With celiac disease on the rise, researchers are racing to pin down any factors that may play a part. Recent attention has turned to the role of respiratory infections in at-risk children.

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Why do some at-risk children develop celiac disease, but others don't?

Celiac disease is an autoimmune condition. When someone with celiac disease eats gluten, which is a protein in wheat, rye, and barley, the immune system attacks the small intestine.

Villi, or small, finger-like projections that are vital for the absorption of nutrients, are damaged.

In the United States, the exact prevalence of celiac disease is not known. However, some have estimated that it affects around 1 in 141 people, with a significant proportion not being aware that they even have it.

Across the world, around 1 percent of the population is thought to have celiac disease, and that proportion seems to be growing.

Although more cases are now picked up due to improved tests and detection rates, experts believe that the increase is not due to this factor alone. So, the race to understand why this condition is experiencing such a surge is on.

Celiac disease runs in families; people with a first-degree relative with the condition have a 1 in 10 chance of developing it during their life. At present, it is not known why some at-risk people develop it while others do not, though it is assumed that environmental triggers set the wheels of celiac disease in motion.

The role of infections in celiac disease

The number of at-risk children - or those with relatives who have celiac disease - who go on to develop the condition seems to be increasing. And recently, Dr. Renata Auricchio, from the University of Naples Federico II in Italy, set out to understand why this might be the case.

Studies have pointed toward infections in childhood as a potential trigger of celiac disease in those who are genetically susceptible. For instance, a 2013 study found that the presence of rotavirus antibodies could predict the onset of celiac disease.

Similarly, in the Norwegian Mother and Child Cohort Study, children who had experienced 10 or more infections before reaching the age of 18 months had a significantly increased risk of developing celiac disease than children who had had four or fewer.

Many earlier investigations into infections and celiac disease relied on parental recall of infections and have included a general cross-section of the population.

However, to gather more detailed information, the new study used a prospective cohort. In other words, the team studied a group of infants known to be at risk of developing celiac disease and followed them for 6 years.

Their findings were recently published in the journal Pediatrics.

As the authors explain, the study's aim was "to explore the relationship between early clinical events (including infections) and the development of CD [celiac disease] in a prospective cohort of genetically predisposed infants."

In all, they followed 373 Italian newborns with at least one relative with celiac disease. They were monitored closely for 6 years, and this included undergoing blood tests every 4 weeks for the first 6 months, every 3 months until the age of 1, every 6 months from the age of 1 to 3, and then once per year until age 6.

Respiratory infections predict onset

Across the study, 6 percent of the children were diagnosed with celiac disease at the age of 3, 13.5 percent at age 5, and 14 percent by age 6. They also found that "[c]ompared with gastroenteritis, respiratory infections during the first 2 years of life conferred a twofold increase in the risk of developing CD [celiac disease]."

When discussing how early infections might impact the later development of celiac disease, the authors write:

"It is possible that [...] early infection stimulates a genetically predisposed immune profile, which contributes to the switch from tolerance to intolerance to gluten."

The much-debated "hygiene hypothesis" states that triggering the immune system as an infant protects against future autoimmune conditions and allergies. These findings, however, show that this may not always be the case.

The study authors write that an "immune response to infections may modulate natural immunity via mechanisms that can drive tolerance as well as intolerance, according to the pathways involved."

Although the authors admit that the sample size for this study was relatively small, it does add more evidence to a growing pile. More research will need to be done, but the connections between early years infections and later development of celiac disease seem to be strengthening.