have Gluten Sensitivity, Right?" 

Not Necessarily. A lack of gut symptoms doesn't mean you're in the clear. Everyone reacts differently to gluten sensitivity. One person can have chronic skin rashes, another may have joint pain, and a third brain fog. In fact, research suggests the majority of people with gluten sensitivity have no gastrointestinal symptoms whatsoever. 
For every person with gut symptoms caused by gluten, there will be eight who have none, despite there being a gluten sensitivity present. 

An undiagnosed gluten sensitivity during pregnancy is in no way a guarantee that your child will develop schizophrenia or other brain disorders either. However, when an expectant mother produces autoimmune antibodies to brain tissue, 86% of their children are on the autism spectrum. 

If mom has an autoimmune mechanism going on inside her body, it can affect the baby. One of the most common food sensitivities associated with neurologic problems is wheat. Only a fraction of people who have a problem with wheat have celiac. Many more have gluten sensitivity. 

Many women —and men—may be better off on a gluten-free diet even though they do not have celiac disease. 
How do you reduce antibodies?

First, screen for antibodies against the brain. Two great tools for screening are the Cyrex Array #5 and the Neural Zoomer. 

If you are producing antibodies, you need to eliminate the trigger(s). The goal is to stop the autoimmune cascade, particularly during pregnancy when the fetus is developing its entire body and establishing its own immune system that will set him or her up for life.

Bacterial Colonies Change in the Vaginal Tract During Pregnancy

In the last trimester of pregnancy, the bacterial colonies in the vaginal tract change completely to the point that there's a very high count of prevotella [bacteria]. 

Most of the time, there are practically no prevotella that are measurable in the vaginal tract at all. The change in the last trimester occurs because the prevotella is the substance that coats the baby as it comes down the birth canal. Prevotella migrates through the baby's nasal cavity and its mouth and goes down to turn on the genes in the gastrointestinal (GI) tract. These genes say, "Okay, this is the mammal that is going to start feeding you. Here are the codes for the protein that's about to come to you for food." 

The baby's digestive tract then starts turning on the digestive enzyme production capability for the specific proteins that are encoded in the prevotella bacteria. 

My Personal Story

When we were first married, my ex-wife and I, despite all efforts, could not get pregnant. I was an intern at the time, and I called the seven most famous doctors I'd ever heard of, holistic doctors, and asked, "What can we do?" 

Because I was an intern, they asked, "Do you know this?" "Do you know that?" I'd say, "No." 

And they would respond: "Learn." 

So I put a program together, and we were pregnant in six weeks.  A lot of people know that this began my study of gluten and the many effects it has on the body.

Since then, I've helped hundreds of couples with infertility, recurrent miscarriages, and hormonal imbalances. There's not much in medicine that's all or every, but this is an every. 

What we learned early was that every person with hormone-related symptoms, whether it was infertility, miscarriages, estrogen dominance, testosterone deficiency, all of them, when tested properly, had a sensitivity to foods that they were eating — foods that they did not know were making them sick. 

When you eat a food that you're sensitive to, it triggers inflammation in the body. The immune system responds to try to protect you from something it considers an invader, and it creates an inflammatory reaction.

I have said this so many times over the years: "Ms. Patient. If you pull at a chain, the chain always breaks at the weakest link. So, the first thing to do is to learn what's pulling on the chain." 

We found out something amazing...

Food Sensitivities Were a Component Every Time

Often there were more, but it was an important component. I found that the most frequent food sensitivity was wheat. So I started reading the literature on wheat way back in 1980. Our daughter was also born in 1980, and I started talking about it shortly thereafter because the studies were blowing me away.

By 2004, I was lecturing professionally onstage about wheat sensitivities with or without celiac disease. That progressed and progressed until 2008, when a nutritional company called Metagenics sponsored me to go around the world. I went to 26 different cities and gave full eight-hour presentations on wheat sensitivity. The presentation dropped everybody's jaw. No one had ever seen these studies about different types of spondyloarthropathy, rheumatoid arthritis, psoriasis, multiple sclerosis, attention deficit disorder, autism, or Alzheimer's and how it would benefit some of those people just by getting off of wheat. They started to get better, sometimes dramatically, but often to some degree.

In 2009, I did the same 26 cities for a full eight-hour presentation on the development of autoimmunity. 

What triggers the development of autoimmunity? And what do you do to address autoimmunity? 

It was infertility, successfully addressed by looking at food sensitivities and a couple of other things that led me into learning about wheat sensitivity; gluten sensitivity; and the trigger of intestinal permeability.

For example, in the United States, 78% of the prebiotic diet is wheat. If you take wheat out of your diet, which is a very important thing, what you're also taking out is the major source of your prebiotics. And prebiotics feed probiotics, which are the good bacteria in your gut.

If you take wheat out of your diet without the right education or mentorship, you lose the main prebiotic source, and, as a result, probiotics in your gut (the good bacteria that need that food) start starving. Some probiotics begin to die off, and the bad guys in your gut that have been kept in check to some degree by those probiotics now become opportunistic and rear their ugly heads. 

This is why it is so helpful to find a certified gluten-free practitioner or nutritionist when you are on a gluten-free diet: This is especially important before and during pregnancy. You want to prepare your body to be free of antibodies prior to conception, and you want the proper nutrition to support both you and a developing baby.