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Celiac Disease, Gluten and Children

By Casey Thaler, B.A., NASM-CPT, FNS
October 15, 2014

Researchers posit introducing gluten at specific points of time during infancy development might be the key to celiac disease prevention. A few recent studies tested the hypothesis on an infant population who were genetically at risk for developing the disease.1

Di Sabatino A, Corazza GR. Coeliac disease. Lancet. 2009;373:1480–1493.
Di Sabatino A, Corazza GR. Coeliac disease. Lancet. 2009;373:1480–1493.

For those unfamiliar, celiac disease is (very simply) defined as an autoimmune disorder, which is caused by a reaction to gliadin.2 Gliadin is a prolamine protein, which is found in wheat.3 Those with celiac disease are usually also sensitive to other proteins, which are chemically similar in structure.4, 5

World J Gastroenterol. Nov 14, 2012; 18(42): 6036–6059.
World J Gastroenterol. Nov 14, 2012; 18(42): 6036–6059.

Surprisingly, the researchers’ hypothesis was disproved.6 The studies exhibited that children developed the disease equally, regardless of the time frame of gluten introduction. Perhaps most surprisingly, breastfeeding didn’t seem to provide any protective benefits either, which is seemingly contradictory to earlier scientific findings.7

BMC Pediatr. 2011; 11: 46.
BMC Pediatr. 2011; 11: 46.

Children with chronic illnesses are known to be more predisposed to emotional and behavioral problems.8 The above chart (MASC Tscore Mean) shows the increased rate of emotional and behavioral problems in children with celiac disease.9 Since the topic of gluten, celiac disease and children is a somewhat sensitive one, it is important for us to look at the likely cause of the disease.10 Causative, not correlative, mechanisms and reasons are, at the end of the day, what’s really important about scientific findings.11 What we seem to have learned from these very well conducted studies, is that celiac disease may be caused almost entirely by genetics.12

World J Gastroenterol. 2012 November 14; 18(42): 6036–6059.
World J Gastroenterol. 2012 November 14; 18(42): 6036–6059.

Almost all people with celiac disease have one of 2 genes, DQ2 or DQ8.13 The above table shows the worldwide frequency and distribution of the genes.14 However, interestingly, about 33% of the population also has one of these genes – but they never develop the disease.15 This leads researchers to think that perhaps there are lifestyle and/or epigenetic factors at play, as well.16

J Clin Invest. 2011;121(6):2126-2132. doi:10.1172/JCI58109.
J Clin Invest. 2011;121(6):2126-2132. doi:10.1172/JCI58109.
Tilg, Herbert et al. Gastroenterology. Volume 136 , Issue 5 , 1476 - 1483
Tilg, Herbert et al. Gastroenterology. Volume 136 , Issue 5 , 1476 - 1483

One hypothesis is that changes may occur, in gut bacteria, before the disease develops.17 This means that things such as antibiotics, refined sugar, artificial colors, gluten and other artificial food elements may be causing detrimental changes in the microbiome.18 This would also mean that intervening with a probiotic might be one possible “fix.”19, 20 Above, we can see how changes in microbiota, sometimes brought upon by diet, affect many changes and processes in the body.21, 22

World J Gastroenterol. Nov 14, 2012; 18(42): 6036–6059.
World J Gastroenterol. Nov 14, 2012; 18(42): 6036–6059.

Hypothetically, it would make sense that the recent rise in celiac disease could be due to our massive shift in diet.23 We have changed our diet, almost totally and completely, since the 1970s.24, 25 Obviously, our genome has not really had much time to adapt to these changes.26

Another interesting factor that has also changed since the 1970s is that children are exposed to fewer germs - and parents are much more vigilant about cleanliness.27 This theory of disease is nicknamed the “hygiene hypothesis.”28 With decreased exposure to harmful environmental elements, which our body then learns to defend itself against, children’s immune systems may be turning inward – attacking the body’s own tissue, instead.29, 30

Though the cause of celiac disease may be genetic, the only cure, as has long been known, is a gluten-free diet.31 On the diet, the small intestinal mucosal injury heals and gluten-induced symptoms and signs disappear.32 If you have children, the best course of action is a screening, to see if they may be at risk for celiac disease.33 This goes doubly if any family members have the disease, as the genetic risk factor makes the likelihood increase.34

However, regardless of your children’s potential risk for developing celiac disease, it is not a good idea to be eat gluten.35, 36 There are many downsides to gluten, and it has many negative effects on the body and mind.37, 38, 39, 40 In fact, one study showed that removing gluten from the diet reduced adiposity, inflammation and insulin resistance.41

Other studies have shown that in some individuals, gluten sensitivity was shown to manifest solely with neurological dysfunction, though this point is somewhat debatable.42, 43, 44 What is interesting, however we previously detailed, is that schizophrenics among others with mental disorders, seem to respond positively to the removal of gluten from the diet.45

As should be obvious by now, you can see the benefits in removing gluten and gluten-like compounds from your children’s diet. Therefore, a Paleo Diet, which is rich in nutrients and avoids problematic proteins like gluten, is the best course of action to take - for both children and adults. You will likely see a decrease in your blood pressure, improve your glucose tolerance and your lipid profile.46 These are all healthy, positive changes – whether you’re young or old.

Wheat Sensitivity: A New Study Shows It’s Not in Your Head, It’s in Your Gut
By Trevor Connor, M.S.


1. Lionetti E, Castellaneta S, Francavilla R, et al. Introduction of gluten, HLA status, and the risk of celiac disease in children. N Engl J Med. 2014;371(14):1295-303.

2. Rubio-tapia A, Murray JA. Celiac disease. Curr Opin Gastroenterol. 2010;26(2):116-22.

3. Thompson T. Wheat starch, gliadin, and the gluten-free diet. J Am Diet Assoc. 2001;101(12):1456-9.

4. Troncone R, Auricchio S, De vincenzi M, Donatiello A, Farris E, Silano V. An analysis of cereals that react with serum antibodies in patients with coeliac disease. J Pediatr Gastroenterol Nutr. 1987;6(3):346-50.

5. Hollén E, Högberg L, Stenhammar L, Fälth-magnusson K, Magnusson KE. Antibodies to oat prolamines (avenins) in children with coeliac disease. Scand J Gastroenterol. 2003;38(7):742-6.

6. Available at: //www.bostonglobe.com/lifestyle/health-wellness/2014/10/05/studies-find-tactics-prevent-celiac-disease-newborns-don-work/zsbjwMAjdYOPFzRsDhriuO/story.html. Accessed October 12, 2014.

7. Norris JM, Barriga K, Hoffenberg EJ, et al. Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease. JAMA. 2005;293(19):2343-51.

8. Hysing M, Elgen I, Gillberg C, Lundervold AJ. Emotional and behavioural problems in subgroups of children with chronic illness: results from a large-scale population study. Child Care Health Dev. 2009;35(4):527-33.

9. Mazzone L, Reale L, Spina M, et al. Compliant gluten-free children with celiac disease: an evaluation of psychological distress. BMC Pediatr. 2011;11:46.

10. Niewinski MM. Advances in celiac disease and gluten-free diet. J Am Diet Assoc. 2008;108(4):661-72.

11. Verhulst B, Eaves LJ, Hatemi PK. Correlation not causation: the relationship between personality traits and political ideologies. Am J Pol Sci. 2012;56(1):34-51.

12. Monsuur AJ, Wijmenga C. Understanding the molecular basis of celiac disease: what genetic studies reveal. Ann Med. 2006;38(8):578-91.

13. Castro-antunes MM, Crovella S, Brandão LA, Guimaraes RL, Motta ME, Silva GA. Frequency distribution of HLA DQ2 and DQ8 in celiac patients and first-degree relatives in Recife, northeastern Brazil. Clinics (Sao Paulo). 2011;66(2):227-31.

14. Gujral N, Freeman HJ, Thomson AB. Celiac disease: prevalence, diagnosis, pathogenesis and treatment. World J Gastroenterol. 2012;18(42):6036-59.

15. Szałowska-woźniak DA, Bąk-romaniszyn L, Cywińska-bernas A, Zeman K. Evaluation of HLA-DQ2/DQ8 genotype in patients with celiac disease hospitalised in 2012 at the Department of Paediatrics. Prz Gastroenterol. 2014;9(1):32-7.

16. Alegría-torres JA, Baccarelli A, Bollati V. Epigenetics and lifestyle. Epigenomics. 2011;3(3):267-77.

17. Nistal E, Caminero A, Herrán AR, et al. Differences of small intestinal bacteria populations in adults and children with/without celiac disease: effect of age, gluten diet, and disease. Inflamm Bowel Dis. 2012;18(4):649-56.

18. Kau AL, Ahern PP, Griffin NW, Goodman AL, Gordon JI. Human nutrition, the gut microbiome and the immune system. Nature. 2011;474(7351):327-36.

19. Tillisch K, Labus J, Kilpatrick L, et al. Consumption of fermented milk product with probiotic modulates brain activity. Gastroenterology. 2013;144(7):1394-401, 1401.e1-4.

20. Cryan JF, Dinan TG. Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour. Nat Rev Neurosci. 2012;13(10):701-12.

21. Tilg H, Moschen AR, Kaser A. Obesity and the microbiota. Gastroenterology. 2009;136(5):1476-83.

22. Tilg H, Kaser A. Gut microbiome, obesity, and metabolic dysfunction. J Clin Invest. 2011;121(6):2126-32.

23. Brown K, Decoffe D, Molcan E, Gibson DL. Diet-induced dysbiosis of the intestinal microbiota and the effects on immunity and disease. Nutrients. 2012;4(8):1095-119.

24. Hurt RT, Kulisek C, Buchanan LA, Mcclave SA. The obesity epidemic: challenges, health initiatives, and implications for gastroenterologists. Gastroenterol Hepatol (N Y). 2010;6(12):780-92.

25. Cordain L, Eaton SB, Sebastian A, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341-54.

26. Tännsjö T. Should we change the human genome?. Theor Med. 1993;14(3):231-47.

27. Okada H, Kuhn C, Feillet H, Bach JF. The 'hygiene hypothesis' for autoimmune and allergic diseases: an update. Clin Exp Immunol. 2010;160(1):1-9.

28. Rook GA. Review series on helminths, immune modulation and the hygiene hypothesis: the broader implications of the hygiene hypothesis. Immunology. 2009;126(1):3-11.

29. Bloomfield SF, Stanwell-smith R, Crevel RW, Pickup J. Too clean, or not too clean: the hygiene hypothesis and home hygiene. Clin Exp Allergy. 2006;36(4):402-25.

30. Romagnani S. The increased prevalence of allergy and the hygiene hypothesis: missing immune deviation, reduced immune suppression, or both?. Immunology. 2004;112(3):352-63.

31. See J, Murray JA. Gluten-free diet: the medical and nutrition management of celiac disease. Nutr Clin Pract. 2006;21(1):1-15.

32. Mäki M. Celiac disease treatment: gluten-free diet and beyond. J Pediatr Gastroenterol Nutr. 2014;59 Suppl 1:S15-7.

33. Aggarwal S, Lebwohl B, Green PH. Screening for celiac disease in average-risk and high-risk populations. Therap Adv Gastroenterol. 2012;5(1):37-47.

34. Rubio-tapia A, Van dyke CT, Lahr BD, et al. Predictors of family risk for celiac disease: a population-based study. Clin Gastroenterol Hepatol. 2008;6(9):983-7.

35. Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011;106(3):508-14.

36. Marziali M, Venza M, Lazzaro S, Lazzaro A, Micossi C, Stolfi VM. Gluten-free diet: a new strategy for management of painful endometriosis related symptoms?. Minerva Chir. 2012;67(6):499-504.

37. Drago S, El asmar R, Di pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006;41(4):408-19.

38. Gluten sensitivity as a neurological illness. Journal of Neurology, Neurosurgery & Psychiatry. 2002;72(5):560.

39. Hadjivassiliou M, Grünewald RA, Kandler RH, et al. Neuropathy associated with gluten sensitivity. J Neurol Neurosurg Psychiatr. 2006;77(11):1262-6.

40. Hadjivassiliou M, Grünewald RA, Lawden M, Davies-jones GA, Powell T, Smith CM. Headache and CNS white matter abnormalities associated with gluten sensitivity. Neurology. 2001;56(3):385-8.

41. Soares FL, De oliveira matoso R, Teixeira LG, et al. Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression. J Nutr Biochem. 2013;24(6):1105-11.

42. Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010;9(3):318-30.

43. Nijeboer P, Mulder C, Bouma G. [Non-coeliac gluten sensitivity: hype, or new epidemic?]. Ned Tijdschr Geneeskd. 2013;157(21):A6168.

44. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013;145(2):320-8.e1-3.

45. Kraft BD, Westman EC. Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and review of the literature. Nutr Metab (Lond). 2009;6(1):10.

46. Frassetto LA, Schloetter M, Mietus-synder M, Morris RC, Sebastian A. Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr. 2009;63(8):947-55.

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