Celiac.com 07/05/2016 - Principal Investigator: Amrit P.S. Narula M.D, F.A.C.P, F.A.C.G, F.A.C.N., A.G.A.F
Study Coordinator: Alicia Mercuri, PA-C

Background
Research estimates that approximately 18 million Americans have gluten sensitivity. That is six times more than patients confirmed with celiac disease. Non-celiac gluten sensitivity is defined as those individuals who cannot tolerate gluten in the diet and experience the same symptoms attributed to celiac disease, but lack antibodies and intestinal damage as seen in celiac disease.

A dietary supplement called ZyGluten was developed from in vitro studies, not in vivo. The primary aim in its development was a supplement which, if taken at the beginning of a meal, would hydrolyze gluten concentration in ingested food. Foods tested included McDonald's hamburger, white sliced bread, a plain bagel, macaroni and cheese, spaghetti, a muffin, and frozen pizza. The amount of gluten was measured at 0, 30 and 60 minutes after the introduction of ZyGluten. In all samples, gluten measured at the end of 60 minutes was less than 20 ppm.

ZyGluten is a compound of amylases, proteases, and lipase enzymes with probiotics, specifically Lactococcus lactis and Lactococcus cremoris. It is derived from plant and microbial sources.

Inclusion Criteria

• Ages 18-80 years
• Physician diagnosed gluten sensitivity by history and experienced symptoms of gluten sensitivity for at least 1 month prior to involvement
• Willing to take supplement twice daily for 2 weeks
• Sign informed consent

Exclusion criteria

• Active Inflammatory Disease
• Celiac disease confirmed by antibodies and duodenal biopsy
• Peptic ulcer disease
• Lactose intolerance
• Pregnant or lactating women
• Received any experimental drug within 30 days of enrollment

Methods
27 patients, all of whom met the inclusion criteria, were selected to take 2 capsules of ZyGlutens before 2 major meals of the day for 2 weeks. 23 patients were female and 4 were male, with ages ranging from 25-77. The following symptoms were assessed at baseline, week 1, and week 2 which was the conclusion of the study:

• Abdominal pain
• Diarrhea
• Constipation
• Headaches
• Joint pain
• Fatigue
• The severity of symptoms was measured as mild, moderate, or severe, and none if symptoms were absent.

All patients were contacted by phone within 48 hours of start of the trial to assess for any adverse effects. Following parameters were checked at baseline, week 1, and week 2:

• Weight
• Height
• Blood pressure
• Pulse rate
• Respiration rate
• Patients were not charged or reimbursed for their participation in the study.

Results
The following number of patients (27) had these symptoms at baseline:

 The following number of patients (23) had these symptoms at week 1:

The following number of patients (23) had these symptoms at week 2: 

The following number of patients rated their symptom improvement as:

• No improvement: 0
• Improved: 4
• Markedly improved: 19

Adverse Effects
No patients reported any adverse effects.

Participants
Twenty-seven participants were enrolled in the study. Two patients withdrew from the study; one of which had a scheduling conflict with follow-up visits and one stopped taking the medication due to increased sleepiness after two pills. Two patients were lost to follow-up. These four patients were excluded from analysis.

Conclusion
In conclusion, ZyGluten study is a 2 week open labeled trial. Our outcome so far has shown to be extremely efficacious with no significant side effects. There was no significant difference found in patients who complained of headaches or joint pain. The majority of the patients found significant improvement in their symptoms of abdominal pain, bloating, changes in bowel habits, and fatigue. In fact, 83% of patients rated that their symptoms markedly improved, and 17% rated an improvement in their symptoms.

Patient Testimonials

• *The medication was known by patients as ‘Gluten Buster' during the clinical trial.
• "Medication has given me more freedom. I am no longer afraid to eat, especially away from home. I am very pleased with the medication".-MF
• "My symptoms have improved. I would like to keep taking this if I can, especially since it's natural, to see how long I can go without an endoscopy".-MH
• "I feel that this pill has made a tremendous improvement in my condition". –BW
• "Bloating is gone. Stools seem to be more formed. Feeling good". –PS
• "It's wonderful to not be limited in what I can eat. It's great not to have the symptoms of pain, etc. when eating gluten foods". –JH
• "Great for bloating".-JF
• "Very little of passing gas. I feel good". -PW
• "Bloating is a lot better". -LW
• "I have not had any cramping or urgency to have a BM after a meal. My bowel movements are now normal. I have had no GI distress since on the meds". –KY
• "Gluten Buster has been a miracle pill. After so many years of having bowel problems, I never knew what it was like to have a regular bowel movement. I have had no problems with digestive system since I starting taking these pills". -JM
• "Medication was very helpful". –KO
• "My experience with the Gluten Buster that Dr. Narula has given me to take has been simply amazing. It has made my quality of life so much better. He is an amazing doctor to help those that otherwise thought there was no hope! I feel great"!-CM
• "Seems a little bit better. Still have IBS. Still have a lot of gas and bloating."-AM
• "It has been helping to go to the bathroom. The weight is going up and the stomach is going down a little bit".-SH
• "Before taking the medicine, mornings were hard because of bloating and diarrhea. Now I feel great in the morning".-GK
• "Gluten Buster is a life changer. Will definitely go on it when available in market." -MC
• "It is helping with bloating and gas. Has improved all of my GI symptoms. Overall, I can eat anything, including French fries and food I could not eat before (Super Pill)". -MK
• "I feel it has improved. Still have bloating, but eating regular food. Diarrhea has improved, no pain in stomach or abdomen". -BS
• "I feel 10x better than I did before starting the medication. No stomach cramps of bloating, I only have a BM twice/day. Feel great!" -JB
• "I am doing 100% better now since I have been taking the Gluten Buster meds". - JZ
• "Passing more gas, feeling better". -ML
• "I'm feeling better. I'm eating anything I want, not sticking with gluten free food. If it's due to taking the Gluten Buster, then I would still take it". -BS
• "It has made a big difference in bloating and abdominal pain. I would like to continue taking it". -JP
• "My stomach feels fantastic when I take the product. This should be available for all people with gluten sensitivity. This would be a great idea for Shark Tank. It needs to be available to the masses! I don't know how my stomach will survive without it, especially at the holidays". -LT

References

1. Am J Gastroenterol. 2011 Mar;106(3):508-14; quiz 515. doi: 10.1038/ajg.2010.487. Epub 2011 Jan 11. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Biesiekierski JR1, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, Shepherd SJ, Muir JG, Gibson PR.
2. The Oslo definitions for celiac disease and related terms. Jonas F Ludvigsson,1,2 Daniel A Leffler,3 Julio C Bai,4 Federico Biagi,5 Alessio Fasano,6 Peter H R Green,7 Marios Hadjivassiliou,8 Katri Kaukinen,9 Ciaran P Kelly,3 Jonathan N Leonard,10 Knut Erik Aslaksen Lundin,11 Joseph A Murray,12 David S Sanders,13,14 Marjorie M Walker,14 Fabiana Zingone,15 Carolina Ciacci16
3. Food Allergy - An Overview (PDF|1 MB). DHHS. NIH. National Institute of Allergy and Infectious Diseases.
4. Gastroenterol Hepatol. 2014 Jun-Jul;37(6):362-71. doi: 10.1016/j.gastrohep.2014.01.005. Epub 2014 Mar 22. [Non-celiac gluten sensitivity: a critical review of current evidence]. [Article in Spanish] Molina-Infante J1, Santolaria S2, Montoro M2, Esteve M3, Fernández-Bañares F3.
5. Gluten Causes Gastrointestinal Symptoms in Subjects Without Celiac Disease: A Double-Blind Randomized Placebo-Controlled Trial. Jessica R Biesiekierski, Evan D Newnham, Peter M Irving, Jacqueline S Barrett, Melissa Haines, James D Doecke, Susan J Shepherd, Jane G Muir and Peter R Gibson.
6. Nutrients. 2013 Sep 26;5(10):3839-53. doi: 10.3390/nu5103839. Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders. Catassi C1, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A.
7. BMC Med. 2014 May 23;12:86. doi: 10.1186/1741-7015-12-86. Non-celiac gluten sensitivity - why worry? Lundin KE.
8. BMC Med. 2014 May 23;12:85. doi: 10.1186/1741-7015-12-85. An Italian prospective multicenter survey on patients suspected of having non-celiac gluten sensitivity. Volta U1, Bardella MT, Calabrò
9. Neurogastroenterol Motil. 2013 Nov;25(11):864-71. doi: 10.1111/nmo.12216. Epub 2013 Aug 12. Non-celiac gluten sensitivity: clinical relevance and recommendations for future research. Mooney PD1, Aziz I, Sanders DS.
10. World J Gastroenterol. 2014 Jul 21;20(27):8837-45. doi: 10.3748/wjg.v20.i27.8837. Irritable bowel syndrome and food interaction. Cuomo R, Andreozzi P, Zito FP, Passananti V, De Carlo G, Sarnelli G.
11. Expert Rev Gastroenterol Hepatol. 2012;6(1):43-55. Problems of an Emerging Condition Separate From Celiac Disease. Amy C Brown
12. Dig Dis Sci. 1999 Jul;44(7):1317-21. Pancreatic supplements reduce symptomatic response of healthy subjects to a high fat meal. Suarez F1, Levitt MD, Adshead J, Barkin JS.

Celiac.com 06/28/2016 - My latest obsession is creating new quinoa recipes, since my eight year old daughter absolutely loves it! Her favorite is warm quinoa with crumbled turkey sausage, broccoli, and lots of cumin. She also loves it with oil and balsamic vinegar. I like it cold with chopped veggies, garlic, and fresh squeezed lemon juice. Just a few weeks ago I tried amaranth for the first time. It seems to be the new craze these days. It cooked up very similarly to quinoa, and had a similar taste and texture. I would say the only noticeable difference is that amaranth does not get as fluffy when cooked. It seems like it would be great in soup! Now for a little history.

Amaranth is estimated to have been domesticated between 6,000 and 8,000 years ago, and was a staple food crop of the Aztec's. The common name, amaranth, represents over sixty different plant species called amaranthus.(1) The amaranth plant is a full, broad leafed plant that has vibrant colors. Amaranth's name comes from the Greek name, amarantos, meaning "one that does not fade." This is due to the plant retaining its vibrant colors even after harvesting and drying. The amaranth plant can contain up to 60,000 seeds.

Amaranth is gluten-free and it contains about thirty percent more protein than rice, sorghum, and rye.(2) Amaranth flour can be made from the seeds and is a excellent replacement for those suffering from celiac disease or gluten sensitivity.

Amaranth flour has a unique chemical composition with a predominance of albumins and globulins and a very small prolamins content with total absence of alpha-gliadin. This makes it very comparable to wheat protein(2). It also has a relatively high content of calcium, iron, potassium, magnesium, and fiber and an almost perfect amino acid profile. It's particularly high in lysine, which is abundantly lacking in wheat and corn.(3)

Another benefit of amaranth is that it is a natural source of folic acid, and in some countries, amaranth is used alleviate birth defects. Amaranth is not a true grain, as it does not come from the Poaceae family, but is considered a pseudo-cereal like it's relative quinoa. Both amaranth and quinoa belong to a large family that also includes beets, chard and spinach.(3)

Quinoa is a broad-leafed plant that produces a small seed. It's a member of the Goosefoot family that is native to South America.(4) Quinoa is considered a complete protein that contains all nine of the essential amino acids necessary to human physiology, and it is the only plant-based source for these nutrients.(5) Quinoa cooks up like a grain, but it is actually a seed, and is an excellent source of protein for vegans and people following a gluten-free diet. According to the American Journal of Gastroenterology, it is also safe for celiac patients.(6)

Like amaranth, quinoa can be ground into a flour and used in cooking or baking. Quinoa is rich in manganese which is vital to activating enzymes crucial to metabolizing carbohydrates and cholesterol. It is also essential to bone development. Quinoa is rich in lysine, an essential amino acid, and helps with the absorption of calcium and the production of collagen and is low on the glycemic index.(5)

Both amaranth and quinoa are great gluten-free options, both as a flour or grain substitute, and have a nutty taste and texture. They readily absorb the flavors they are cooked with, but are also tasty on their own. They can be made hot or cold, combined with other foods, added to soups or baked goods, and made into hot porridge or cereal. They are both versatile, easy to work with, and have a high nutritional content. If you're looking for an easy, healthy, gluten-free option, why not try amaranth or quinoa? It's a staple in our home!

References:

1. Open Original Shared Link
2. Vopr Pitan. 2014;83(1):67-73., Amaranth flour: characteristics, comparative analysis, application possibilities.
3. Howard, B. C. (August 12, 2013), Amaranth, Another Ancient Wonder Food, But Who Will Eat It?, Retrieved from Open Original Shared Link.
4. Laux, M. (June 2012). Iowa State University. Agricultural Marketing Resource Center. Retrieved from Open Original Shared Link.
5. Norek, Danna. (June 15, 2010), Quinoa Gives the Perfect Protein Source to Vegetarians and Vegans. Retrieved from Open Original Shared Link.
6. Victor F Zevallos PhD1, L Irene Herencia PhD2, Fuju Chang MD, PhD3, Suzanne Donnelly PhD1, H Julia Ellis PhD1 and Paul J Ciclitira MD, PhD1 (January 21, 2-14). Gastrointestinal Effects of Eating Quinoa (Chenopodium quinoa Willd.) in Celiac Patients. Am J Gastroenterol 2014; 109:270–278.

Celiac.com 06/20/2016 - One evening in October 1999, while in my academic office at Open Original Shared Link, my professional and personal life changed in an instant. I had recently had the idea of testing stool for gluten sensitivity to possibly prove that patients with microscopic colitis, whom displayed an epidemiologic, pathologic, and genetic overlap with celiac disease but who rarely had positive blood tests against gluten (because they rarely had the small bowel villous atrophy of celiac disease; they had colitis which is inflammation in the colon). I had remembered that previous researchers in Scotland invasively placing tubes into certain patients without villous atrophy had been able to find antibodies to gluten deep inside the small intestine when they were absent from the blood. They called these patients latent celiacs. However, they never reported results of testing stool, which would have been a lot easier to collect because it did not require the multiple hours and patient invasion of placing tubes deep inside the intestine.

That October afternoon I received the first set of results from my laboratory of a newly improved method we had developed for testing stool for the presence of antigliadin IgA, the main antibody against wheat gluten. It was about 7:00PM, it was dark outside, and late enough in the office for everyone to have gone home, allowing me a quiet setting to review these results. What I saw that night seemed like a window into the future and a medical-scientific Pandora's box, all at the same time. Not only did I see that about 75% of the microscopic colitis patients had a positive fecal antigliadin test but 25% of asymptomatic volunteers did also. I quickly did the math, and realized that celiac disease at a prevalence of even 1% would pale in comparison to these statistics, revealing that hundreds of thousands of people in the US and the world may be gluten sensitive without having celiac disease. I knew that I had just been given information that no one else in the world knew, and that it would likely have major public health implications resulting from a new dietary-induced disease paradigm. That the main staple food of Western civilization may be causing large percentages of the population to have symptoms and syndromes, not only colitis, but perhaps also irritable bowel syndrome, autoimmune syndromes, short stature in children, multiple allergies and chemical sensitivities, and even idiopathic psycho-neurologic syndromes like depression, Parkinson's Disease or Lou Gehrig's disease. Not to mention what it might mean for me as the holder of this information.

Then it happened—the most significant moment of my life up to that point—it felt like someone had tapped me on my left shoulder. Though I knew I was alone in the office, I turned to the left and looked upward for some reason for what or whom might have tapped me on my shoulder. And though, while I saw no one there, I immediately knew there was a presence with me at that moment, a spiritual or angelic presence. And then I heard these words in my head "You have to leave this place". And within minutes, the decision came to me that I indeed did have to leave my academic post of 15 years to bring the results of this new fecal testing method to the public: to the 25% of otherwise asymptomatic people reacting to dietary gluten with the same immunologic reaction measured in celiac disease, antigliadin antibody, as well as to the 75% of patients with microscopic colitis and perhaps other GI ailments and syndromes who, with a gluten-free diet, might heal their chronic refractory inflammatory bowel conditions.

This was a bold line of thinking for me, as I had been on a professional trajectory toward the normal milestones of a successful young academic medicine career, becoming head of a sub-specialty medical department (for me, Gastroenterology), the prospects for which had just begun to surface in my life. Yet, I had just been called it seemed, by an encounter with a supernatural force, to an assignment of sorts with a mission to fulfill. And so, the idea of creating a specialty intestinal laboratory to make this new line of testing available to those in need of its benefits was born, EnteroLab.com (entero means intestine in Greek and in medical terminology). A "dot com" I thought? Yes, this form of testing should originate "in the comfort of your own home". Why make people with GI problems fly on an airplane half way across the country merely to give stool specimens for lab analysis (the practice of my Dallas hospital for decades up until that time). If I could create a mechanism whereby only the specimens but not the person could do the flying, then we could deliver results and follow-up dietary recommendations electronically, and the healing would begin shortly thereafter with dietary elimination of the causative antigenic foods. And if the client desired, they could have a paid phone consult with me or my nurse and still not have to spend the time, money, and difficulty flying to Dallas. And I have to admit, in 2000 it was kind of exciting to be the first doctor in the world to turn his entire medical career over to the internet, as well as to have created the first clinical laboratory serving people directly without the need of a prescription or previous doctor's visit, both incredibly bold and revolutionary ideas at the time (and perhaps still).

I had learned from similar major paradigm shifts in my field of gastroenterology (specifically, in 1983 when doctors in Australia found in their research that ulcers might be caused by bacteria, but whom were laughed at and ignored for about 15 years, yet later in 2005 received a Nobel prize) that it would likely take 15-20 years before anyone in the medical field would believe my new research findings relating to non-celiac gluten sensitivity and its simple diagnosis with fecal testing. This, even though I was regarded even at my young age as an expert in the field, with a significant track record for developing unique and successful ideas for diagnosis and treatment of GI diseases (see my CV at www.intestinalhealth.org/CV), and having been trained by one of the most successful and respected gastroenterologists of all time, Dr. John Fordtran. While my medical peers might not believe my results for some time, people suffering the symptoms would not care whether or not it was too soon for a scientific paradigm to shift, because they would want to try a gluten-free diet to get better. And try, they did. Following positive stool test results from EnteroLab, they got better in droves going gluten-free, and in most cases with complete healing of long-standing symptoms and syndromes. And eventually I predicted, with such remarkable improvements that had never been possible before, their health practitioners (at least the honest, inquisitive, and non-egotistical ones) would ask them what had brought on such improvement. Eventually these practitioners would begin sending other patients for the same testing that had opened the door to the dietary miracle the gluten-free diet posed for those previously tested.

Beyond the consequences of having to leave my academic positions and stature behind, I had to withstand some public and more often professional criticism for undertaking a bold and somewhat maverick professional move without the permission of my peers in doing so. This does not always go over smoothly in scientific and medical professional circles. Despite having been a highly respected young published researcher at that time (40 publications by the time I was in my mid-30's), my submissions both to professional GI society meetings and GI journals (journals that I had served as a reviewer for years) were rejecting my research submissions relating to this new paradigm of non-celiac gluten sensitivity. And it seemed, the rejections were not for objective reasons, but more subjective and for principle. Other researchers in this specific field and other fields have had to endure similar treatment. Sadly, submissions to these journals addressing paradigm-shifting topics are not always reviewed in unbiased, objective ways if they deal with a subject or contain conclusions that go against what the reviewers inherently believe to be true at that time (the "I'll see it when I believe it" scenario rather than "I'll believe it when I see it"). And yet, despite submissions of excellently performed and written studies that were rejected for these reasons by a system that seemed unready for this new paradigm, the most common public and professional criticisms of my methods primarily centered around my "lack of publication". This seemed circular and nonsensical to me. After all, had Michael Dell ever published his methods of making computers delivered in a revolutionary way (mail order) to its customers? These computers worked and served its customers well without a published method? Why is lack of publication of a medical technologic method equated with lack of Truth or efficacy? My response was and still is to remain true to my own data and experience, and my desire to serve and help people, and to not proceed according to the needs and critical dictates of others having no experience with my techniques.

And so, 15 years later, as EnteroLab approaches our millionth patient tested, and with the current number of referring health practitioners in excess of 1,500, EnteroLab.com stands as a successful purveyor of medical Truth and public service. I ask people "How could hundreds of thousands of people be satisfactorily served over 15 years if what we are doing was not worthy and True?"; at some point, a person's or business' track record has got to stand for something positive and meaningful. And it seems my estimate of the time it would take for other researchers or mainstream practitioners to begin getting on board with the new paradigm was correct. Non-celiac gluten sensitivity has recently been further researched and substantiated to exist, just as I reported in public and professional lectures as early as 1999 (but published by others as early as 1980). And it has only been in the last 2 years or so that I have seen the question being raised at national and international GI meetings by "celiac researchers", but at least they are now doing so. Yet, the public has been the patron of the paradigm all along. In the last 4-5 years gluten-free food companies have carried the ball farther down the field than ever before. Yet interestingly, this focus on the food has mistakenly led people to regard this serious clinical syndrome as "a diet" not a disorder. And as we all know, "diets" come and go for people, even week to week. This is not healthful for any diet, but especially not for a gluten-free diet where the immune system can be hyperstimulated by repeatedly withdrawing and reintroducing such an immunogenic food. And yet, whether or not people choose to test for the syndrome with our stool test (the only test available to sensitively detect non-celiac gluten sensitivity), if they decide to go gluten-free, that must be a lifelong dietary decision. Otherwise, the test should be employed to help determine how serious the circumstances might be, and to further reinforce the clinical need of its permanency. Because after all, 25% of people, even when asymptomatic, have detectable immune reactions to gluten, and in many of these, damage to the intestine can be detected as well (measurable by EnteroLab from a fecal fat test from the same stool specimen).

We have stood firm on the Truth of our research and clinical results, patiently waiting these 15 years for the public and professional paradigm-thinking to catch up. And catch up it has. Everyone today has at least heard about gluten, and people are not called crazy because going gluten-free makes them better physically, mentally and/or emotionally. But our work is not done. There are many millions more children and adults suffering not only from gluten sensitivity, but from other food sensitivities as well, and other diet-related maladies (obesity, endocrine problems including diabetes, eating disorders, food addictions, etc.). I am appreciative of the support and respect given to me and EnteroLab by Celiac.com and its founder, Scott Adams, who also knew early on there was something real about gluten sensitivity. His 14 year old "Journal of Gluten Sensitivity" is evidence of that.

And so now, we are proud to partner with Celiac.com by allowing them to be the first company outside our own to offer our proprietary EnteroLab tests for sale, having created some special gluten-oriented testing panels for them. And as we go into the next decades of service, I leave you with a hint of the next, new paradigm… which is really the old paradigm. Gluten sensitivity is not limited to wheat, barley, and rye, but often includes oats as well (not just because of wheat contamination of the oats). This was the clinical standard from its beginning by the founder of the gluten-free diet, Dr. Willem Dicke, but that got changed in the last 10-15 years by substandard research methods based only on celiac disease as the end point and bias toward wanting to find such a result (all studies contain bias by the researchers, it's the nature of the mind influencing reality). So for the first time anywhere, we are using a diagnostic test for non-celiac oat sensitivity, and showing that about 50% of people reacting to wheat, barley, and rye, also react to oats with a similar immunologic reaction detectable in stool. But more on this as the information and paradigm-acceptance develops. Hopefully, this one won't take another 15 years to be accepted.

We at EnteroLab and my non-profit public educational institute, The Intestinal Health Institute (www.IntestinalHealth.org), have been greatly honored to serve all our patrons to date, and we look forward to meeting and serving more of you in the future. For more information on testing at EnteroLab.com, please call 972-686-6869 or go to Open Original Shared Link. Thank you for reading this historic account.

The adult gut has between 10 trillion and 100 trillion bacteria that make up the microbiome or surface of the intestines. The goal for digestive wellness is to be sure that there are more GOOD bacteria than BAD bacteria in the microbiome. Food choices, antibiotic use and lifestyle play an important part in creating that balance. Endocrine disrupting chemicals in plastics, along with artificial sweeteners all influence the bacteria or microbiome levels.

The bacteria content of the gut begins at birth. A vaginal delivery results in a microbiome from the mother while a cesarean section produces a microbiome from everyone who handles the infant. Gut bacteria levels are also influenced by breast feeding versus the use of infant formula.

Diets deficient in fruits and vegetables mean less antioxidants are consumed so free radicals can destroy digestive and immune function. In addition, fruits and vegetables provide fiber for bacteria to grow on. Current research from the Journal of Clinical Nutrition indicates high fiber diets yield more bacteroides bacteria growth that helps control body weight. Low fiber diets result in more firmicute bacteria which produces weight gain and can lead to obesity.

Microbiological safety in fresh produce continues to gain prominence in the media. Fresh cut, RTE (ready to eat) produce in convenient packages leads the way in food safety recalls. Fruits and vegetables are prone to microbial contamination from irrigation water, soil, fertilizers, insects, animal feces and field workers during pre-harvest processing. After harvest, the washing and sanitation procedures lack oversight. Remember to wash all raw fruits and vegetables to minimize food poisoning potential.

Listeria monocytogenes is one of the leading causes of death from food borne illness. It is found in raw milk, cheese, and packaged deli meats. Flu-like symptoms can last days to weeks, and in pregnant women listeria infection can lead to miscarriage.

Noroviruses make the news regularly, especially on cruise ships. Common food sources include raw produce and shellfish such as clams, mussels, scallops and oysters. Symptoms begin as early s 12 hours after ingestion and the malaise disappears 3 to 4 days later.

Salmonella continues to plague many with chills, nausea, joint pain and headaches beginning 12 hours post ingestion. Eggs, poultry and raw produce are major sources of salmonella.

Probiotics are an important addition to the celiac diet for balancing the bacteria levels in the GI tract. They should be taken WITH food to reduce the degradation in an acid stomach. Research has shown that urinary tract and vaginal infections have an improved management rate when lactobacillus and bifidobacterium multi-species probiotics are used.

Probiotics are live bacteria which have been shown to reduce inflammation in the gastrointestinal tract. They also reduce intestinal permeability and influence serotonin and melatonin production in the gut.

So since the human gut contains 10 times more bacteria than all the human cells in our body, keeping a healthy balance of bacteria in the gut is critical for digestive wellness.

Celiac.com 06/11/2016 - It's never become so clear to me how much our health and quality of life are dependent upon the food we eat since seeing myself, my family and more than my share of celiac friends and acquaintances make the transition to grain-free from gluten-free. This is evident in witnessing such positive results just from eating a biologically appropriate diet, the paleo diet, which is grain-free and thus gluten-free. Some have this simple diet termed as the caveman diet, the paleolithic diet and what-have you, but in essence it has been deemed "man's original" diet.

In my approaches to the topics of the paleo diet, I discovered the affects this diet has on man's health as a low glycemic alternative to man's diet, aiding ills and physical betterment through glycemic control. In my research and through working with many professionals over the years I've explored a variety of diet, health and lifestyle regimens and looked in depth into the prevailing topic of non-responsive celiacs, also known as refractory celiac disease.

The paleo gluten-free diet is based on the premise that humans do best eating the foods our ancestors ate prior to the advent of agriculture and animal husbandry around 10,000 B.C. This proven theory is that modern humans do best on paleolithic nutrition because human genetics have largely remained the same since the pre-agricultural era, and thus our genetic makeup is best suited to the ancestral human diet—no grains at all. Taking our current bodies and then applying how man ate back in the day has been having profound effects on the general health and well-being within research and study results.

According to research, pre-agricultural humans were free of the diseases of the civilized world such as cardiovascular disease, cancer, obesity, and autoimmune diseases. Modern studies, including clinical studies, have shown as well that eating paleo gluten-free can help or reduce risks of a variety of serious health conditions. This includes issues associated with high insulin and blood sugar levels, which can lead to a variety of diseases and health conditions such as hypertension, high cholesterol levels, obesity, type 2 diabetes and gout. That's because many foods on the paleo gluten-free diet are low-glycemic, which is evidenced in the ills they are void of, which we now classify as "normal" or aging, or an aging "disease".

Grains are biologically similar to table sugar, causing an unhealthy spike in insulin upon consumption. Most of the carbohydrates consumed on the paleo gluten-free diet, consisting of a variety of vegetables, fruits, proteins and healthy fats are low-glycemic. Honey, maple syrups, etc. are currently debatable and this is another topic all together.

What's the big deal about the Glycemic Index? According to studies, a low-glycemic diet can help with obesity, type 2 diabetes, polycystic ovarian syndrome, cardiovascular disease, as well as other conditions such as Alzheimer's, depression and non-responsive celiac disease. Some of the benefits of low glycemic eating include: improved weight loss, decreased hypoglycemia, steadier moods, mental clarity, sleep improvement, and reduced food cravings, which means less binge eating. This also means less overweight children with early onset diabetes, which is truly a rapidly growing concern.

It is to our benefit that we all take a good look at our diets and the effects that the carbohydrate intake of the currently prevailing "standard" gluten-free diet has on our bodies. Let's determine if what we are eating could be causing health conditions that could possibly be reversed or avoided. Should we be willing to entertain the idea of change? The change could be as simple as taking a sincere look at man's original diet, the diet we were biologically designed to live on.

Could our original diet of no grains, low carbohydrates and high "good" fats be a door we need to open, step through with our eyes wide open and be willing to learn about? I truly believe this topic answers many mysteries and unresolved diagnoses.

Celiac.com 05/01/2015 - In his article titled "Open Original Shared Link," published in the November 3, 2014 issue of The New Yorker, Michael Specter likens the Gluten and Allergen Free Expo to "a travelling medicine show" in the first paragraph (1). Just in case a reader was half asleep and missed the bias embodied in that phrase, Specter ends the same first paragraph with: "There was even gluten-free dog food." It's hard to miss the harsh, cynical tone, and it is a shame that he usurped the name of Melissa Diane Smith's informative book to title his invective.

What, we must wonder, is the source of his bias? He does offer some detailed explanations of the bond between glutenin and gliadin, and how carbon dioxide from the fermentation process is trapped as bread and other pastry rises, making light, fluffy bread and pastry. He has done some detailed, even impressive investigation into cooking with gluten. However, he also asserts that wheat-breeding practices haven't induced any changes that might explain the increased incidence of celiac disease since World War II. He then goes on to say: "But something strange is clearly going on. For reasons that remain largely unexplained, the incidence of celiac disease has increased more than fourfold in the past sixty years." Mr. Specter acknowledges that celiac disease is on the rise and, according to Specter, there have not been any major changes to the genetics of wheat that might explain this increase.

This perspective appeared in a very prestigious, highly regarded publication—The New Yorker. Many people will believe these claims just because of where they were published. And here is the problem I have with that. Mr. Specter has the genetic information all wrong: Norman Borlaug was awarded a plethora of honors for his work in developing more than 6,000 new wheat hybrids, which included several strains of disease resistant, semi-dwarf wheat that increased per-acre yields by seven to ten fold, thereby leading to wheat independence in a number of third world nations. For these scientific accomplishments he was awarded the Nobel Peace Prize, the Presidential Medal of Freedom, and a Congressional Gold Medal. Several books have been written about Dr. Borlaug and his achievements, and several foreign governments, science academies, and institutions have bestowed him with awards, honorary degrees and memberships. Borlaug has even had streets, university wings, and assorted other places and artifacts named after him and has even been mentioned in popular television shows. He has been called the father of the "green revolution" and has enjoyed very widespread recognition for having been instrumental in saving many millions of lives through increasing the world's food supply in the form of wheat. It is my belief that this venerable and compassionate man of science deserved every honor that was bestowed on him (2).

However, I also think that it besmirches Dr. Borlaug's memory when Specter dismisses all those genetic changes to wheat as a possible factor in "the growing number of cases" of celiac disease based on the statement by Dr. Donald Kasarda that he was unable to find "evidence that a change in wheat-breeding practices might have led to an increase in the incidence of celiac disease". One person's failure to find evidence for something does not prove the absence of that phenomenon. Mr. Specter also quotes Dr. Joseph Murray, the very popular and famous (at least in the gluten sensitive community) gastroenterologist at the Mayo Clinic, as an expert in wheat genetics, and quotes Dr. Murray as asserting that wheat genetics haven't changed much over the past fifty years. I'm skeptical that Dr. Murray would profess expertise in the realm of cereal grain genetics. Regardless of whether this is Mr. Specter's construct, or Dr. Murray did actually make this claim to expertise in wheat genetics and the assertion that little has changed in wheat genetics since World War II, the statement is at least incorrect when it comes to wheat genetics.

The conundrum Mr. Specter has created by ignoring Dr. Borlaug's work sets up an article in which he attacks what he calls "gluten anxiety". He says that "nearly twenty million people contend that they regularly experience distress after eating products that contain gluten." The implication is clear. Mr. Specter would have us believe that these people are confused about changes to how they feel, and/or whether those changes resulted from switching to a gluten-free diet—apparently all twenty million of them are so confused that they now need Mr. Specter to lead them out of the darkness of their own self-delusion, and begin to appreciate that wheat, in its present genetic form, has been consumed for at least 10,000 years and it's "a staple food that has sustained humanity for thousands of years". I'd like to point out that the Levant, where wheat was first grown, was not host to all of humanity at that, or any other time. Many humans, after leaving Africa about 85,000 years ago, evolved in a variety of environmental niches where gluten grains have not been available until quite recently.

And there are many genetic variations of wheat. Which ones, I wonder, is Mr. Specter saying have been with us for so long? Contrary to his assertions, it is this variability that serves as one of the greatest barriers to the development of genetic strains of wheat that are "safe" for consumption by people with celiac disease. Dr. Sachin Rustgi, one of the scientists who is trying to develop such a safe wheat also said that: "Different celiac patients are sensitive to different 'gluten' proteins (prolamins). If one feeds peripheral blood cells sampled from a patient or a small group of patients (from a specific geographical location) with gluten proteins derived from a wheat genotype, it is expected either to see a reaction (monitored by the production of interferon gamma) or no apparent effect. But in the latter case it does not mean that the wheat genotype is non-toxic to all celiac patients" (3). Since different proteins or protein fractions (peptides) are recognized by different celiac patients' immune systems, there is an enormous number of peptides and proteins that are potentially toxic to at least some people with celiac disease. Extrapolating from that point, people with non celiac gluten sensitivity may well be reacting to any of the proteins or derivative peptides from any of the multitudinous variants of wheat.

Mr. Specter also makes the claim that: "Humans have been eating wheat, and the gluten in it, for at least ten thousand years." Yet the geneticist, Dr. Martin Richards, and his colleagues report that about three quarters of Europeans are descendants of hunter-gatherers, rather than the early farmers from the Levant (4). So a large majority of people of European descent have not been eating cereal grains for more than 10,000 years. Just how long they have been consuming them depends on where they lived in Europe, which may explain the variability in the frequency of celiac disease across Europe. It is worthy of note that incidence of celiac disease is particularly increased in Scandanavia, Scotland, and Ireland, where climate and topography combined to make cereal grain cultivation more difficult. Thus, one might reasonably interpret this to suggest that these populations experienced limited past exposure to these grains. It is only with modern transportation systems, combined with the abundant excesses of wheat made possible by the work of Dr. Norman Borlaug and many others, in addition to the erroneous belief that wheat is a healthy food, that we now have almost worldwide over-consumption of gluten grains. Increased consumption has led to the increased frequency of celiac disease in these relatively grain-naive populations.

Much of the rest of the world's populations have only recently begun to eat these grains. Even in the lowlands of England, where grain cultivation is relatively easy and successful, these grains have only been there for the about the last 5,000 years. Worldwide exposure to these grains varies somewhere between several thousands of years to less than 100 years. And what data supports the notion that even 10,000 years is sufficient time for humans to make the complex adaptation to eating them? Dr. Marlene Zuk has implicitly made such a claim, through reporting on much more rapid adaptations to adult consumption of dairy products (5). However, since we are mammals, and are almost universally able to consume human milk as infants, the adaptation required for the digestion of lactose into adulthood is, comparatively speaking, quite minor. Still, more than two thirds of the world's populations are unable to do so. Mr. Specter's resistance to recognizing gluten as a dietary hazard appears to be rooted in bias, rather than a thoughtful examination of the relevant data.

It also appears that Mr. Specter either failed to learn, or failed to mention, that humans do not have the necessary complement of digestive enzymes needed to break some of the bonds between amino acids in the storage proteins of gluten grains, so we can fully digest them (6). Surely, if we were fully adapted to eating them, we should be able to digest these proteins.

Nonetheless, Mr. Specter repeatedly disparages and dismisses the disease entity of non-celiac gluten sensitivity, and goes on to say: "The most obvious question is also the most difficult to answer: How could gluten, present in a staple food that has sustained humanity for thousands of years, have suddenly become so threatening?" Of course, this question is only difficult to answer if one ignores the many genetic manipulations of gluten grains and a substantial body of medical research into a variety of human ailments.

For instance, Dr. Curtis Dohan and his colleagues were the first to publish a report on the connection between some cases of schizophrenia and gluten grains titled "Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet" in 1969 (7). This research was conducted in a locked psychiatric ward. Similarly, seven years later, Singh and Kay followed with publication of an affirming research report that, using a different study design, identified wheat as a pathogenic factor in some cases of schizophrenia (8). This work was also conducted in a locked ward where total control of the patients' food intake could be controlled. Further, neither of these reports asserted a connection between celiac disease and schizophrenia. Over the following two decades, several reports, based on sloppy, poorly designed research, were published in the medical literature, and the notion that gluten grains could be a factor in schizophrenia was quickly forgotten. Mr. Specter would have been pleased with these latter reports. Another critic of Dr. Dohan's work, Dr. Donald Kasarda, a cereal scientist at the USDA, was quite happy to make statements such as: "Dohan wasn't much of a scientist" (9). Yet it was this same individual, Don Kasarda, whose name appeared as one of the authors of a report that asserted that a subset of schizophrenic patients mount a novel immune reaction against gluten (10). Dr. Dohan and his colleagues discovered a disease process, and an effective treatment for it, forty years ahead of the group that Dr. Kasarda worked with. Yet the earlier work was unscientific—until the publication of the work led by Dr. Samaroo, with contributions from Dr. Kasarda. Did Dr. Dohan suddenly become competent? Or is there another, more reasonable explanation? I don't understand the contradictions here.

I'm also struggling to understand Mr. Specter's quoting Dr. Kasarda in his attack on non celiac gluten sensitivity. After all, Dr. Kasarda was one of the authors who published the report of non celiac gluten sensitivity in a subset of schizophrenic patients.

On another front, Dr. Marios Hadjivassiliou and colleagues have been reporting, over the last twenty years, on celiac disease and non-celiac gluten sensitivity in connection with a variety of neurological diseases. These include depression, cerebral palsy, neurological dysfunction, alcohol induced cerebellar degeneration that results in gluten sensitivity, ataxia, ganglionopathy, a gluten induced condition that mimicks amyotrophic lateral sclerosis, inflammatory myopathy, chorea, headaches, balance disturbances, and neuromuscular disorders. They have also reported that antibodies against one of the protein families in gluten are found in the brain (IgG class anti-gliadin antibodies) and they also attack brain tissues (11). Others have reported connections between gluten and seizure disorders in non-celiac gluten sensitivity (12), and cerebral calcifications with seizures (13). Further, several forms of gluten induced brain damage have been reported in the context of celiac disease, which suggests a similar dynamic for those with non-celiac gluten sensitivity and brain damage. Gluten induced brain disorders include headache/migraine, attention-deficit/hyperactivity disorder, epileptic seizures, mental retardation, cerebellar ataxia and behavior disorders (14) in the context of celiac disease. Any and all of these may also suggest a similar dynamic for those with NCGS.

I have worked with learning disabled students who have shown remarkable recoveries on a gluten-free diet, similar to those described by Alexandra Blair, in her 2003 Times article about dyslexic children who improved enormously on a gluten-free diet (15). Unfortunately, these data were not published in the peer reviewed literature, so they are unlikely to persuade researchers to investigate this matter further. Nonetheless, given the data on gluten's impact on neurological and brain tissues, it does seem very possible that many learning disabilities are, at least partly, the result of non-celiac gluten sensitivity, and that they may benefit from gluten avoidance. Time and space limitations prevent me from exploring the research that identifies the psychoactive properties of protein fractions in wheat, first identified by Christine Zioudrou et al, in her 1979 publication (16), or the Hudson and colleagues' report in 1976 showing that a single subgroup of gluten proteins, called gliadins, are toxic to any of a wide variety of human cells (17). Yet Mr. Specter, calling it "gluten anxiety" would have us dismiss all of this and much, much, more peer reviewed research that identifies gluten as toxic to many people who do not have celiac disease.

It has never been clear to me why people such as Mr. Specter are quite willing to attack new ideas and discoveries that others have made on their quest for improved health. The attackers seem to want to mock those of us who have found an answer for ourselves. He interviewed several people, whom he quoted in his article, who were just convinced that they felt better when avoiding gluten. Mr. Specter derides those gluten sensitive individuals who were generous enough with their time to allow him to interview them, apparently at the Gluten Free Expo he attended, then compared with "a travelling medicine show". It is difficult to tell whether Mr. Specter was making news or reporting it when he interviewed these people.

Please recall the fall issue of the Journal of Gluten Sensitivity, in which I explored the flaws of the research by Dr. Biesiekierski and colleagues in Australia (18). Mr. Specter cites Professor Gibson, one of the authors of the same study, as one of his sources for discrediting the notion of non-celiac gluten sensitivity. Mr. Specter goes on to present himself as having a superior insight into the issue of non-celiac gluten sensitivity, attacking Dr. William Davis, cardiologist and author of the popular book, Wheat Belly (19), and Dr. David Perlmutter, a neurologist and author of the similarly popular book, Grain Brain (20). Are we to ignore the now thousands of researchers whose peer reviewed reports are now characterizing non-celiac gluten sensitivity as a disease entity? And should we ignore the scores of popular books asserting the same thing? Or should we ignore Mr. Specter and the flawed research from Australia? I know what I'm going to do.

Sources:

1. Open Original Shared Link
2. Open Original Shared Link
3. Adams S. Discussion with Assistant Research Professor Sachin Rustgi on the genetic modification of wheat to make it safe for celiacs. Journal of Gluten Sensitivity. 2014; 13(2): L11-14.
4. Richards M, Macaulay V, Hickey1 E, Vega1 E, Sykes B, Guida V, Rengo C, Sellitto D, Cruciani F, Kivisild T, Villems R, Thomas M, Rychkov S, Rychkov O, Rychkov Y, Gölge M, Dimitro D, Hill E, Bradley D, Romano V, Calì F, Vona G, Demaine S, Papiha S, Triantaphyllidis C, Stefanescu G, Hatina J, Belledi M, Di Rienzo A, Novelletto A, Oppenheim A. Tracing European Founder Lineages in the Near Eastern mtDNA Pool. American Journal of Human Genetics, 2000; 67; 5: 1251–1276.
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19. Davis W. Wheat Belly. Rodale Inc. NY, 2011.
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