Celiac Disease, Gluten And Children

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

Celiac Disease - Diagram 1

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

Celiac Disease - Diagram 2

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

Celiac Disease - Diagram 3

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

Celiac Disease Table 1

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

Celiac Disease Diagram 3

J Clin Invest. 2011;121(6):2126-2132. doi:10.1172/JCI58109.

Genetic and diet-induced obesity are associated with alterations of (i) the composition and (ii) the functional properties of the gut microbiota. (A) Leptin-deficient ob/ob mice rapidly gain weight. Development of obesity correlates with a shift in the abundance of the 2 dominating divisions, the Bacteroidetes and the Firmicutes. Compared to lean ob/+ or +/+ littermates, obesity was associated with a 50% reduction in Bacteroidetes and a proportional division-wide increase in Firmicutes. Moreover, ob/ob mice showed an increase in environmental gene tags that matched Archaea, methanogenic microorganisms that might promote bacterial fermentation by removing one of its end products, namely hydrogen (H2). The metagenomic analysis of the obese gut microbiome revealed an increase in glycoside hydrolases, capable of breaking down otherwise indigestible alimentary polysaccharides. Furthermore, the obese microbiome showed enrichment for transport proteins and fermentation enzymes further processing breakdown products. As a consequence, ob/ob mice have an increased capacity to harvest energy from their diet. (B) The interrelationship between diet, intestinal microbial ecology, and energy homeostasis was investigated in a mouse model of diet-induced obesity.28 The microbiota of mice fed a high-fat/high-sugar prototypic Western diet was compared with the microbiota of mice receiving a low-fat/high-polysaccharide diet. Again, as in the ob/ob model, the Western diet was associated with an increased body weight, a lower relative abundance of Bacteroidetes, and a higher relative abundance of Firmicutes. However, unlike in the ob/ob model this shift was not division-wide. The overall diversity of the Western diet-associated gut microbiota dropped dramatically. The reason was a bloom in a single class of the Firmicutes—the Mollicutes. The Western diet gut microbiome was enriched for genes involved in import and fermentation of simple sugars and host glycans, enriched for genes for beta-fructosidases, and depleted for genes involved in motility. Gastroenterology Volume 136, Issue 5, Pages 1476–1483, May 2009 .

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

Prevalence of celiac disease worldwide. N/A: Not available. 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.

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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.

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