-
Welcome to Celiac.com!
You have found your celiac tribe! Join us and ask questions in our forum, share your story, and connect with others.
-
Celiac.com Sponsor (A1):
Celiac.com Sponsor (A1-M):
-
Get Celiac.com Updates:Support Celiac.com!
Search the Community
Showing results for tags 'ncgs'.
-
Celiac.com 01/01/2024 - A recent review by researcher Evan D. Newnham delves into the evidence concerning the effects of gluten ingestion on gastrointestinal symptoms and small intestinal injury indices in individuals without celiac disease, but who may be gluten intolerant. Newnham, affiliated with the Eastern Health Clinical School in Australia, conducted a literature review focusing on interventional studies to address this issue. The findings highlighted a lack of comprehensive exclusion of celiac disease in some studies. In particular, an unblinded study that identified symptomatic responses to gluten didn't effectively exclude celiac patients, as many exhibited intraepithelial lymphocytosis. However, a more robust double-blinded, randomized, placebo-controlled re-challenge trial was reported. This trial included patients where celiac disease had been ruled out based on either normal duodenal histology on a gluten-containing diet or the absence of the HLA DQ2 or DQ8 haplotype. During the trial, participants were randomly assigned to receive 16 grams per day of either gluten or a placebo for six weeks. All participants experienced improved gastrointestinal symptoms on a gluten-free diet (GFD) for at least six weeks before enrollment. The study, comprising 19 participants receiving gluten and 15 receiving a placebo, revealed that the change in overall symptom severity from baseline to the final weeks was more significant for those receiving gluten. Within one week, symptoms like pain, bloating, satisfaction with stool consistency, and tiredness were worse for the gluten group compared to the placebo group. However, the mechanisms behind symptom induction were not identified. The study underscores the existence of non-celiac gluten intolerance and emphasizes the need for future research to address critical issues like determining the required gluten dose and understanding the mechanisms of action in non-celiac individuals. Read more in the Journal of Gastroenterology and Hepatology
- 7 comments
-
- gastrointestinal symptoms
- gluten
- (and 6 more)
-
NCGS is my final diagnosis, methinks. I was born with a Nightshade Food intolerance. I'm 54 years young, as a kid we were poor. Mom made beans, taters, and cornbread EVERY day. Sometimes twice a day with little meat in our early developmental years. I'm now intolerant to potatoes and beans (of ANY kind) and the CORN (4x higher lectins than other foods). Lectins cause me a burning in my joints like psoriatic arthritis...but NO PsA detected. Corn also gives me psoriasis. Tricky these food issues are! Suffering stomach issues my entire life, I became mentally & physically ill. Lost my vision, hearing, balance, horrible incontinence, and eventually a HUGE precancerous tumor in my colon that almost killed me. Been 2 yrs since that surgery. Recovery seems to be a decade long process. I've been on a LTGFDWC for almost 4 yrs now, along with dairy, soy & Nightshade free for 2 yrs. These illnesses have destroyed my brain & my body. My muscles and connective tissues throught my body are damaged. And it's painful to just move around at times. I suffer from cognitive decline due to gluten ataxia. Slower thought processes, reaction times etc. TWO Differences (for me) put me in the NCGS diagnosis. 1st) NO DAMAGE TO INTESTINES and 2nd) DO NOT TEST POSITIVE FOR GLUTEN ANTIBODIES **IF anyone had explained THIS to me I feel I could've began figuring out my health problems a LOT sooner. Gluten IS tricky. So are Nightshades bc everyone in my family has a different level of sensitivity to it. My youngest family member to have passed from Colon cancer died at just 19 yrs of age. BE CAREFUL what u put in your bodies. EVERYTHING has a direct affect on the brain. Negative or positive. Be a POSITIVE foodie. Our bodies weren't made for processed foods. OR the wheat, dairy and soy that are in EVERY processed food on the shelf. Take care & love yourself
-
Hello! I am new to this site and I have been debating whether to post my situation or not, but here goes! Since early March, I have been having daily hives. Typically they present as an itchy area of skin (sometimes showing small bumps), and when I scratch them they become more pronounced and the area becomes red and puffy. They happen just about anywhere on my body, even though I take an antihistamine daily. I had also been experiencing dermatographia, some digestive issues and bloating. I decided to start with going to a GP to find some answers. They suggested bloodwork. I had been attempting to research similar stories/symptoms, leading me to ask if they could include a gluten panel. The bloodwork was done in June, and all of the tests except the gluten panel came back normal. Based on the results of the gluten panel, I was told I did not have to eliminate gluten, but should limit it to some point. I asked if I could be having an allergic reaction to wheat. I was told no, based on the absence of elevated levels of something else in the bloodwork (which I forget). Craving relief, I cut gluten out completely for 6 weeks. During this, my symptoms lessened significantly. I even had days of no hives at all. I recently tried eating gluten intentionally again, and it has brought back my symptoms. At least I think it is gluten that is the culprit. That leads me to why I am posting. Other than the digestion issues/bloating, which were not extremely significant, but noticeable nonetheless, I am not convinced my skin symptoms are typical of a gluten sensitivity. I am planning on going to an allergist for formal skin testing, though it is difficult to get an appointment at the place I am trying to go to, so it will be a bit before I get that testing done. Has anyone experienced anything similar? Also, I would post pictures of my gluten panel/skin issues but I cannot seem to figure out how to do it just yet…
-
To All, I came across this article and research and haven't been able to post it till now and I thought it deserved it's on thread topic. I will probably post in the Magnesium, Magnesium, Magnesium thread at a later date. Maybe it will help some one else. https://blog.organicolivia.com/magnesium-deficiency-associated-high-histamine-levels-allergies/ And this research they quoted entitled "Blood and mast cell histamine levels in magnesium-deficient rats" https://pubmed.ncbi.nlm.nih.gov/6445415/ Where they note Histamine Levels are elevated to 6 to 7X compared to a healthy person with normal Magnesium levels. There seems to be an direct relationship (IMHO) between a Magnesium deficiency and a disordered immune systems IE a Magnesium deficiency could be the trigger for a Histamine Intolerance leading to a Histamine Storm... This would explain well this research as well entitled "Effects of magnesium deficiency on dermal mast cells in rats]" https://pubmed.ncbi.nlm.nih.gov/2438197/ I hope this is helpful but it is not medical advice. Posterboy,
- 36 replies
-
- allergies
- histamine intolerance
-
(and 3 more)
Tagged with:
-
To All, I came across this Old Live Journal blog a few years ago doing research on Zonulin and/or Niacin to see if I could find a "Metabolic link" to Pellagra in Celiac disease and I never had a good opportunity or chance to use it......but thought it was research worth discussing so I thought I would start a thread about it to see what others thought about it? https://alobar.livejournal.com/2930798.html#%2F2930798.html Could Zonulin be the body's way to tell the body it needs more Niacin? This researcher seems to think so and the research seems to indicate.....and I tend to agree with it/them what do others think about this? quoting from the blog post... "For a number of years I have mentioned some articles talking about gluten and corn protein having the effect of opening up the permeability of the intestines WHEN (and only when) the animals were niacin deficient at the time of exposure." And also a little lower in the blog post see this quote... "Jon Pangborn and I have had conversations about a shift that may have occurred since he began looking at plasma amino acid profiles years ago and saw many with elevated tryptophan. I don't see elevated tryptophan that much, but I do see a lot of reports (20%) that don't have a figure for tryptophan. I think this is because it was not detected, although I WISH the labs were clearer about SAYING that instead of just leaving it blank. One reason for my suspicion that the blank field means "not detected" is that I've seen repeat tests from some children, and on other tests, they had measurable tryptophan but it was very, very low. Regardless, tryptophan was above the mean in only about 15% of my database, and below the mean in 81% of the ones where there was a number there. That is nothing like a normal distribution! So, maybe there is something about having low niacin that suddenly makes peptides from gluten (and to some extent corn zein) become signalling molecules, and the raised level of zonulin may just be a "reasonable" response to that signal. In other words, this (Zonulin) might be a "Plan B for niacin" signal. You will see, in the first article below, they did find low plasma tryptophan in people with celiac disease and an altered low neutral amino acid to tryptophan ratio." He was remarking about this study in Celiac children... Entitled "Plasma precursor amino acids of central nervous system monoamines in children with coeliac disease.....American spelling Celiac disease. https://pubmed.ncbi.nlm.nih.gov/1773952/#:~:text=A significantly lower ratio of plasma tryptophan to,children and was more pronounced in untreated children. Here is the full abstract for anyone who wants to read it. Abstract "Some children with coeliac disease show behavioural disorders such as depression and other signs which have been correlated with reduced central monoamine metabolism. We have therefore investigated the brain availability of the monoamine precursors tryptophan and tyrosine in 15 untreated children with coeliac disease and 12 treated children with coeliac disease as well as in 12 control children. Significantly decreased plasma concentrations of tryptophan were found in untreated children (mean (SD) 13 (4) mumols/l, p less than 0.001) compared with treated children (31 (13) mumols/l), and in both groups of coeliac children when compared with control children (81 (22) mumols/l). A significantly lower ratio of plasma tryptophan to large neutral amino acids (tyrosine, valine, isoleucine, leucine, and phenylalanine) was also observed, which could indicate impaired brain availability of tryptophan in coeliac children and was more pronounced in untreated children. The impaired availability of tryptophan could produce decreased central serotonin synthesis and in turn behaviour disorders in children with coeliac disease." I would be interested what people think.....is impaired tryptophan metabolism in children with celiac disease proof enough for you to convenience you that at least at a "Metabolic" level Pellagra is occurring in Celiac disease going undiagnosed? This same metabolic maker of impaired tryptophan metabolism has also been found in adult Celiac's as well! I hope this is helpful but it is not medical advice. Posterboy,
- 2 replies
-
- celiac disease
- corn
- (and 8 more)
-
FPIES Model for Celiac disease and or NCGS triggered by Low and or NO Stomach Acid in Children and Adults by the Posterboy of Low and No Stomach acid I started a thread about this topic Low and No Stomach Acid as trigger for food alelrgies……. but it was part of a larger more general topic Here it is if you want some background But this topic about FPIES is important enough…..it needs to be explained some more and deserves it own blog post on this topic and/or an article about it on the journal of gluten sensitivity….. Maybe Scott will consider editing this blog post and making an article out of it someday…. Here is the link to the Autumn Issue https://www.celiac.com/celiac-disease/journal-of-gluten-sensitivity/autumn-2022-issue/ I woke up tossing and turning thinking about this topic…..and I knew I needed to write one more Posterboy blog post…. explaining the FPIES Model for Celiac disease…… Mainly because Nobody else could or would write it…. To those who might read the rest of this blog post…..KNOW this will probably be another WTL: DR……(Note: this is only about 1/3 as long as normal) because I choose to focus on the food allergy trigger of Low/NO Stomach instead of trying to bite off more than I can chew in one blog post..... (See what I did there) and I left appropriate and proper supplemention to help support your Celiac symtpom's triggered, in large part (IMO) by being low in stomach in the first place etc....in the rambling eclectic Posterboy style…..I am infamous for….for another blog post (If I have the time and decide it is worth exploring some more)......Scott already has a nice thread on Supplementing to help your Celiac recovery..... This builds on my other Posterboy blog posts……(for those who have not read the other ones)……they go something like this LOW Stomach and/or NO Stomach is the trigger for your food allergies! I can’t make it any simpler than this…. This blog posts is based on this article about this topic…. Entitled “Anti-acid medication as a risk factor for food allergy” I have subtitled the FPIES Model for Celiac disease….. because it elegantly explains what is happening… Here is the Abstract link….. https://pubmed.ncbi.nlm.nih.gov/21121928/ For those who like to do more thorough reading/research on this topic…..it is a “Gold Mine” of information about Low/NO Stomach Acid and why Antiacid medicines can trigger a food allergy…. Here is the full citation…. https://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2010.02511.x Which makes it approx…12 years old now……and most people and doctor’s don’t have a clue….. low stomach acid is the trigger for their food allergies…. As I like to say……why isn’t this information on the front page of every “newspaper” in the country….. Recently Celiac.com did a nice summary on this topic…..confirming this very fact IMO! And it was very widely read and popular article and why I knew I needed to write another Posterboy blog post on this topic…. Entitled “Acid Suppression Drugs and Antibiotics Given to Infants Strongly Associated with Celiac Disease” And can be read at this link… The Mounting Evidence is overwhelming in IMHO when you know and are aware that the stomach is the “Gate Keeper” for the Small Intestine and what triggers someone to develop food allergens…..in the first place. When you consider that 35+ years ago Low and NO stomach was found to be common in Celiac’s and predictable of DH in Celiacs! See this research about it entitled “Gastric morphology and function in dermatitis herpetiformis and in coeliac disease (aka Celiac disease) .” https://www.ncbi.nlm.nih.gov/pubmed/3992169 And this article as summarized on Celiac.com entitled “Do Proton Pump Inhibitors (aka PPIs) Increase Risk of Celiac Disease” Add to that the recent article on PPIs in Children and you have a “Trifecta” of sorts….. Or three strikes and your out (affect)……however you would like to look at it/think abou it???? So what does FPIES have to do with Celiac disease and or NCGS…. Because FPIES also happen when we as children are low in Stomach acid…..and why children will often outgrow their food allergies as their stomach acid strengthens enough (as they age)….and it (stomach acid) become strong enough to cut up food proteins in their diets…. One of the main and primary differences of FPIES of Celiac disease and NCGS in children is the level of Vomiting…. IE if you vomit as a kid (like I did)…..then it is a FPIES allergy like Lactose Intolerance etc.…..and Not NCGS and /or Celiac disease etc….. But the trigger is the same…..Low and /or NO stomach acid. How do we know this or can we? And why??? Now, I want to quote from the “Anti acid medication (and or Low/NO Stomach Acid) as a risk factor for food allergy” article….. To scientifically establish this point and why this matters….. in Celiac disease and or NCGS…. Quoting… “Adult values of gastric pH, as well as the full digestive capacity and the complete mucosal barrier function, are reached at an age of approximately 2 years only….” Not surprisingly the age when babies begin to outgrow a FPIE allergy….. The keyword here is “Begins to outgrow” their food allergies…..Not when it stops being a problem… It is not to/till age 5 or 6 often that children completely outgrows their childhood food allergies…. This is because or Longer Term Immune System Memory is about 2 years…..from the last time the food allergen triggered the immune system and why it can take another 2 or 3 years to fully outgrow a babies (childhood) allergy…..and important to note this is why many Vaccines A La, like the COVID-19 vaccine etc.....need "Boosters" to retrain the immune systme to fight this virus.... Because after a few years......it will forget it ever saw this virus before etc... And this it should be noted…..is only present in full term infants……with delayed stomach acid production lasting even longer in Pre-term babies…. Quoting again… “Similarly, the mean acid output in 21-month-old children after histamine stimulation was found to be only 50% of that observed in adults and is roughly similar to adult levels only by the end of the second year of life (54, 55). Therefore, peptic digestion may not be complete during early life, and protein remnants of the diet could act as allergens. Together, these facts may contribute to the higher incidences of food allergies in children.” And what is what noting and very interesting to say the least……antibodies to food allergens have been shown to be passed off to their off spring in mammals…. See again quoting. “When we fed pregnant mice with fish protein in context with anti-ulcer medication, we observed not only allergy induced in the mother animal but also a Th2 bias in the offspring (91).” And why Celiac disease can be inherited from mother to child without a genetic bias being involved…. .it is just our immune system has been preprogramed to avoid gluten, lactose etc…..by our mothers existing food allergy…… and High Stomach acid explains exactly how, why and when a child will outgrow a FPIE allergy. And it is worth noting from the article (paragraph) “Impaired digestion lowers threshold levels of food allergens”. Quoting again… “Moreover, in histamine release test, the dose of native allergen eliciting positive reactivity was 10,000x times lower than with predigested allergen (77). This implies that in settings of impaired digestion, lower levels of allergens may be able to induce hypersensitivity reactions. These data might finally also explain why some food-allergic patients develop symptoms of different intensity at different time points: their actual symptom intensity may depend on the current functional capacity of the digestive system.” IE whether your stomach acid is low at the time of the gluten consumption! To read more about this topic and it’s relation to a gluten allergy read this excellent work by Eva Untersmayr. Entitled "New Study Shows that Antacid Use Leads to More Allergies: Q&A with Eva Untersmayr MD, PhD" https://asthmaallergieschildren.com/new-study-shows-that-antacid-use-leads-to-more-allergies-qa-with-eva-untersmayr-md-phd/ Anybody that has a child with a food allergy should really read these two very authoritative articles…..one as an interview and one as a full citation of the original work on food allergens as a trigger for FPIES (IMO) explaining the childhood diagnosis of NCGS and or Celiac disease in Children. Or any adult still struggling from a food allery ESPECIALLY if they are/were or continue taking PPIs and are still suffering from food allergies! I am not surprised by this anymore……and by now….neither should you be either…. Acts 28:24 "And some believed the things which were spoken, and some believed not." I can only tell you it helped me to treat my co-existing, comorbid Low/NO stomach in helping my many GI symptoms! 2 Timothy 2: 7 “Consider what I say; and the Lord give thee understanding in all things” this included. I hope this is helpful but it is not medical advice......but I sometimes with the mounting evidence of Low/NO stomach acid being widespread and common in Celiac disease and/or NCGS and IBS etc. I honestly wonder whether it should be or not??? IBS, IBD, GERD aka Heartburn, UC etc. has a Biderectional Link via the Low/NO Stomach connection/trigger for/ too Celiac disease and this too was recently proven to be true!!! Now it will just take another 15 to 20 years before Medical Science integrates this into their model for NCGS and/or Celiac disease etc.... IMHO or at least I have found this to be true....in my life! To Whomever who read this too the end.....Good luck and God speed on your continue journey(s) in Life! And I wish us all good health soon! Posterboy by the grace of God,
- 1 comment
-
- celiac disease
- celiac posterboy
- (and 7 more)
-
To All, I am just trying to start this resource for others that shows how Low Stomach Acid can lead to a food allergy problem. Maybe someone will read it and it will make sense to them. Eva Untersmayr has done the most work on the topic. I will quote a couple research articles by her.....demonstrating that food allergies happen when we get low in Stomach Acid. Starting with this one entitled "The influence of gastric digestion on the development of food allergy" https://pubmed.ncbi.nlm.nih.gov/28616101/ And this one entiteld "The role of protein digestibility and antacids on food allergy outcomes" https://pubmed.ncbi.nlm.nih.gov/18539189/ Food allergies happen when are stomach acid is no longer strong enough to digest proteins into harmless peptides. See also this excellent article (recently found) that explains how Antacid use can trigger food allegies again by Eva Untersmayr. "New Study Shows that Antacid Use Leads to More Allergies: Q&A with Eva Untersmayr MD, PhD" https://asthmaallergieschildren.com/new-study-shows-that-antacid-use-leads-to-more-allergies-qa-with-eva-untersmayr-md-phd/ When I get a chance I will check back in......and see what others think about this new cutting edge research.....has Eva found the trigger for food allergies? What do you all think? I hope this is helpful but it is not medical advice. Posterboy by the grace of God,
- 3 replies
-
- celiac disease
- food allergens
- (and 5 more)
-
To All, I came across this great article where they are interviewing Eva Untersmayr the pioneering researcher that explains how food allergens develop and I thought it was a "Must Read" for anyone with food allergies. I hope you will read it ALL yourselfselves. It really a great overview of how these things happen.......and it IMHO confirms my hunch about how Low/NO Stomach Acid is the "Gate Keeper" for the Small Intestine and helps fight off food allergens.....or at least helps keep them out of the small intestine in the first place. I will quote select sections but the article is not too long.....that you shouldn't read it for yourself in it's entirety. Entitled "Protect Your Digestion, (or IE Stomach Acid the Gate Keeper) the First Line of Defense Against Food Allergies" https://asthmaallergieschildren.com/protect-your-digestion-the-first-line-of-defense-against-food-allergies/ I was STRUCK by how quickly this can happen when one takes PPIs (and recent research in children has also confirmed these connections etc.) quoting from the article "Eva: The change in the gastric milieu takes place very quickly. You are right that approximately 5-6 days of PPI intake elevates the gastric pH to around 5. But long-term use of anti-ulcer drugs seems to especially increase the risk for need of anti-allergy medication, which we could also prove in our current study." quoting again... "One mechanism, which we also highlight in our paper, could be the direct effect on the immune response as immune cells have H2 receptors, PPIs can induce mast cell activation and the aluminum-containing Sucralfate might act as an adjuvant. Moreover, anti-ulcer drugs have an enormous effect on microbiota, which is even more prominent than the effect of antibiotics when considering the entire population due to longtime intake of this medication. So there are different layers of mechanisms that might explain our results." This article only summarizes the earlier work......and I am fond of saying "Why isn't this on the front page of every newspaper in the country"..... It is summarizing this ground breaking research now almost 12 years old!!! Entitlted "Anti-acid medication as a risk factor for food allergy".....I would say this includes Low/NO stomach acid from STRESS in our lives as well! https://onlinelibrary.wiley.com/doi/full/10.1111/j.1398-9995.2010.02511.x But taking PPIs and H2 blockers just acclerates this process by which our bodies activates antibodies to food allergens including Wheat etc....because the way PPIs and H2 blockers change the way our Mast Cell's react to food.....see above article that explains this in much better/more detail.....it involved the use of Aluminum that perks "Ups the Ears" of our immune system and makes the food we were eating WHEN we were taking PPIs and H2 Blockers now a food enemy!!! where before it was a friendly food etc... I will quote the full abstract because It is instructive to us to know how this process works in the body.... "Abstract An important feature for oral allergens is their digestion-resistance during gastrointestinal transit. For some oral allergens, digestion stability is an innate feature, whereas digestion-labile antigens may only persist in times of impairment of the digestive system. In this review, we collect evidence from mouse and human studies that besides the inherent molecular characteristics of a food protein, the stomach function is decisive for the allergenic potential. Gastric acid levels determine the activation of gastric pepsin and also the release of pancreatic enzymes. When anti-ulcer drugs inhibit or neutralize gastric acid, they allow persistence of intact food allergens and protein-bound oral drugs with enhanced capacity to sensitize and elicit allergic reactions via the oral route. Mouse studies further suggest that maternal food allergy arising from co-application of a food protein with anti-acid drugs results in a Th2-biased immune response in the offspring. Especially, anti-ulcer drugs containing aluminum compounds act as Th2 adjuvants. Proton pump inhibitors act on proton secretion but also on expression of the morphogen Sonic hedgehog, which has been related to the development of atrophic gastritis. On the other hand, atrophic gastritis and resulting hypoacidity have previously been correlated with enhanced sensitization risk to food allergens in elderly patients. In summary, impairment of gastric function is a documented risk factor for sensitization against oral proteins and drugs." Eva has figured it out!.....but nobody want to follow her.....your enviroment (and things in it) are a trigger for food allergens via Low/NO Stomach acid! As always I hope this is helpful but it not medical advice. 2 Timothy 2: 7 “Consider what I say; and the Lord give thee understanding in all things” this included. Posterboy by the Grace of God,
- 3 replies
-
- celiac disease
- food allergens
- (and 5 more)
-
To All, This work is by Eva Untersmayr that establishes your Stomach Acid as the "Gate Keeper" against food allergens. I quote the whole abstract because it is instructive to us. https://pubmed.ncbi.nlm.nih.gov/23160973/ Abstract "True food allergens are considered as digestion stable proteins, which are absorbed through the gastrointestinal epithelium in an intact form leading to sensitization and causing systemic symptoms. According to classifications, allergens, which are digestion-labile, cause local symptoms by their cross-reactivity towards inhalative allergens. Our recent studies revealed that digestion labile allergens can also have sensitizing capacity if gastric digestion is hindered. The increase of gastric pH via acid-suppression by proton pump inhibitors, sucralfate or antacids, interferes with protein digestion, and leads to sensitization and allergic reaction in mouse models as well as in human patients. Furthermore, the inhibition of digestion increases the risk for anaphylactic responses in sensitized individuals.Even though also other factors, such as sphingolipid metabolites, are associated with the development of food allergies, it is without any doubt that the stomach has an important gate keeping function against food allergies." This medical research was published 10 years ago and we still don't understand it is low stomach acid that is the trigger for food allergies in our diet! Even older research has been done testing Acid reducers and the onset of food allergens while using PPIs.....and yes their use triggered food allergies.....up to and including an allergy to Wheat......why isn't this research on the front page of every newspaper in America and/or the world! See this research 17+ years old entitled "Anti-ulcer drugs promote IgE formation toward dietary antigens in adult patients" https://pubmed.ncbi.nlm.nih.gov/15671152/ quoting "In an observational cohort study, we screened 152 adult patients from a gastroenterological outpatient clinic with negative case histories for atopy or allergy, who were medicated with H2-receptor blockers or proton pump inhibitors for 3 months. IgE reactivities to food allergens before and after 3 months of anti-acid treatment were compared serologically. Ten percent of the patients showed a boost of preexisting IgE antibodies and 15% de novo IgE formation toward numerous digestion-labile dietary compounds, like milk, potato, celery, carrots, apple, orange, wheat, and rye flour. If you consider the 10% who had already had a food allergy.....it more than doubled food allergens one had after only 3 months of PPIs or H2 receptor blockers use. Or totaled togther 1/4 of those taking a PPIs or H2 Blocker either had a worsened response or a new response to foods like milk, wheat (gluten) and rye etc. Pretty convincing evidence IMO that PPIs and H2 Blockers are a trigger for a NCGS and/or Celiac diagnsosis. And agrees with research reported on Celiac.com I am just trying to help those who have started taking them realize what harm they are doing to their bodies.....in hope they will find the courage to quit them for good! I hope this is helpful but it is not medical advice. Posterboy,
- 3 replies
-
- celiac disease
- food allergens
- (and 5 more)
-
To All, A few years ago Celiac.com featured an article on Cytokines (aka different Interleukins) that are produced in response to a gluten challenge and it got me thinking? Here is the article as summarized by Jefferson Adams if you would like to scan the summary... Here is the length to the full study if somebody wants to read through/scan and explain to me and other on the Celiac.com forum. https://www.science.org/doi/10.1126/sciadv.aaw7756 A recent discussion lead me do some more research on this topic? Could poor nutrition be a trigger for Cytokine reslease and I found YES it could be! Here is the research that I wanted to lead with.....their is other research that can be included but this is just to get the ball rolling/started you might say... Here is looking at you Blue-Sky @Blue-Sky 30+ years old and the medical community has forgotten how Cytokine/Interlukin production is triggerd/controlled by poor nutrition! See this research on Zinc Entitled "Role of zinc in interleukin 2 (IL-2)-mediated T-cell activation" https://pubmed.ncbi.nlm.nih.gov/2345864/#:~:text=In a serum-free culture containing no zinc%2C zinc,was completely inhibited by anti-IL-2 receptor (CD25) antibodies. This one is also worth your time explains B-Vitamins role in Cytokine production in the body as sign of Inflammation. Entitled "The effects of vitamin B on the immune/cytokine network and their involvement in depression" https://www.maturitas.org/article/S0378-5122(16)30299-7/fulltext What do other's think......which came first (the poor nutrition) or the inflammation (IE triggering) the Immune response? I wish us all good health soon! STRESS Kills us.....but it MAIMS us first! I hope this is helpful but it is not medical advice. Also in tribute to Blue-Sky it is worth noting Blue-Sky's great blog post on a Zinc deficiency as a possible trigger for IBS......which is the best article on Celiac.com IMO on the topic of Zinc!!! as it relates to GI problems like IBS etc. Posterboy by the grace of God,
- 2 replies
-
- celiac disease
- il-2
-
(and 7 more)
Tagged with:
-
To All, This research was quoted by RMJ and I thought it was worth sharing! And I wanted to start a conversation about it considering how and what role B-Vitamins have in Cytokine production and/or the management of our Immune System(s) since we know B-Vitamins are involved in controlling Cytokine production we know they play a role in activating and controlling our immune responses. I will start with this research. Entitled "Thiamine and riboflavin inhibit production of cytokines and increase the anti-inflammatory activity of a corticosteroid in a chronic model of inflammation induced by complete Freund’s adjuvant" https://www.sciencedirect.com/science/article/abs/pii/S1734114016302729 I hope this is helpful but it is not medical advice. Posterboy,
-
Celiac.com 09/19/2022 - A team of researchers recently set out to calculate rates of non-coeliac gluten sensitivity (NCGS) in a group of fibromyalgia patients, to evaluate their clinical response to a six-week gluten-free diet, any improvement in symptoms, rates of diet responders who did not meet non-coeliac gluten sensitivity diagnostic criteria, and any baseline characteristics associated with diet response and diagnostic criteria fulfillment. The research team included Miriam Almirall, Francesc Casellas, Joan Dot, Inés de Torres, Hegoi Segurola, Sara Marsal. They are variously affiliated with the Department of Pathology, Department of Endoscopy, Department of Rheumatology, and the Nutritional Support Unit ant the Hospital Universitari Vall d’Hebron, Barcelona, Spain; the Rheumatology Research Group, Vall d’Hebron Research Institute; the Digestive System Research Unit Gastroenterology; and the Department of Morphological Sciences, Autonomous University of Barcelona. The team carried out an uncontrolled prospective experimental study in a group of patients with fibromyalgia from a specialized hospital ward. The team analyzed the percentage of patients who met the Salerno Experts’ Criteria, responded to a gluten-free diet, improved their symptomatology and baseline characteristics, and met diagnostic criteria. In all, the team found a non-coeliac gluten sensitivity rate of about 6% in 142 patients. About 22% of those showed an improvement in intestinal symptoms on a gluten-free diet. In total, 74.2% of the responders did not fulfil the Salerno Experts’ Criteria. The presence of diarrhea and intraepithelial lymphocytosis and lower levels of anxiety were predictive factors of gluten-free diet response. No predictive factors of non-coeliac gluten sensitivity criteria fulfilment were found due to the low number of discriminators between gluten and placebo. These results show that patients with fibromyalgia have non-coeliac gluten sensitivity at rates similar to the general population. That means a gluten-free diet won't be appropriate for all patients with fibromyalgia. However, it could be useful for patients with diarrhea or intraepithelial lymphocytosis, at least to assess any improvement in intestinal symptoms. Read more in Rheumatology
-
- fibromyalgia
- gluten-free diet
- (and 4 more)
-
To All, Knitty Kitty started a thread on Thiamine, Thiamine, Thiamine, once upon a time, so now is the time to start a thread on Magnesium as a resource for others who don't have the time to do the research and wonder if taking Magnesium might help them! Maybe it will be helpful to others as Knitty Kitty's thread on Thiamine deficiency. I will start with one on IBS and Magnesium Deficiency. Entitled "Magnesium and inflammatory bowel disease" aka IBS quoting there entire abstract because it is instructive. Abstract "Mg deficiency is a frequent complication of inflammatory bowel disease (IBD) demonstrated in 13-88% of patients. Decreased oral intake, malabsorption and increased intestinal losses are the major causes of Mg deficiency. The complications of Mg deficiency include: cramps, bone pain, delirium, acute crises of tetany, fatigue, depression, cardiac abnormalities, urolithiasis, impaired healing and colonic motility disorders. Serum Mg is an insensitive index of Mg status in IBD. Twenty-four-hour urinary excretion of Mg is a sensitive index and should be monitored periodically. Parenteral Mg requirements in patients with IBD are at least 120 mg/day or more depending upon fecal or stomal losses. Oral requirements may be as great as 700 mg/day depending on the severity of malabsorption." Or simply stated up to almost 90% of IBS patients are or could be low in Magnesium. This youtube webinar that summarizes a lot of Magnesium links to allergies in about a 30 minute video. https://www.youtube.com/watch?v=NYeuSw86bzk This one for anyone who has asthma entitled "Role of magnesium in regulation of lung function" https://pubmed.ncbi.nlm.nih.gov/8509592/ This one entitled "Magnesium (Deficiency) in Infectious Diseases in Older People" https://pubmed.ncbi.nlm.nih.gov/33435521/ This one entitled "Possible roles of magnesium on the immune system" https://www.nature.com/articles/1601689 This is enough to get this thread started I/you/we can always add more research latter. I always said the Lord being my help......I was lucky I found Magnesium early and I still believe that! I hope this is helpful but it is not medical advice. Posterboy by the grace of God,
- 2 replies
-
- beri beri
- celiac disease
- (and 7 more)
-
Celiac.com 03/08/2022 - There's been some evidence to connect celiac disease with an imbalance in gut microflora. However, researchers still don't know much about how gluten exposure in people with well-controlled celiac disease might influence microbial balance in the gut. A better understanding of this connection could help to improve our knowledge of celiac disease activity and its symptoms. To get a better idea of such a possible connection, a team of researchers recently set out to evaluate the impact of gluten exposure on the gut microbiome in patients with celiac disease and non-celiac gluten sensitivity (NCGS). The research team included Nobel, Yael R. MD; Rozenberg, Felix BA; Park, Heekuk PhD; Freedberg, Daniel E. MD, MS; Blaser, Martin J. MD; Green, Peter H.R. MD; Uhlemann, Anne-Catrin MD, PhD; and Lebwohl, Benjamin MD, MS. They are variously affiliated with the Celiac Disease Center, Columbia University Irving Medical Center, New York, New York, USA; the Microbiome and Pathogen Genomics Collaborative Center, Columbia University Irving Medical Center, New York, New York, USA; the Center for Advanced Biotechnology and Medicine, Rutgers University, New Brunswick, New Jersey, USA; the Department of Epidemiology, Mailman School of Public Health, Columbia University Irving Medical Center, New York, New York, USA; the Division of Infectious Diseases, Department of Medicine, Columbia University Irving Medical Center, New York, New York, USA. The team conducted a 14-day gluten challenge of 5 grams of gluten per day on nine patients with celiac disease and eight with NCGS, all of whom had been on a gluten-free diet. They then compared the results from the two groups against results from eight control subjects on a standard gluten-containing diet. The team used 16S rRNA gene and metagenomic sequencing before, during, and after the gluten challenge, to conduct fecal microbiome analysis on patient stool samples. They assessed symptoms using two 2 validated clinical scales. The results showed that patients with celiac disease and NCGS showed no significant fecal microbial changes in response to the gluten challenge. Interestingly, gut microbiome composition differed between all thee groups at baseline, and these differences continued regardless of gluten exposure. Celiac and NCGS subjects reported worse symptoms and general health in the middle of gluten challenge, and slightly better by the end. However, the symptoms and general health issues showed no consistent connections with the composition of the gut microbiome. In this study, fecal microbiome diversity remained unchanged by gluten challenge in adult subjects with celiac disease and NCGS. These results indicate that celiac disease and NCGS activity and severity may be unrelated to gut microbiome status. Since the gut microbiome is crucial to good health, it may be some comfort to people with celiac disease and NCGS that gluten exposure doesn't seem to damage the microbiome balance, and so is unlikely to worsen disease symptoms, at least in the short term. Read more in Clinical and Translational Gastroenterology: December 2021
- 6 comments
-
- celiac disease
- gluten sensitivity
-
(and 5 more)
Tagged with:
-
Celiac.com 01/31/2022 - As intestinal permeability and innate immune system activation emerge as possible pathophysiological mechanisms in non-celiac gluten sensitivity (NCGS), a number of researchers have become interested in markers for gut integrity and inflammation. The idea being that thesis markers might help to reveal pathological changes that occur with non-celiac gluten sensitivity. A team of researchers recently set out to assess relevant biomarkers in non-celiac gluten sensitivity by analyzing serum levels of gut integrity and permeability markers, pro-inflammatory cytokines and antigliadin IgG in patients with suspected non-celiac gluten sensitivity on a gluten-free diet, and compare them to serum levels in patients with irritable bowel syndrome (IBS) and healthy controls (HC). The research team included Hanna Fjeldheim Dale, Julianne CH Johannessen, Ingeborg Brønstad, and Gülen Arslan Lied. They are variously affiliated with the Centre for Nutrition, Department of Clinical Medicine, University of Bergen, Bergen, Norway; the Division of Gastroenterology, Department of Medicine, Haukeland University Hospital, Bergen, Norway; and the National Centre of Functional Gastrointestinal Disorders, Haukeland University Hospital, Bergen, Norway. Their team analyzed serum samples collected from twenty patients with suspected non-celiac gluten sensitivity patients on a gluten-free diet, twenty with IBS, and twenty healthy sex and age matched control subjects. The team used IBS severity scoring system (IBS-SSS) to assess gastrointestinal symptom severity. Compared to heathy control subjects, suspected non-celiac gluten sensitivity and IBS patients had higher IBS-SSS scores. Their analysis showed no significant differences in serum levels of any of the gut integrity and permeability markers, cytokines or antigliadin IgG antibodies between the three groups. However, they did see positive correlations between claudin-1 and i-FABP, and between claudin-1 and antigliadin IgG antibodies. The team's assessment showed no differences in serum levels of gut integrity and permeability markers, pro-inflammatory cytokines or antigliadin IgG antibodies among patients with suspected non-celiac gluten sensitivity patients on a gluten-free diet, IBS and healthy control subjects. The findings suggest that these biomarkers do not offer a way to spot possible pathophysiological mechanisms in non-celiac gluten sensitivity. Stay tuned for more on this and related stories. Read more at DovePress.com.
- 2 comments
-
- celiac disease
- gluten
- (and 7 more)
-
Celiac.com 04/26/2021 - Doctors are still figuring the best way to tell celiac disease from non-celiac wheat or gluten sensitivity. A team of researchers recently assessed some key differences between celiac disease and non-celiac wheat or gluten sensitivity. The research team included A. Rej, I. Aziz, and D.S. Sanders. They are variously affiliated with the Academic Unit of Gastroenterology, Royal Hallamshire Hospital, Sheffield Teaching Hospital NHS Foundation Trust, Sheffield, UK; and the Department of Infection, Immunity and Cardiovascular Disease, Academic Unit of Gastroenterology, University of Sheffield, Sheffield, UK Celiac disease and non-celiac wheat or gluten sensitivity (NCWS/NCGS) are both common gluten‐related disorders, with similar presentations. Because both conditions can present with gastrointestinal and extra-intestinal manifestations, it can be difficult for doctors to tell them apart. Around 7% of individuals self‐reporting symptoms in relation to gluten ingestion have celiac disease. That's a significant number. For this reason, it is important that patients undergo a thorough workup to assess for the diagnosis, including celiac serology, as well as the exclusion of classic wheat allergy. Celiac disease is diagnosed by assessing serology and histology, but there are no clear biomarkers for the diagnosis of NCGS. Complicated celiac cases should be referred to a specialist, since even with recent developments in noninvasive celiac screening, histological assessment via duodenal biopsy remains the gold standard. Both conditions are treated with a gluten‐free diet, but the length and strictness of the gluten-free diet regime needed to properly treat NCGS is unclear. Following a GFD can be challenging for both celiacs and NCWS/NCGS sufferers, alike. While wheat/gluten is a known trigger for symptom generation in NCGS, it is unclear which components of wheat trigger symptoms in this group, and additional research required to understand the development of the condition. Their paper on the subject, titled "Coeliac disease and non-coeliac wheat or gluten sensitivity," offers a detailed and comprehensive discussion of the two conditions. Read the full paper at the Journal of Internal Medicine (PAYWALL)
-
- celiac disease
- ncgs
- (and 4 more)
-
How Solid is the Evidence for Non-celiac Gluten Sensitivity?
Jefferson Adams posted an article in Latest Research
Celiac.com 05/15/2017 - For all the talk of studies touting evidence for non-celiac gluten sensitivity, the actual data don't stack up very well, according to an recent assessment by two researchers, whose results appear in Clinical Gastroenterology and Hepatology. In an effort to determine the accuracy of using a double-blind, placebo-controlled study to confirm diagnosis of non-celiac gluten sensitivity in patients who respond to a gluten-free diet, researchers Javier Molina-Infante, and Antonio Carroccio recently set out to assess data on a series of such studies. Both researchers are affiliated with the Department of Gastroenterology, Hospital Universitario San Pedro de Alcantara in Caceres, Spain. For their study, the pair analyzed data from 10 separate double-blind, placebo-controlled, gluten-challenge trials on a total of 1,312 adults. The available studies varied significantly in many ways. The duration of the gluten challenge, for example, varied from 1 day to 6 weeks. The daily doses for those gluten challenges varied from 2 grams to 52 grams, with 3 studies administering 8 grams or less each day. The composition of the gluten-free placebo also varied considerably between tests; including variation by gluten-free product type, and levels of xylose, whey protein, rice, or corn starch containing fermentable carbohydrates. Most of the studies did find gluten challenge to significantly increase symptom scores compared with placebo. However, out of 231 NCGS patients, only 38 patients (16%) showed gluten-specific symptoms. Moreover, nearly half (40%) of these patients showed similar or increased symptoms in response to placebo; something researchers term a 'nocebo' effect. That leaves just 6 or 7 patients out of 231 showing gluten-specific symptoms. The researchers also point to heterogeneity and to potential methodology flaws in gluten challenge studies. They also present powerful questions about gluten as the trigger for symptoms in most patients with presumptive NCGS. Lastly, they highlight the importance of the nocebo effect in these types of studies. These results certainly invite more careful, rigorous studies on the matter, and challenge researchers to provide solid data from well-crafted double-blind placebo controlled studies. Basically, what little evidence we thought we had to support the existence of non-celiac gluten sensitivity has been shown to be thin at best. Until solid evidence arrives, the status of non-celiac gluten sensitivity will remain open to question and doubt by both researchers and potential sufferers. Source: Clin Gastroenterol Hepatol. 2017;15(3):339-348.- 5 comments
-
- evidence
- gluten sensitivity
-
(and 2 more)
Tagged with:
-
Can Serum Zonulin Help Diagnose Non-Celiac Gluten Sensitivity?
Scott Adams posted an article in Latest Research
Celiac.com 04/20/2021 - Non-celiac gluten sensitivity (NCGS) is marked by intestinal and extraintestinal symptoms triggered by gluten-containing foods, but with no celiac disease or wheat allergy. There are currently no known biomarkers to diagnose non-celiac gluten sensitivity, and the gold standard double-blind placebo-controlled gluten challenge is clinically impractical. A team of researchers recently set out to investigate the role of serum zonulin as a diagnostic biomarker of NCGS and to develop a diagnostic algorithm. The research team included Maria Raffaella Barbaro, Cesare Cremon, Antonio Maria Morselli-Labate, Antonio Di Sabatino, Paolo Giuffrida, Gino Roberto Corazza, Michele Di Stefano, Giacomo Caio, Giovanni Latella, Carolina Ciacci, Daniele Fuschi, Marianna Mastroroberto, Lara Bellacosa, Vincenzo Stanghellini, Umberto Volta, and Giovanni Barbara. They are variously affiliated with the Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy, the First Department of Internal Medicine, San Matteo Hospital Foundation, University of Pavia, Italy; the Department of Clinical Medicine Public Health Life Sciences and Environment, University of L'Aquila, Italy; the Department of Medicine, Surgery, and Dentistry Scuola Medica Salernitana, University of Salerno, Salerno, Italy, and the Department of Medical and Surgical Sciences, University of Bologna, Italy. For their multi-center study, the team enrolled 86 patients with either self-reported or double-blind confirmed non-celiac gluten sensitivity, 59 patients with diarrhea-predominant IBS (IBS-D), 15 patients with celiac disease, and 25 asymptomatic control subjects. The team assessed Zonulin serum levels, and calculated the associated diagnostic power. They recorded any clinical and symptomatic data. They also assessed the effect of diet on zonulin levels in a subgroup of patients with non-celiac gluten sensitivity. Compared with asymptomatic control subjects, the non-celiac gluten sensitivity patients, regardless of diagnosis modality, and celiac patients showed substantially increased levels of zonulin, as did both non-celiac gluten sensitivity and celiac patients, compared with IBS-D patients. Self-reported non-celiac gluten sensitivity showed increased zonulin levels compared with double-blind confirmed and not-confirmed non-celiac gluten sensitivity. There's been a lot of talk about gluten-free diets benefiting non-celiac gluten sensitivity patients, but this study found that six-month wheat avoidance significantly reduced zonulin levels only in non-celiac gluten sensitivity patients with positive HLA-DQ2/8. Wheat withdrawal was associated with reduced zonulin levels only in non-celiac gluten sensitivity with the HLA genotype. Zonulin levels were 81% accurate in distinguishing non-celiac gluten sensitivity from IBS-D. By excluding celiac disease, a diagnostic algorithm combining zonulin levels, symptoms and gender increased that accuracy to 89%. Certainly finding a reliable new biomarker for non-celiac gluten sensitivity would be a big deal. This study shows that zonulin can be an accurate diagnostic biomarker for non-celiac gluten sensitivity. When combined with demographic and clinical data, Zonulin levels can differentiate non-celiac gluten sensitivity from IBS-D with high accuracy. Expect more investigation into the use of zonulin levels as an accurate diagnostic biomarker for non-celiac gluten sensitivity. If it pans out, expect to see it developed for clinical practice, though that may take some time. Source: Gut, 2020 Nov;69(11):1966-1974.- 1 comment
-
- celiac disease
- epithelial barrier
- (and 6 more)
-
Celiac.com 02/22/2021 - The skin has long been thought to be the body's largest organ. Recently, however, researchers discovered that the largest organ might actually be the interstitium, which lies just beneath the skin's outermost layers. It is that interstitial tissue that is the focus of a new biometric skin patch that may eventually diagnose numerous ailments faster and easier, and more cleanly than traditional blood tests. However, this is no easy task, as the interstitial tissue won't give up its secrets easily. Even though it's close to the skin, and close to blood, getting enough useful fluid from the interstitial tissue to get accurate test data is a bit like squeezing blood from a stone. Getting even a thousandth of a tablespoon, an amount still hundreds of times smaller than a standard blood draw, remains a challenge. A new development might offer a way around that challenge. In a recent paper, researchers at Washington University in St. Louis report using disposable micro-needle patches to capture ISF biomarkers, and to measure them up to about 800 times greater sensitivity than comparable biomarker tests. The thin rectangular patches contain hundreds of plastic micro-needles, each less than a millimeter long. To use them, simply press the patch against your finger, then dip the patch into a liquid solution of nanoparticles, which will sense and reveal presence of the certain known proteins. Because blood based testing can present logistical and financial challenges for poor and/or rural populations, such a test represents a logistical, scientific and financial breakthrough. "Currently, the new skin patches work on just a few biomarkers, but by significantly improving the sensitivity of immunoassays,” says Srikanth Singamaneni, a materials scientist who led the study, researchers may be able to help to meet the "need for bio-diagnostics in low- and middle-income countries—and even in rural parts of the United States.” The test can detect cytokine IL-6, and research has shown that detecting cytokines may be the best way to diagnose gluten sensitivity. A cheap, portable, reliable test that could spot celiac disease, gluten sensitivity and other health conditions, could be a major benefit to large numbers of people who remain undiagnosed, and for whom traditional blood tests are often out of reach. The team's data appears in Nature Biomedical Engineering. Read more on this in an excellent article by Wired.com
-
- blood test
- celiac disease
- (and 7 more)
-
Celiac.com 02/01/2021 - Non-Celiac Gluten Sensitivity (NCGS) is poorly understood, particularly in terms of its neurological effects. A team of researchers looking into the matter first conducted a prospective postal survey to investigate its neurological presentation and symptom course. Based on the results of the survey, they conducted a brain MRI study to follow-up, and to note potential diagnostic biomarkers for future research. The research team included Iain D. Croall, Nigel Hoggard, Imran Aziz, Marios Hadjivassiliou, and David S. Sanders. They are variously affiliated with the Department of Infection, Immunity & Cardiovascular Disease, University of Sheffield/INSIGENO, Sheffield, United Kingdom; the Academic Unit of Gastroenterology, Royal Hallamshire Hospital, Sheffield Teaching Hospital NHS Foundation Trust, Sheffield, United Kingdom; and the Academic Departments of Neurosciences and Neuroradiology, Sheffield Teaching Hospitals NHS Trust, Sheffield, United Kingdom. The team recruited 125 patients with NCGS from a clinical center. Each patient completed a prospective postal questionnaire summarizing the symptoms, their severity and their course. The team used Chi-squared analysis to compare onset time to data from 224 celiac disease patients from the same centre. Five gluten-free respondents who self-reported brain fog then received MR brain imaging and questionnaires, both before and after a gluten challenge. The team recorded this “baseline” data, and looked for abnormalities. They then compared symptom severity and cerebral blood flow (CBF) both before and after the gluten challenge. Neurological symptoms included headaches in more than half of patients, brain fog in just under half, balance issues in about one-third of patients, and tingling in about 20%. Symptoms typically began with 90 minutes, and resolved within 48 hours. The pattern of symptom onset was similar to that seen in celiac patients. Extra-intestinal symptoms worsened by nearly 40% during a typical reaction. The combined survey and brain imaging analysis showed that non-trivial neurological symptoms are common, and may be studied within 2 hours following gluten ingestion. The team suggests that further brain imaging studies may help reveal physiological damage, and the physiological response to gluten. The researchers stress the need for diagnostic biomarkers for NCGS, and notes that there is limited research showing AGA is raised in NCGS patients compared to the general population This first-of-a-kind neuro-imaging study revealed numerous clinical variables, which may be helpful for further studying the pathophysiology of NCGS. The positivity rate in patients for this study was about 18%, compared to just under 13% for healthy volunteers, which is an insignificant difference. This generally supports previous literature showing that AGA is not a good way to diagnose typical NCGS. A better understanding of how gliadin positivity interacts with neurological outcomes may be helpful, as research indicates that these antibodies may harm the brain. Read more at PLOS.org
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8-M):
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8-M):