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Toddlers....gluten And Behavior?

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i know that behavioral issues can be triggered by food....and sensory and anxiety issues can be heightened by food, and food can cause sleep problems and hyperactivity. i

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Well, hon...I think I'd get a big bottle of something and lock the door.

My son is a positive reinforcement kid. Drives me up the freaking wall. He has to have immediate enforcement/consequences and you have to be consistent for a week or more. Repeat. He needs a carrot every day. Makes me NUTS.

I just had him tested for Celiac and am waiting. May try gluten-free regardless, maybe milk free too. I understand the confusion and frustration.

Perhaps you need to keep pushing the diet. Maybe they need more detox. Perhaps there were subtle changes in parenting style that relaxed after the first few weeks? I know I get tired and slack off then bam, Obnoxious Child is back. It's hard to pinpoint what they respond to, compared to what we want them to respond to.

Yes, people have emotional and behavioral consequences from gluten. I really don't know what to say other than it may be worth a try if you want to.

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my 3 yr old was terrible before gluten free, said the tv was too loud, 3 hr tantrums, very clingy, 1 month later she is a different kid. I'd give gluten free a try, what harm can it do?

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My own personal experience is that as much as food can effect how the body reacts and behaves sometimes you just need a professional to help you get some answers. My second who was diagnosed with coeliac at 7 has suffered from eating issues, behavioural issues, learning issues and none have been any different since him being gluten-free (he is now 11). We are going to see a peadiatrition next year (4 month wait here to see one privatly grrrr) in hope to have some answers.

I hope you find some answers because it can be really difficult in dealing with it and your right a lot of people dont understand and that makes it even more frustrating

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My daughter was 4 at the time of her celiac diagnosis. Her behaviors were similar....antagonistic towards her older sister, whiny, irritable (she crashed/melted every day around 3-4pm and making supper was a disaster!) Extremely clingy and attached to me, would not play independantly, no interest in playing, coloring etc just wanted to lay around and watch tv, extremely hungry and tired 24/7 even though she slept great at night, dark circles under eyes, pale skin, constipation, and sensitive to noise. (HATES fire alarms, vaccuums etc). Once off of gluten she improved very quickly and quite dramatically. It is easy for me to tell when she has gotten gluten accidentally because these behaviors return. I would try for a blood test before going gluten free. Once gluten free you are unable to test because the damage repairs itself and the antibodies are no longer elevated. It was hard waiting for a biopsy (the worst actually) but we are thankful to have the confirmed diagnosis from a GI specialist. I think it makes it easier to stick to the gluten-free diet and helps with others (SCHOOL!) accepting it as well. Good luck.

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thank you for your response divamomma...

i debate so much between behavioral, or sensory, or food...or maybe it is just kids being kids...but

when i read posts like yours it makes me think maybe i am on to something. i had hoped that

removing the artificials would have been this amazing 'ah-ha' moment, but it hasn't...so now I am

considering digging deeper, but i am also afraid i am creating a problem that isn't there. i'm just

struggling with how to handle this. so thanks for your replies!!

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thank you for your response divamomma...

i debate so much between behavioral, or sensory, or food...or maybe it is just kids being kids...but

when i read posts like yours it makes me think maybe i am on to something. i had hoped that

removing the artificials would have been this amazing 'ah-ha' moment, but it hasn't...so now I am

considering digging deeper, but i am also afraid i am creating a problem that isn't there. i'm just

struggling with how to handle this. so thanks for your replies!!

If you have a pretty good pediatrician, you may even be able to convince them to do the bloodwork for Celiac's Disease. They may be sensitive to gluten without having Celiac's, but if they did have it you would definately have an answer. Regardless it sounds like it may be worth going gluten free even if they tested negative.

My daughter's biggest issues were failure to thrive, but behaviorally she is a nightmare when she has consumed gluten. By 9 months old she was throwing herself on the ground if the tiniest thing ticked her off. Now, at 18 months I can tolerate being around her (in other words, she doesn't scream at me constantly).

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Hi -

My 3 year old son is autistic, not celiac, so I may not be a good person to respond b/c our situations are different. But his primary issues are a language delay, social issues (not knowing how to interact with peers), and repetitive behavior (spinning objects, opening and closing doors, etc.). We had him tested and he did not show a wheat allergy. But we tried the gluten free diet anyway starting in January and it made a huge difference for him. Over the course of 6 months he went from having a "severe language delay" to testing at age level (!). His repetitive behaviors went down, and he made great strides socially. He was/is getting ABA therapy, so it's hard to know what can be attributed to the diet vs. the therapy but the biggest thing for us that told us the diet helps was when we tried to reintroduce gluten. He was a mess. Big potty training regression, aggression (which is so not him - if anything he is overly passive), meltdowns (again not typical for him) ... We got a note from his teacher, who we did not tell we were giving him gluten, asking what on earth was going on with him and saying "I have never seen him like this."

Anyway my point is that sometimes the only way you know sometimes is to try the diet. We have always been in favor of interventions with low or minimal risk and we felt like the gluten free diet fell in that category. I'd say try it, give it a certain amount of time, and then "test" it. If it helps, then great. If it doesn't, then I agree with you that there is no reason to continue with the diet. Another option is to just limit gluten. We have found that my son can tolerate occasional gluten, like cake at a birthday party for example, as long as we are careful not to overdo it and not close together.

If you are worried something else is going on (you mentioned ADHD symptoms), you could also have your children tested by a developmental pediatrician. Even if you don't want to medicate, having a diagnosis if there is one can give you big clues on some interventions.

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hi Kelleybean.

just hearing those of you who had strictly behavioral (as opposed to physical) improvements does help me..so thank you for sharing.

i kind of keep bouncing from cause to cause trying to understand their behaviors...first i felt it was sensory, then simply behavioral, then back to sensory, now maybe i'm thinking it is food so i tried removing all artificials and preservatives and that didn't work too well, so now i am moving on to gluten. if i find something it will all be worth it...but i am so afraid that i am going to pull out every random allergen and spend hundreds in specialty food stores, and put my kids through all of this (again, basically just my 7yo who has a hard time at school etc), but what if i do all of this and in 10 years i look back and think 'omg, what was i thinking'?! so, that being said, your positive stories really are uplifting and give the rest of us the hope that we will have success stories of our own!

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    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
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    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
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