November 16, 2015
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Early gluten intake increases risk for celiac disease in at-risk infants

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A recent study found that gluten intake before age 2 years is associated with at least a twofold increased risk for celiac disease among genetically at-risk children.

“The role of gluten intake in infants and the risk of later developing celiac disease has long been debated,” Carin Andrén Aronsson, MSc, from the department of clinical sciences at Lund University in Sweden, said in a press release. “Our study provides convincing evidence that the amount of gluten ingested at an early age plays a role in disease course, particularly in children with genetic risk of developing celiac disease.”

As part of the TEDDY study, Aronsson and colleagues performed a nested case-control study of Swedish children genetically at risk for celiac disease to determine whether the amount of gluten intake before age 2 years increases their risk for developing the disease. They used a database of genetically at-risk children to generate 436 sex-, birth year- and HLA genotype-matched pairs of children screened from September 2004 to February 2010, 146 of whom were diagnosed with celiac disease.

These children were screened yearly with a tissue transglutaminase auto-antibody (tTGA) assay, and those who tested positive had celiac disease confirmed by intestinal biopsy. Three-day food records quantifying gluten intake were collected for all children at ages 9, 12, 18 and 24 months.

The median breastfeeding duration was 32 weeks and the median age at first gluten intake was 22 weeks, both of which were comparable between children with and without celiac disease. Children with celiac disease had a median gluten intake of 4.9 g per day while children without celiac disease had a median gluten intake of 3.9 g per day, which was reported at the visit before tTGA seroconversion (OR = 1.28; 95% CI, 1.13-1.46). Before testing positive for tTGA seroconversion, children with celiac disease more often had greater than 5 g gluten intake per day (upper tertile) compared with children without celiac disease (OR = 2.65; 95% CI, 1.7-4.13).

Notably, they found comparable risk increases between children homozygous for DR3-DQ2 (OR = 3.19; 95% CI, 1.61-6.3), heterozygous for DR3-DQ2 (OR = 2.24; 95% CI, 1.08-4.62) and those who were not DR3-DQ2 carriers (OR = 2.43; 95% CI, 0.9-6.54).

“This finding offers insight into why some, but not all, children at genetic risk develop celiac disease,” Aronsson said.

The researchers concluded that “high intake of gluten during the first 2 years of life is associated with an increased risk of [celiac disease]. This association was similar in children carrying any of the major HLA-risk genotypes for [celiac disease]. Since these HLA-risk genotypes also are widely distributed in the general population, our findings may therefore have consequence for future infant feeding recommendations.” – by Adam Leitenberger

Disclosures: The researchers report no relevant financial disclosures.