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    Evaluation of Safety and Efficacy of Dietary Supplement ZyGluten In Patients with Gluten Sensitivity


    Amrit P.S. Narula M.D


    • Journal of Gluten Sensitivity Winter 2015 Issue


    Image Caption: Image: CC--Health Gauge

    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


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    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:

     

    None

    Mild

    Moderate

    Severe

    Abdominal Pain/Cramping

    1

    1

    16

    9

    Bloating/Distention

    0

    3

    9

    15

    Diarrhea

    10

    4

    2

    11

    Constipation

    16

    2

    3

    6

    Headaches

    11

    5

    7

    4

    Joint Pains

    12

    2

    9

    4

    Fatigue

    3

    4

    5

    15

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

     

    None

    Mild

    Moderate

    Severe

    Abdominal pain/Cramping

    10

    7

    4

    2

    Bloating/Distention

    9

    10

    1

    3

    Diarrhea

    16

    5

    2

    0

    Constipation

    20

    1

    1

    1

    Headaches

    17

    2

    3

    1

    Joint Pains

    14

    2

    4

    3

    Fatigue

    7

    8

    3

    5

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

     

    None

    Mild

    Moderate

    Severe

    Abdominal Pain/Cramping

    15

    4

    2

    2

    Bloating/Distention

    14

    6

    1

    2

    Diarrhea

    21

    1

    1

    0

    Constipation

    21

    1

    0

    1

    Headaches

    16

    5

    1

    1

    Joint Pains

    17

    3

    2

    1

    Fatigue

    10

    7

    1

    5

    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.
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    WILL THIS BE ON THE MARKET SOON ? I WOULD LOVE TO TRY IT.

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  • About Me

    Amrit P.S. Narula, M.D., F.A.C.P., F.A.C.G., F.A.C.N., A.G.A.F. is currently practicing gastroenterology in Pottsville, PA with Integrated Medical Group, and is a principal in the company that makes ZyGluten.

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    Susan Costen Owens
    Celiac.com 07/17/2015 - This article originally appeared in the Spring 2015 edition of Journal of Gluten Sensitivity.
    Why is a researcher whose field for twenty years has been autism now writing an article about celiac disease and its possible relationship to oxalate? This takes a little explaining.
    My training in graduate school was all about looking into old literature to find pieces of research that had been lost, or were never incorporated into current models. I learned that new science could provide a different context for old findings. The importance of this process came home when more than a decade ago I was sitting at an enormous oval table at the National Institutes of Health where an important meeting was addressing how the heads of various National Institutes of Health and the CDC would handle a theory about a possible environmental trigger related to autism. One scientist rose to the floor, and began to explain his reason for discounting the new theory's importance. He proposed that this theory did not fit into previous models of autism, and began to say that the scientific process worked like the construction of a brick wall. Everything added to that wall should fit into the foundation and bricks that had already been laid.
    How often does this view of science as being a construction of human beings, rather than a discovery of nature, keep us from accepting new lines of research? Has scientific consensus ever ended up wrong after the appearance of new findings? Yes, many times.
    In this meeting at the NIH, at that moment, a senior scientist, Dr, Bernard Rimland, rose to the floor. Those who knew this man realized he had singularly changed the view about the science of autism twice, accomplishing these major shifts of thinking during different decades. I don't have a transcript from that meeting, but Dr. Rimland rose to say something like this: "My experience is very different. I find that science is more like a crossword puzzle, in that you may have been working at the puzzle from one end and filled in places that looked correct until you began working from another side and discovered that something you filled in before must have been wrong. That's when you erase the part that you thought had been right, and you find another answer that will make the parts fit from both directions."
    That speech has been a guiding light to my own research since then, helping me have the motivation to recover all the pieces that were lost or misunderstood or left out from the past whose absence left a model that only approximately provided a place for all the known pieces, but left many other pieces "loose" and unable find a proper fit.
    In 2005 after spending ten years studying the biological roles of sulfate in the body, I began to investigate another negatively charged ion that travels on the same transporters. I reviewed the published literature on oxalate in any condition, looking at basic science and clinical research over the last two centuries. I was looking for gaps and opportunities for improving the identification of oxalate-related diseases outside the kidney. My work for twenty years had focused most intensely on autism, and I had found that oxalate was high in autism, but this finding needed to be put in context and studied formally. It was mystifying to me why work from basic science about oxalate was only being applied to patients with kidney disease. How could we identify others with oxalate-related disorders?
    In the fall of 2005, along with several associates, we started our Oxalate Project. Using the same methodologies I had developed in the previous decade using the internet to interact with a broad range of patients, we began seeking those with any condition that was already related to oxalate in the literature, and patients with other conditions where the science took us. Included in this effort was setting up a project at the Autism Research Institute that we named the Autism Oxalate Project.
    In October of 2006, I attended the International Celiac Disease Symposium in New York City. I was hoping that the findings in oxalate research on malabsorption and intestinal disease, and specific findings on oxalate in celiac disease published since the 1970's were being discussed at this conference. I heard not a word about oxalate there. These scientists probably did not realize that when oxalate levels in the blood become high, it can get stored all over the body where it can produce effects in any potential organ…not just the kidney. I had learned that systemic effects from oxalate could change the course of a condition in patients over years of time. For patients with celiac disease, this storage might have occurred primarily during the years before diagnosis when problems with fat digestion would have increased the percent of oxalate absorption from the diet.
    In autism, I had learned that, as in celiac disease, some investigators had noticed oxalate's elevation in urine in isolated individuals, but they had been taught by articles in peer-reviewed literature to dismiss this finding as irrelevant when those individuals didn't have kidney stones. Basically, the literature kept saying that kidney stones would always be the first presentation of an oxalate problem—but was that true? Why would that be true? As I began to attend numerous world conferences on oxalate, I was very surprised to find that the only people there besides botanists, were those involved in kidney research. My previous studies in the literature had identified many articles describing oxalate producing effects all over the body and in multiple systems. New work on oxalate transport was finding regulation of oxalate's movement all over the body. Why wasn't this research being applied to patient care outside the kidney and why were certain laboratories insisting on a kidney diagnosis before they would even measure oxalate?
    Since my own work at that point included running a support group for people reducing oxalate and our doors were open for people with any condition, we had seen patients with more than twenty different conditions report an easing of their symptoms or even complete cures when they brought their oxalate levels down. Would the scientists be able to catch up with this wealth of experience that today has involved more than 17,000 families?
    Here is an example: I worked with a team of oxalate and autism researchers in Poland to establish the prevalence of oxalate's elevation in autism. The study that this work produced became available online in 2011, but officially went to print in September of 2012 in the European Journal of Paediatric Neurology. It was the first study to examine whether the levels of oxalate in blood plasma would correlate to the levels in 24 hour collections of urine in those who were not in kidney failure. We discovered that the levels in these two compartments did not correlate at all, especially in the controls. This meant that the oxalate field's dependence on urine tests as sufficient to identify those with oxalate problems was probably misplaced. It made sense that the two compartments would not "agree" because oxalate's movement between tissues, we now know, is regulated and its regulation would be different in different organ systems. How many other conditions were experiencing effects from elevated oxalate in blood that were not accurately reflected by only using urine tests? What did we know about variability from day to day, or even rhythms within the day, for oxalate secretion in other conditions? What did we know about how any variability should affect the interpretation of lab results, or our interpretation about the timing and presentation of symptoms in other conditions?
    A striking finding in our paper seemed to have been also referenced in a paper from Mayo Clinic, showing that urine oxalate in normal controls seemed to stay below the reference level of 0.46 mmol/1.73 m2 (24 hr.) Perhaps the point of the kidneys regulating that level so tightly was to protect the kidneys from risks of kidney stones or nephrocalcinosis, but that particular control of urinary secretion seemed lacking in autism. Scientists were beginning to discover secretion to other compartments, such as the intestines, the lungs, and the skin for example. Why would someone doing research even think to measure oxalate secretion and regulation in these other sites in clinical settings? In the past, everyone had assumed that measuring urine was sufficient. The graph of plasma versus urine looked completely different in those with autism compared to controls. What would a similar graph look like in celiac disease? Would the graph show different patterns at different ages, or before and after treatment with a gluten-free diet? Data from a study from Saccomani et al. may suggest that a limit to urinary secretion may be preserved in children with celiac disease, but would limiting secretion in the kidney sometimes lead to a greater accumulation of oxalate in tissues?
    Our autism study revealed that there are problems with assuming that a single urine test could be used to screen patients when oxalate could be elevated in blood and causing problems in the rest of the body. More than fifteen years ago (not published but presented at a think tank) I noticed problems in lab tests in autism with what looked like it could be caused by a variability in creatinine secretion. This would create a problem in interpretation for any urine test ratioed to creatinine, but the reason we would see this variability in autism made sense when a rat study recently found that oxalate in the kidney changes the movement of creatinine out of blood and into urine when oxalate was made to be high experimentally. This type of study urgently needs to be replicated in humans before anyone can have confidence that this affect on creatinine isn't compromising our data from spot urine tests. Suddenly it seems very sensible that in the oxalate field, it has become common practice to use 24 hour tests. Readers need to realize that this issue would affect anything measured in urine and ratioed to creatinine, not just oxalate! From data I've reviewed and analyzed statistically from more than a thousand organic acid tests, and from other literature, I also doubt that this single mechanism is solitary in contributing to problems in interpreting urine tests that use this ratio.
    Can we still legitimately think that physicians should not worry about oxalate levels unless their patients have developed kidney stones? Celiac disease is one of many conditions where high oxalate levels have frequently been found in patients. Some of the other conditions include bariatric surgery, cystic fibrosis, inflammatory bowel disease, short bowel syndrome, autism and more.
    Are doctors and nutritionists understanding that patients with these disorders will experience risks from oxalate to the rest of their body? Are they noticing when these patients develop issues outside the kidney that their symptoms might be related to oxalate? I've learned that the answers to these questions is most often, no.
    In our project's work with such patients we have reduced body oxalate levels through strategies of dietary modification, and by the use of specific vitamins, minerals and probiotics that have been shown to reduce oxalate. We've seen these changes alter the expression of their presenting disease in unforeseen but positive ways. It will take decades before all our findings from ten years of work in dozens of conditions can be confirmed by scientific studies. That does not mean these patients have to wait for academic studies to be published to see for themselves if reducing their exposure to this clearly recognized toxin will help improve their own health.
    Do physicians know that research on kidney stone patients have identified issues in their kidneys that lead to their increased risks of forming kidney stones from oxalate levels that would not produce stones in others? Could oxalate that was elevated in blood and tissues (and currently not being secreted at high levels in urine) cause problems to other parts of the body, contributing in unknown ways to comorbidities like those found in celiac disease?
    At the celiac symposium I attended, there were so many issues that were being discussed as being unresolved by the use of a gluten-free diet. That surprised me. Could those issues have been triggered by oxalate that was absorbed into the body before a gluten-free diet had resolved steatorrhea? Steatorrhea is the condition where excess fat stays in the feces, possibly causing the stool to float or have an oily appearance. Studies had shown that untreated celiac disease often was associated with steatorrhea. This condition elevates fat in the gut and that fat travels undigested all the way to the colon. Oxalate scientists had found that the fat left in the intestines during the journey to the colon would tie up calcium that ordinarily binds oxalate from the diet. About 80% of the calcium that travels through the gut stays in the gut. The purpose may involve the formation of a calcium oxalate salt in the feces that limits oxalate's absorption in the colon. Otherwise that oxalate could be transferred to blood if it is not first metabolized by the microbes in the gut. This is a bigger problem than the higher amount of oxalate in the diet. This might become a more serious problem when people with celiac disease use new grains that are gluten-free but which we know now are extremely high in oxalate.
    During the mid-nineteen thirties, prominent groups began recommending adding vitamin D to milk to prevent rickets, knowing that vitamin D enhances the absorption of calcium from the gut. Back then, oxalate research had not yet found a protective role for most of the calcium to remain in the gut to protect us from oxalate. Physicians had advised kidney stone patients to avoid calcium, but later determined that calcium in the diet was protecting patients from absorbing oxalate.
    Later studies showed that oxalate that remains in the intestines as a free anion (unbound to calcium) can and will be absorbed into the body once it reaches the colon. When this unbound oxalate is taken into the blood, there it was found to be able now to tie up free calcium that was needed to protect our bones and work in our metabolism.
    Free oxalate could a lso be taken into cells via oxalate transporters where it could disrupt calcium signaling inside cells and wreak havoc in the mitochondria and endoplasmic reticulum. Free oxalate can disrupt activity also in the nucleus where nature has supplied a specific oxalate binding protein. Is this protein sometimes overwhelmed when oxalate gets too high?
    Before I attended this celiac symposium, I had not heard that some of the autoimmune and cancer risks associated with celiac disease may still be there even with a gluten-free diet. Who was asking what else besides gluten could be contributing to these risks and were they being studied? Was oxalate one of those risks? People on our listserves that help people reduce dietary oxalate were telling us they experienced improvements in autoimmune conditions on a low oxalate diet. No one has had time to examine these reported changes formally yet, but could oxalate have a potential connection to the risks of autoimmunity or even transformed cells in celiac disease patients?
    I learned to ask these types of questions in graduate school and in the years that followed as I continued to find science that had been learned "out of order", and rejected as an important piece of the science because at the time there were missing pieces that were only discovered later. My intense study of medical literature's missing links brought to my attention so many valuable scientific discoveries that at the time they were published had been cast off as irrelevant. As I started to look intensively for more and more of these lost pieces, I made another astonishing discovery. I learned that we do not fund researchers to go digging through past scientific work to find links that may never be rediscovered after scientists with other priorities and agendas direct research efforts into other directions.
    Does science proceed linearly? Why should it? Are you personally one of the types of people that when doing a jigsaw puzzle, you first find all the outside pieces, and then start grouping colors and actually have a plan for which piece you will try to find next? My plan is to keep looking for pieces that didn't fit into models in the past to see if today's new findings will finally reveal how they now fit in well with today's insights.
    I don't think laboratory scientists or clinicians are the best equipped to do this sort of work, but organizations funding science expect that to be where this sort of integrative work will originate. I have found instead that most investigators who are up to their ears in current scientific projects or who are developing protocols for others to follow will not take very much time to dig deeply for lost pieces. There are rare exceptions to this observation. I have actually met a lot of this special breed of scientist, who loves to think outside the box and has respect for what might have been lost and loves to dig through old findings. Nevertheless, sociologists who study such things tell us that most scientific studies are never read outside of a small group of narrow interest and will only have influence for a few years. With this being the general expectations, who is left to do the work of recovering lost work from the past? Who also brings in work from other disciplines previously thought unrelated to a condition?
    In the oxalate field, molecular biologists have now discovered that oxalate shares transport with sulfate and bicarbonate, which means oxalate also gets into the regulation of pH. While these transporters regulate these ions, they also move a lot of water across cell membranes. In some places, oxalate shares transport with iodine, and of course, that makes us think of things related to the thyroid and all the histories of later onset thyroid disorders and autoimmune conditions. Pathologists found that the older you are, the more your thyroid gland will fill with oxalate, and this can be associated with a loss of thyroid activity. That makes sense now that we understand that these substrates are linked in the way the body handles them.
    But what about anemia that can develop in celiac disease? Scientists found that transferrin's carbonate ion can be replaced by oxalate if oxalate can gain access to this site at sufficient concentrations. When that happens, unlike the carbonate ion, the oxalate anion won't let go of the iron, so it sequesters iron irreversibly. This mechanism has never been thought to be related to the anemia in celiac disease.
    What about the tendency towards osteoporosis or osteopenia in celiac disease? Some remarkable studies conducted in the late 1930's (actually after Popeye made his appearance) fed groups of rats a basal diet deficient in a good calcium source, but they made up the rat "RDA" for calcium by using either turnip greens or spinach. Turnip greens are high medium in oxalate content, but spinach is extremely high. The rats fed the spinach, during their lifetime (and many died prematurely), had impaired growth (also seen with celiac disease). They had bones and teeth that wouldn't mineralize. The rats on spinach were unable to reproduce except for one litter of two pups that were quickly devoured by their mother at birth. In contrast, the rats fed turnip greens, which are roughly otherwise equivalently nutritious, completed the study in great health with shiny coats and all the perks of being a healthy rat. Did Popeye deceive us about the benefits of what has become a much more popular food, often called "the healthiest food there is?" By the way, one of these studies was conducted by Campbell Soup Company!
    Our oxalate project, which makes its home at www.lowoxalate.info with its associated support groups on Yahoo and Facebook, has now served more than 17,000 families in helping them discover for themselves how oxalate has been contributing to health issues…with problems that resolved as they brought down their body burden of oxalate. We've seen this one change fundamentally alter the course of more than twenty disorders, and these disorders are not very much alike. Some are genetic and some are probably not genetic, but are you wondering why they aren't alike if they are all associated somehow with oxalate?
    With new genetic tools and new basic science to help us, it is now a lot easier to figure that out. Members of the SLC26 family of oxalate transporters that move a special set of nutrients across cell membranes are expressed at different levels and in different combinations in different organs and cell types. Scientists are just now starting to ask the questions about how they may be regulated, or "turned on" or "turned off". When is the immune system involved in this regulation? When may we find genetic differences in the use or expression of these transporters? We already know a few observations related to their expression in the lungs and in the inner ear and in the mucosa, but at this stage in the game, there is much more science about their regulation that we don't know compared to what we already have discovered.
    We do know now that it was a mistake to think oxalate was only secreted in urine. How many studies in the past based their conclusions on urine being the only place to look? Oxalate is now known to be secreted in the lungs where scientists in Russia have been making much progress in understanding its roles in asthma and COPD, but I would just about guarantee that your immunologist or your pulmonologist doesn't know about that research yet, but it has been going on for years and years.
    Oxalate is also secreted to the skin and can cause terrible rashes. Is it related to dermatitis herpetiformis? Who has measured for oxalate in those lesions associated with gluten sensitivity? In primary hyperoxaluria, secretion of oxalate to the skin has led to serious lesions that can even turn into gangrene. People on our listserves have reported the swelling of blood vessels in the skin termed livedo reticularis, and others have described and pictured all sorts of skin lesions, including an odd appearance of glitter in the skin that appears imbedded, but glistens beautifully in the sun. No, these people were not vampires!
    Our bodies not only get oxalate from dietary sources. The body is also producing oxalate internally as a by-product of certain metabolic processes that normally keep oxalate levels low. In the genetic condition, Primary Hyperoxaluria Type I, still believed to be found in only one in a million individuals, these individuals lack a B6-dependent enzyme that ordinarily converts a normal byproduct of metabolism to a very safe amino acid. When this enzyme activity is lacking from this genetic defect or from B6 problems, oxalate builds up inside the cells where it is made and where it might produce local damage. The amount of oxalate produced with the genetic defect is so high that it spills out into the body, primarily from the liver, and produces a condition called oxalosis where oxalate damages tissues all over the body, and in the bones, and the heart, and often leads to death by kidney failure.
    Through the work of Marguerite Hatch and other scientists, we have learned that signals now being studied will instruct intestinal cells to take oxalate out of blood and secrete it into the stool. Even though a vast literature has associated inflammatory bowel diseases with producing an increased absorption of dietary oxalate through a leaky gut, that is apparently not the whole story.
    The body has mechanisms to rid itself of normal levels of excess oxalate, but in primary hyperoxaluria Type I, these efforts seem never enough to protect the body. In Mayo's database it was reported that 59% of those with this genetic disease experience abdominal pain. Oxalate is a known inflammatory molecule. Does oxalate secretion to the gut produce inflammation and pain? This certainly needs to be studied by gastroenterologists but does that discipline even know about this oxalate research? Who is showing them this science? Have you ever wondered if there is anyone who ensures that discoveries from basic science are applied by the physician to patient care when the finding isn't related to drug development?
    We humans do not have genes to degrade oxalate. That is why oxalate, once absorbed into blood can collect in our tissues and cause damage. Nature has provided a way for increased oxalate in our blood to join the contents of our intestines so that it can find and bind calcium in the gut and then can leave in the feces. That is not the only reason oxalate from blood is sent there. The gut is home to microbes that are capable of degrading oxalate. This purposeful removal of a substance toxic to humans happens only if the oxalate-loving microbes are there and healthy enough to perform this service for us. This wonderful system fails, however, in conditions like cystic fibrosis, where continuous use of antibiotics may have killed the microbes that perform this service for us. Unfortunately, even in those without cystic fibrosis, many commonly used antibiotics, like the Z-Pack, can kill our oxalate degrading microbial friends.
    Another problem is that widely used antibiotics can also kill back the biotin producing microbes in the gut. Why is that relevant to oxalate? An important class of enzymes called biotin-dependent carboxylases, were found to be invaded by oxalate when higher levels of oxalate travel to where these enzymes function. Since these enzymes function in critical roles in the mitochondrion (with only one enzyme of this type serving us in the cytosol) scientists learned that oxalate may seriously impair their enzyme activity, putting our mitochondria in great distress. Scientists also found this interference is fairly easily addressed by high doses of biotin.
    Many years ago, I realized that doses of biotin being recommended by physicians and others were in all likelihood too low to provide effective restoration of the function of biotin-dependent carboxylases whenever oxalate had become elevated in mitochondria . I read about doctors treating dystonia caused by a thiamine transport defect with high dose biotin at 5-10 mgs/kg/day. Children with this thiamine transport disorder were kept on this dose of biotin for years with no problems, but when the dose was lowered, the dystonia came back. Why are some physicians worrying about giving 5 to 20 mgs a day to grown adults?
    I can only guess that they were unaware of the literature on biotin's safety and were never able to witness how their patient's lives might change on higher doses. Competition at enzyme active sites will matter much more than blood or urine levels. Unfortunately, we have no way of measuring tissue or organelle levels of oxalate in routine patient care. Clearly, more work needs to be done in this area to see where and when higher doses are needed.
    Unfortunately, many doctors are in unfamiliar territory with higher doses of biotin, and may be unaware of biotin's track record of great safety even at very high doses. We must ask, if someone is dangerously high in oxalate, which choice will cause more harm to them, taking high dose biotin, or failing to take higher doses of biotin when that could lead to a loss of function of those important enzymes? Do scientists and doctors realize that anything which damages mitochondrial function might also lead to villous atrophy? Did elevations of oxalate happen before the changes that lead to a diagnosis of celiac disease?
    There are actually many other mitochondrial enzymes known to be inhibited by oxalate. If oxalate seriously affects mitochondrial function, what might that have to do with what else we know about celiac disease? Right now, the first two articles that come up in pubmed when searching on celiac disease and oxalate are articles that should get us thinking. The first is an article entitled, "Subclinical celiac disease and crystal­ induced kidney disease following kidney transplant". Its abstract says, "Subclinical celiac disease is commonly overlooked and hyperoxaluria is not usually investigated in kidney patients." This article described a patient with hyperoxaluria, but this patient was lacking overt diarrhea, fat malabsorption, or nephrocalcinosis. The article that comes up next on this search speaks of measuring children with celiac disease, and concludes, "In contrast to adults, increased urinary excretion of oxalate was not detectable in children with celiac disease." Was that happening because oxalate that was getting into the blood was being secreted at this age more appropriately to the gut, or the lungs, or the skin, instead? Or had their oxalate been collecting in tissues like the gut, where it might be starting to impair mitochondrial function, possibly leading in time to villous atrophy?
    It would be hard not to notice that currently in the US, it is becoming popular to try gluten-free eating even if someone does not have celiac disease. That situation also describes several members of my own family who do not have celiac disease, but found out about twenty years ago that being gluten-free turned around our health so significantly that we never were tempted to go back to eating gluten. I had actually gotten the idea to try life without gluten from autism research which had been looking at a different reason to be sensitive to gluten, termed "the opiate excess theory".
    When I was at the medical library doing research when I was in graduate school, I found this theory discussed in a decades old book talking about schizophrenia. Soon I was privileged to know two of the major scientists working in this area, Paul Shattock and Kalle Reichelt. They found a protein in wheat (gliadin) and in milk (casein) that as they were digested formed peptides that had opioid activity. These peptides were capable of producing signals at opiate receptors meaning they might produce reactions or side effects seen when taking opiate medications.
    Later work also discovered opioid peptides in soy. The reason that this research might be important to celiac disease is that part of the benefit seen by removing gluten may come from eliminating these opioid signals, but these signals may continue to be a problem if you are still consuming large amounts of milk or soy.
    Recently, some further implications have appeared in this research area. Another of my autism colleagues, Richard Deth, found at his laboratory that the peptides that form opiates also block the absorption of cysteine across cell membranes. This unexpected finding probably has its biggest implications in the gut (preventing sulfur absorption) and in the brain, where sulfur is regulated a little differently. I recommend his recent paper to tell you more details, but it simply means that some of the benefits people with celiac enjoyed on a gluten-free diet may have been related to this other characteristic of opioid peptides. These same individuals may find that their health will improve even more if they controlled milk and soy.
    In the second year of our project on oxalate, I spoke at a conference in Germany and was invited for lunch in the home of a family with a child with autism on a gluten-free diet, but I noticed that this child and the children with autism I met in Germany were not doing as well as I was used to seeing in the USA. As I sat at their table, I found out that most of their gluten-free bread was made with buckwheat as a major ingredient. Buckwheat is, a very high oxalate grain. Was this keeping their son from getting better?
    Because I knew so many children with autism who had done much better than before after they eliminated gluten and casein, this to me seemed a sufficient reason not to reintroduce these foods to children already off these foods as we looked into the role of oxalate in autism. That's why, as we began our research on oxalate, I purposefully set out to test the raw ingredients being used commercially and in households for individuals on gluten and dairy-free diets. Our project discovered that there was a problem with buckwheat, amaranth, quinoa, and two late arrivals, chia seeds and hemp. We already knew oxalate was high in seeds like sesame seeds and poppy seeds, and also high in nuts like almonds which were now being made into milks for those on dairy-free diets. Soy is also high in oxalate, meaning soy has two problems—its opioid peptides and its oxalate level. In grains, most of the oxalate is in the bran, so the more "whole grain" a product is, the higher it will be in oxalate. Our listserve was literally flooded with individuals who found they got "sick" soon after they adopted what they thought was a "healthy diet". Another issue was the high levels of oxalate in chocolate and carob, which are used extensively in gluten-free "comfort foods".
    Last year, I attended a gluten-free expo in my city and picked up a cookbook full of new exciting recipes that were put together for this expo, and I saw that most of the recipes contained grains, or nuts or seasonings that were extremely high in oxalate. I couldn't help but wonder: Is this going to backfire for people, and will they recognize what is happening if by using these recipes and foods that they will find their health does not improve and may even get worse?
    In helping so many thousands of people reduce oxalate, our oxalate project has learned one thing clearly, and that is that giving someone a one page list of foods to avoid rarely successfully reduces oxalate in anyone. We have been told this most often by kidney stone patients who were given these lists by their doctors. Patients have told us hundreds of times that health improvements were not realized until they made this diet more like calorie counting. This is what we do in our support groups where people also monitor the contribution to their total oxalate level that comes from medium oxalate foods.
    This is why I would ask those reading this article to please seek our help if you wish to reduce oxalate, and do not strike out into the unknown on your own or confine yourself to the use of lists you might find on the Internet or at your doctor's office. Hundreds of Listmates have told us these lists had serious inadequacies and misinformation and little overlap with what they actually had been eating.
    We have also learned something else that is critically important. People who have been on an extremely high oxalate diet and then have reduced their diet's oxalate content too quickly, have gotten themselves in trouble. Some have ended up in emergency rooms in metabolic crisis with the doctors there unable to help them, because the doctors had never had training about why someone in this situation would get so sick.
    Even before our project started, we knew from studying the literature on those with primary hyperoxaluria, that when oxalate supply is reduced quickly by removing the liver that was putting out so much oxalate into their bodies, after replacing it with a normal liver, the amount of oxalate that suddenly began to leave the tissues of their body could potentially damage the replacement organ. Doctors have reported a very high death rate with these patients, which is reported to be much higher than death rates from other reasons for liver transplants.
    But what about what happens when reducing dietary oxalate? The food industry's recommendation of multiple fruits and vegetables has happened at the same as they began promoting many foods as super-foods and nutrient rich. Unfortunately, many of these same foods are so high in oxalate that they can keep someone from being able to retain and utilize minerals that are coming from other foods in the same meal. This can promote hyperabsorption of oxalate and increase risks of mineral imbalances. Our support groups have been deluged with individuals coming to us now with diets containing thousands of milligrams of oxalate putting their urine oxalate levels in ranges formerly seen only in the genetic hyperoxalurias. A low oxalate diet tries to keep the total oxalate load to between 40-60 mgs per day in adults As we said before, people who have been eating extremely high levels of oxalate need to reduce oxalate very slowly while the body adapts to the change. We have amassed a lot of experience with helping such individuals. The need for caution and more gradual change should not surprise us, because scientists are now telling us how quickly dietary changes can alter the function and composition of our microbial community and can also quickly alter cellular regulation of whatever enters and exits cells. These are compelling reasons to change the oxalate level slowly.
    Our website is www.lowoxalate.info. Our Yahoo group and our Facebook group are both called Trying_Low_Oxalates. We are partnering with non-profits and scientists from many fields around the world to fill in the missing science for a long list of disorders. Our work has gone far beyond autism, and we have been monitoring labwork on many conditions. We want to help make this dietary alteration as easy and safe as possible. We hope some of you readers will begin to get educated in this area. If you begin to reduce your oxalate, please let us know what reducing oxalate accomplishes for you.
    Since my early years in autism research, I have been convinced of one main principle. People with a condition will know their own bodies well. They are more likely to make important observations of change compared to a professional who comes in with too many preconceived expectations and has only a limited acquaintance with their subject's previous life.
    The first step in the scientific process really happens before scientific steps are put into use. The first "pre-step" is observation of something that does not fit old models. Frankly, after twenty years in research on autism, I don't believe the first step is best done by scientists and/or physicians. Why? Often someone new seeing a problem for the first time will notice aspects of that problem that people relying on old models will think is irrelevant and leave alone. That is why, to me, careful observations of hundreds and thousands of patients interacting can become the opportunity for forming new hypotheses that a scientist can later be recruited to test. This coordination of this volume of patient input was impossible before the internet allowed patients to find each other. But now, I think this is the most fertile field there is for making new scientific discoveries.
    Please, let's not confuse those two processes. First, we need to observe changes without layering expectations on what we see that comes from experience with only one type of patient. By looking at a broader diversity of patients, and discovering the overlap of their observations, we have a much better chance at noticing unexpected patterns that are significant. When people with no expectations of what ought to be ignored end up making the same observation time and again when they don't know each other, THEN you have something to legitimately research. At that point, the scientist can get involved with the second step, which is verifying the observations and seeing how widely they apply in one disorder or even more broadly. Using both steps, and both sets of eyes, and the marvelous ability to combine observations from thousands of individuals using the internet, we are now likely to begin to understand the complex role of oxalate in celiac disease and in many other disorders.
    From the author:
    If you have ever been diagnosed with an autoimmune disease and have been trying to lower oxalate, will you participate in the development of this science by filling out a survey?
    We would also like to find out whether reducing oxalate has affected your autoimmune condition.
    The link to our survey is here: https://www.surveymonkey.com/r/CMN5KK7
    References:
    Baker PW, Bais, R, Rofe, AM Formation of the L-cysteine-glyoxylate adduct is the mechanism by which L-cysteine decreases oxalate production from glycollate in rat hepatocytes. Biochem. J. (1994) 302, 753-757 Capolongo G, Abul -Ezz S, Moe OW, Sakhaee K . Subclinical celiac disease and crystal-induced kidney disease following kidney transplant . Arn J Kidney Dis . 2012 Oct ;60(4) :662-7 . Halbrooks PJ, Mason AB , Adams TE, Briggs SK, Everse SJ . The oxalate effect on release of iron from human serum transferrin explained . J Mol Biol. 2004 May 21;339 (1):217-26. Kohman, E.F. Oxalic acid in foods and its behavior and fate in the diet. The Journal of Nutrition, 1940 18(3): 233-246. Konstantynowicz J, Porowski T, Zoch-Zwierz W, Wasilewska J, Kadziela -Olech H, Kulak W, Owens SC, Piotrowska-Jastrzebska J, Kaczmarski M. A potential pathogenic role of oxalate in autism . Eur J Paediatr Neurol . 2012 Sep;l6(5) :485-91 Monico, CG, Persson, M, Ford CG, Rumsby, G, Milliner, DS. Potential mechanisms of marked hyperoxaluria not due to primary hyperoxaluria I or II. Kidney International, 2002 Aug;62(2):392-400. PubMed PMID: 12110000 Nishijima S, Sugaya K, Hokama S, Oshiro Y, Uchida A, Morozumi M, Ogawa Y. Effect of vitamin B6 deficiency on glyoxylate metabolismin rats with and without glyoxylate overload. Biomedical Research, 2006 Jun; 27(3):P93-P98. Novartis Foundation Symposium 273, Epithelial anion transport in health and disease: The role of the SLC26 transporters family. John Wiley and Sons, Ltd. 2006. Rare Kidney Stone Consortium Mayo Clinic. http://www.rarekidneystones.org/hyperoxaluria/physicians.html  Saccomani MD , Pizzini C, Piacentini GL, Boner AL , Peroni DG . Analysis of urinary parameters as risk factors for nephrol ithiasis in children with celiacdisease . J Urol. 2012 Aug ;188(2):566-70 . Speirs, M. The utilization of the calcium in various greens, The Journal of Nutrition, 1939 17(6), 557-564. Trivedi MS , Shah JS, Al-Mughairy S, Hodgson NW , Simms B, Trooskens GA, Van Criekinge W , Deth RC . Food-derived opioid peptides inhibit cysteine uptake with redox and epigenetic consequences . J Nutr Biochem . 2014 Oct ;25(10) :1011- 8 .

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 12/15/2015 - Newly diagnosed with celiac disease, late in 1993 or early in 1994, I was reading a paper that turned my perception of this disease upside down. I learned that it takes more than susceptible genes and eating gluten to cause celiac disease. There is some added, as yet unknown factor in the onset of celiac disease. The report I was reading suggested that a fairly common viral infection might be that missing co-factor. It went on to say that 89% of subjects with untreated celiac disease also showed blood evidence of a particular viral infection called adenovirus 12, while fewer than 12% of control subjects showed evidence of past or present infection with this virus. It is a microbe that makes its home in our small intestines. The report went on to say that this particular virus contains an amino acid sequence that is identical to a sequence that forms part of a protein in gliadin, which is found in wheat, while similar proteins with the same triggering impact on our immune systems are also found in rye and barley. I was electrified by this insight. It offered a window through which I could begin to understand this enigmatic disease that made me react to a food that almost everyone I knew seemed to tolerate without any problems.
    I looked to see who had written the article. The lead author was listed as M. F. Kagnoff, but my attention was drawn to Donald Kasarda’s name, also listed as an author, because I had seen that name before. Several years later, I attended a CSA/USA conference in Seattle. The name of one of the speakers was familiar. After a little checking, I realized that he was the lead author of the study that had touched off my imagination.
    Dr. Kagnoff’s lecture followed immediately after a presenter who had repeatedly asserted that celiac disease is a very difficult diagnosis. Almost as soon as he got up on stage, Dr. Kagnoff said something to the effect that celiac disease is only a difficult diagnosis if you aren’t looking for it. The room suddenly became very quiet.
    The presentation went well, and he outlined the criteria for diagnosing celiac disease, and stated why he felt that it was a simple diagnosis. The speaker who followed him began by stating that celiac disease is a difficult diagnosis, despite Dr. Kagnoff’s assertions to the contrary. I left that conference with a strong sense of appreciation for Kagnoff on several levels: as a gastroenterologist, as a researcher, and as an independent thinker who was quite willing to offer a dissenting opinion where he disagreed.
    Six or seven years later, a mutual friend introduced me to Marty Kagnoff at a cocktail party in New York city. It was a pleasure to finally meet him in person. I told him that I was most impressed with, and intrigued by his work with adenovirus 12. I also told him that I enjoyed hearing his assertion, at the Seattle conference, that celiac disease is a simple diagnosis. He seemed a little surprised that I was aware of his research from more than twenty years previous, and he said that his work had been eclipsed by newer work that explored other infectious agents. He was interesting and interested, and the three of us engaged in a lively discussion about some of the politics regarding celiac disease and its diagnosis. He was brilliant, creative, and independent; all the things that a researcher should be.
    His passing is a huge loss to the medical profession, the celiac and gluten sensitive community, as well as to the biological research community. His contributions and discoveries shaped much of what we now understand about celiac disease, the intestinal mucosa, and intestinal immunity.
    Source:
    Kagnoff MF, Paterson YJ, Kumar PJ, Kasarda DD, Carbone FR, Unsworth DJ, Austin RK. Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease. Gut. 1987 Aug;28(8):995-1001

    Betty Wedman-St Louis, PhD, RD
    12/22/2015 - Eating Gluten-Free is not complicated and certainly not less nutritious than conventional menu choices. But there are challenges for the person with celiac disease. Gluten containing substances are used throughout a wide variety of convenience foods—soups, sauces, salad dressings, etc.—so a gluten-free label became necessary to minimize the possibility of gluten contamination.
    Those celiacs wanting to minimize cooking were excited when more Americans started to endorse gluten-free eating. Now supermarkets were filling the shelves with gluten-free flour blends, baking mixes, brownie mixes, chocolate chip cookie mixes, and even a banana bread mix.
    Keep in mind, the gluten-free label in the United States means that the gluten level in that product must be less than 20 ppm. This level may still be too high to tolerate for those with gluten enteropathy—even very low levels of gluten very sensitive individuals may mean continued symptoms. Also realize that there is NO independent or government agency overseeing the truth in labeling that celiacs expect from the gluten-free label.
    It is also important to consider the nutritional value of gluten-free products. Recently eleven gluten-free products were purchased from local supermarkets and tested for quality and convenience. Here is a summary of the evaluations:
    King Arthur Flour gluten-free Banana B read mix made a delightful bread but sugar is the first ingredient. One slice= 16g or 4 teaspoons sugar. Whole grain brown rice flour was the second ingredient which added more nutritional value than white rice flour.
    Chocolate chip cookie mixes from Betty Crocker (13g or 3+ teaspoons sugar per 2 cookies), Hodgson Mill (15g or ~4 teaspoons sugar per 2 cookies) were crispy and delicious but could have reduced sugar content like Among Friends Double Chocolate Cookie Mix (8g or 2 teaspoons sugar per 2 cookies). King Arthur Flour gluten-free cookie mix allows customization of your cookie so nutrition labeling indicates 7g or ~2 teaspoons sugar BEFORE adding chocolate chips or dried fruit.
    Hodgson Mill Brownie mix (13g or 3+ teaspoons sugar) and King Arthur Flour Company Brownie mix (18g or 4 1/2 teaspoons sugar) list sugar as the first ingredient so moderation in consumption is recommended.
    Among Friends Baking Mix for fruit crisp (8g or 2 teaspoons sugar before adding fruit) is oat based providing a whole grain topping for peaches, strawberries, or blueberries. Some celiacs may not tolerate oats even when processors certify that they have been milled on dedicated equipment.
    Hodgson Mill Cookie mix offers 5 recipe choices from one mix. The nutrition label indicates 13g or 3+ teaspoons sugar in the basic mix before chocolate and sugar for one variation or chocolate pieces for another are added to the batter.
    XO Baking Company All Purpose Flour offers the combination of tapioca (cassava) flour, potato starch, and coconut flour for use in cookies, brownies, cakes, pancakes, muffins, etc. No sugar is in the flour blend so the baker can determine how much sugar or what kind of sweetener to use.
    Pillsbury All Purpose gluten-free Flour Blend features a chocolate chip cookie recipe on the package. It is a blend of rice flour, potato starch, pea fiber, and tapioca starch so the sweetener of choice can be determined by the cook.
    Seven out of eleven baking mixes contained xanthan gum. It is a frequent food additive in baking products to make the dough sticky or moist. Xanthan gum is derived from the bacteria Xanthomones campestris which is used as a thickener in salad dressings and sauces. This bacteria strain is the same one that causes black mold on broccoli, cauliflower and leafy green vegetables which results in a slimy coating.
    For those wanting to limit their exposure to genetically modified foods, xanthan gum is not recommended. In the USA it is derived corn. Since no studies have been done on sensitivities to xanthan gum, those with gastro-intestinal sensitivities would be wise to limit or avoid products containing it since labels do not state the carbohydrate source used in production.
    Celiacs with intestinal bloating and gas issues may find that similar symptoms can be caused by too much xanthan gum. In addition, as a thickening agent (salad dressing, ice cream or egg substitute products like egg beaters) xanthan gum can act as a very effective laxative.
    Convenience products can be a lifesaver for someone who does not like to cook or has limited time. Many convenience mixes like those evaluated above can be high in sugar and fat. Foods with high sugar have a high glycemic index which has been shown to contribute to chronic diseases like diabetes, high blood pressure and cardiovascular disease.
    Whole foods offer better nutrition for people with celiac disease. Convenience foods and bakery products are a treat—they can add variety to a gluten-free diet—but a paleo diet is the healthiest choice for anyone, including those on a gluten-free diet.

    Tina Turbin
    Celiac.com 12/29/2015 - I discussed the possibility of a Low Glycemic Paleo Diet as an entertaining idea as a beneficial diet for celiac in the last issue, Winter 2015. In closing, I stated I would reveal more about this topic in the coming issue. So, let's dive in and open our eyes to some facts and even some revealing possibilities that may very well help improve our health and quality of life.
    As a celiac myself, (2 of my three kids have celiac disease and my grandfather died from undiagnosed celiac disease) I was more than happy to follow the gluten-free diet diligently once finally diagnosed after many years of distress, bone loss, declining health not to mention non-stop bone aches, bowel inconsistency and severe lack of muscle tone. I will spare you further details but there was no doubt a major beneficial change that occurred once I eliminated all gluten from sources of wheat, rye and barley and all its "relatives" or any possible cross contamination. Eventually I was thrilled to be able to eat baked good substitutes that did not hurt my belly, cause my joints and bones to ache and were absolutely delicious and healthy, as they were gluten-free!
    Soon after I became an active advocate (and for many years) I was thrilled to be able to speak broadly to help raise awareness about celiac disease and the NEED for the gluten-free diet. I was also soon working closely with many gluten-free companies (as a tester, consultant and promoter) becoming blind to the fact that the boxes that were arriving to my door by the truckload were all desserts, loaded with carbohydrates and sugars.
    At the time I wrote and spoke often (in interviews and on radio) about Type 2 diabetes and celiac disease but never put two and two together. If lifestyle and diet change can address Type 2 permanently, what were these diet changes that were so effective? Also, even more to the point, why was Type 2 diabetes so common as a diagnosis after being diagnosed with celiac disease and going on the gluten-free diet?
    Research suggests an association between Type 1 diabetes and celiac disease, but there does not appear to be a link between celiac disease and type 2 diabetes. Type 2 is not an autoimmune disorder and doesn't share genes with celiac disease. According to the Celiac Sprue Association, individuals can be genetically predisposed to Type 2 diabetes, but those genes don't increase the risk of celiac disease.
    Let's look at the immense increased ingestion of glucose, sugars and carbohydrates and fiber while one is on the gluten-free diet by indulging in baked goods, desserts and grains! Gluten-free foods and grains are typically made with rice starch (or brown rice starch), tapioca starch, cornstarch and potato starch. All of which have virtually no fiber. Hence straight into the blood stream spiking the blood sugar bite after bite and quickly.
    The latest attempt is many companies and cooks trying to improve nutrients by baking with higher fiber gluten-free grains with higher nutrient value. Such as teff, millet, buckwheat etc. These are all still VERY HIGH in carbohydrates and very little fiber to slow the glycemic entrance into the blood system, still resulting in spiking the blood sugar rapidly. I must mention that most people do not just eat 2-3 bites of millet or a ¼ cup of cooked buckwheat. This would be easier on the body, but it seldom occurs.
    Carbohydrates are a type of nutrient in foods and some feel we need this to survive physically and some MD's are saying we need far less than we ever thought. The three basic forms are sugars, starches and fiber. Different types of carbohydrates have properties that affect how quickly your body digests them and how quickly glucose enters your bloodstream. When we eat or drink anything with carbs, the body breaks down the sugars and starches into a type of sugar called glucose. Glucose is the main source of energy for cells in the body. Fiber passes through your body undigested. The unused glucose for energy is quickly taken out of the blood stream by the insulin and "stocked" away in the cells for future energy as fat. It is the body's amazing way of survival.
    To elaborate a bit more, the two main hormones from the pancreas help regulate glucose in the bloodstream. Insulin moves glucose from the blood into the cells. Glucagon helps release glucose stored in your liver when the blood sugar (blood glucose) level is low.
    I suggest to anyone to take a look at the nutritional value on all packages and foods and get familiar with the amount of carbohydrates you are ingesting through your meals, snack and drinks. Get familiar with the carbohydrate, sugar and fiber levels in the food you buy and have in your home. Getting educated is the first step to learning and then you can make changes to suit your health and body goals.
    A healthy paleo or gluten-free diet is a low glycemic one at the very least. A low glycemic diet can improve all manner of current health situations. By statistics and more than abundant research, it will deter diseases quiet commonly associated with a high glycemic diet.
    We will expand on this topic next time.
    At this point I would like to refer you to some highly respected professionals and allow you to do further research and come to your own conclusions. Please look further into DrPerlmutter.com, Mercola.com, WheatBellyBlog.com, BulletProofExec.com, ChrisKresser.com, MarksDailyApple.com.
    As always, wishing you the best in your life and health!

  • Recent Articles

    Jefferson Adams
    Celiac.com 07/16/2018 - Did weak public oversight leave Arizonans ripe for Theranos’ faulty blood tests scam? Scandal-plagued blood-testing company Theranos deceived Arizona officials and patients by selling unproven, unreliable products that produced faulty medical results, according to a new book by Wall Street Journal reporter, whose in-depth, comprehensive investigation of the company uncovered deceit, abuse, and potential fraud.
    Moreover, Arizona government officials facilitated the deception by providing weak regulatory oversight that essentially left patients as guinea pigs, said the book’s author, investigative reporter John Carreyrou. 
    In the newly released "Bad Blood: Secrets and Lies in a Silicon Valley Startup," Carreyrou documents how Theranos and its upstart founder, Elizabeth Holmes, used overblown marketing claims and questionable sales tactics to push faulty products that resulted in consistently faulty blood tests results. Flawed results included tests for celiac disease and numerous other serious, and potentially life-threatening, conditions.
    According to Carreyrou, Theranos’ lies and deceit made Arizonans into guinea pigs in what amounted to a "big, unauthorized medical experiment.” Even though founder Elizabeth Holmes and Theranos duped numerous people, including seemingly savvy investors, Carreyrou points out that there were public facts available to elected officials back then, like a complete lack of clinical data on the company's testing and no approvals from the Food and Drug Administration for any of its tests.
    SEC recently charged the now disgraced Holmes with what it called a 'years-long fraud.’ The company’s value has plummeted, and it is now nearly worthless, and facing dozens, and possibly hundreds of lawsuits from angry investors. Meantime, Theranos will pay Arizona consumers $4.65 million under a consumer-fraud settlement Arizona Attorney General Mark Brnovich negotiated with the embattled blood-testing company.
    Both investors and Arizona officials, “could have picked up on those things or asked more questions or kicked the tires more," Carreyrou said. Unlike other states, such as New York, Arizona lacks robust laboratory oversight that would likely have prevented Theranos from operating in those places, he added.
    Stay tuned for more new on how the Theranos fraud story plays out.
    Read more at azcentral.com.

    Jefferson Adams
    Celiac.com 07/14/2018 - If you’re looking for a simple, nutritious and exciting alternative to standard spaghetti and tomato sauce, look no further than this delicious version that blends ripe plum tomatoes, garlic, olive oil, basil, and firm sliced ricotta to deliver a tasty, memorable dish.
    Ingredients:
    12 ounces gluten-free spaghetti 5 or 6 ripe plum tomatoes ¼ cup extra virgin olive oil 2 cloves garlic, crushed ¾ teaspoons crushed red pepper ¼ cup chopped fresh basil 2 tablespoons chopped fresh parsley Kosher salt and black pepper ⅓ cup pecorino Romano cheese, grated ½ cup firm ricotta, shaved with peeler Directions:
    Finely chop all but one of the tomatoes; transfer to large bowl with olive oil and ¼ teaspoon salt.
    Cook spaghetti until al dente or desired firmness, and drain, reserving ¼ cup cooking water. 
    Meanwhile, chop remaining tomato, and place in food processor along with garlic, red pepper, and ½ teaspoon salt; puree until smooth. 
    Gently stir mixture into the bowl of chopped tomatoes.
    Add cooked spaghetti, basil and parsley to a large bowl.
    Toss in tomato mixture, adding some reserved pasta water, if needed. 
    Spoon pasta into bowls and top with Romano cheese, as desired.

    Jean Duane
    Celiac.com 07/13/2018 - I went to a friend’s home for dinner.  A few days before, she called and asked me what I could eat.  I asked her what she was planning to make, and she said she was grilling meats with side dishes.  I said, “Great.  Please just grill a piece of chicken for me with salt and pepper, and I’ll be happy to bring a side.” She said, “No need to bring a side.  I’ve got this.” When I arrived, she greeted me and said, “I spent all day cooking tonight’s dinner so you can eat it. Hey would you just check this salad dressing to see if it is OK for you?” I looked at the ingredients and it contained gluten and dairy, both of which I cannot eat.  Then I glanced around the kitchen and saw evidence of wheat cross-contamination, including buns being toasted on the grill, and gluten-containing barbeque sauce spilling on the grill where my “clean” chicken was cooking. She had other guests to tend to, and I couldn’t offer instruction or read the ingredients of everything she used in the meal. 
    At social gatherings, I’ve been challenged too by those who ask if I am really “allergic,” or just eating gluten free as a “fad.” I’ve been told many times by hosts and hostesses that, “a little won’t hurt you,” or “everything in moderation,” or “if it is made with loving hands, it is good for you to eat.”  Of course, all of this is bunk for those with food allergies or celiac disease.  A little bit may kill us, and whether made with loving hands or not, it will certainly make us sick. 
    Those of us with food allergies and/or celiac disease walk a tightrope with friends and relatives. The old rules of etiquette just don’t work anymore.  We don’t want to insult anybody, we don’t want to be isolated, and we also don’t want to risk our health by eating foods that may contain ingredients we cannot tolerate.  So what do we do? 
    Etiquette books advise us to eat what is put in front of us when we are guests in someone’s home. They caution us at all costs not to insult our hostess. Rather, we are instructed to compliment the hostess on her good cooking, flavor combinations, and food choices.  But when foods are prepared in a cross-contaminated environment with ingredients we are allergic to, we cannot follow the old social constructs that do not serve us.  We need to work together to rewrite the rules, so that we can be included in social gatherings without fear of cross-contamination, and without offending anyone.
    Let’s figure out how to surmount these social situations together.  
    Each edition of this column will present a scenario, and together, we’ll determine appropriate, polite, and most importantly, safe ways to navigate this tricky gluten-free/food allergies lifestyle in a graceful way.  If someone disagrees with our new behavior patterns, we can refer them to this column and say, “Here are the new rules for those of us with food allergies or celiac disease.”  When we are guests in someone’s home, we can give them links to this column so they understand the plight we are faced with, bite after bite. Perhaps this will help those of us living with us to understand, be more compassionate, and accepting of our adaptations to keep ourselves safe. 
    This column will present a scenario such as the one above, and ask that you comment on how you would navigate it. Let’s talk about it. Let’s share ideas.  Using the example above, here’s the scenario for this issue:
    What would you do?
    Your kind-hearted friend invites you to dinner and insists on cooking for you.  You arrive and the first thing she says is, “I’ve spent all day making this for you. Oh, I bought this salad dressing for you, but you might want to read the ingredients first.”  You do, and it contains malt vinegar.  You look around the kitchen and notice evidence of cross-contamination in the rest of the meal.  What do you do? 
    Please comment below and feel free to share the tricky scenarios that you’ve encountered too.  Let’s discuss how to surmount these social situations.  What would you do?

    Jefferson Adams
    Celiac.com 07/12/2018 - Previous research has shown that the oral administration of Bifidobacterium infantis Natren Life Start super strain (NLS-SS) reduces of gastro-intestinal symptoms in untreated celiac disease patients. The reduction of symptoms was not connected with changes in intestinal permeability or serum levels of cytokines, chemokines, or growth factors. Therefore, researchers suspected that the reduction of symptoms might be related to the modulation of innate immunity.
    To test that hypothesis, a team of researchers set out to assess the potential mechanisms of a probiotic B.infantis Natren Life Start super strain on the mucosal expression of innate immune markers in adult patients with active untreated celiac disease compared with those treated with B. infantis 6 weeks and after 1 year of gluten-free diet.
    The research team included Maria I. Pinto-Sanchez, MD, Edgardo C. Smecuol, MD, Maria P. Temprano,RD, Emilia Sugai, BSBC, Andrea Gonzalez, RD, PhD, Maria L. Moreno,MD, Xianxi Huang, MD, PhD, Premysl Bercik, MD, Ana Cabanne, MD, Horacio Vazquez, MD, Sonia Niveloni, MD, Roberto Mazure, MD, Eduardo Mauriño, MD, Elena F. Verdú, MD, PhD, and Julio C. Bai, MD. They are affiliated with the Medicine Department, Farcombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada; the Small Intestinal Section, Department of Medicine and the Department of Alimentation at Dr. C. Bonorino Udaondo, Gastroenterology Hospital and Research Institute at the Universidad del Salvador in Buenos Aires, Argentina.
    The team determined the numbers of macrophages and Paneth cells, along with the expression of a-defensin-5 expression via immunohistochemistry in duodenal biopsies.
    Their results showed that a gluten-free diet lowers duodenal macrophage counts in celiac disease patients more effectively than B. infantis, while B. infantis lowers Paneth cell counts and reduces expression of a-defensin-5.
    This study documents the differential innate immune effects of treatment with B. infantis compared with 1 year of gluten-free diet. The team calls for further study to better understand the synergistic effects of gluten-free diet and B. infantis supplementation in celiac disease.
    Source:
    J Clin Gastroenterol

    Jefferson Adams
    Celiac.com 07/11/2018 - For people with celiac disease, finding decent gluten-free bread is like searching gold. Many have given up on bread entirely and others begrudgingly relate themselves to the ignominious frozen aisle at their supermarket and content themselves with one of the many dry, shriveled, flavorless loaves that proudly tout the gluten-free label. 
    For these people, the idea of freshly baked bread is a distant, if comforting, memory. The idea of going to Paris and marching into a boulangerie and walking out with a warm, tasty, gluten-free baguette that was freshly baked on the premises that morning, is like a dream. Now, in some Parisian bakeries, that dream is becoming a reality. And the tear of joy from the thankful gluten-free masses are sure to follow.
    These days, a single sign on the awning speaks to hungry customers who peruse the tarts and chou buns, and the loaves that fill the cooling on racks behind a glass pane at Chambelland boulangerie and café in Paris’ 11th arrondissement. The sign lettered in French translates: “artisan baker; flour producer; naturally gluten free.” That’s right. Naturally gluten-free. At a bakery. In Paris. 
    Only the flat, focaccia-style loaves, and the absence of baguettes, tells customers that this bakery is something different. Chambelland opened its doors in 2014 and continues to do a brisk business in delicious, freshly baked gluten-free breads and other goods.
    The boulangerie is the work of Narhaniel Doboin and his business partner, Thomas Teffri-Chambelland. They use flour made of grains including rice, buckwheat and sorghum to make delicious gluten-free baked goods. Doboin says that customers queued in the rain on the first day, hardly believing their eyes, some began to cry. 
    For gluten-free Parisians, there was a time before Chambelland, and the time after. If you find yourself in Paris, be sure to search them out for what is sure to be a gluten-free delight.
    Or maybe book your ticket now.
    Read more at: Independent.co.uk