Celiac disease, which damages the lining of the gut and is triggered by eating food containing gluten, occurs more often as adults age, according to a study suggesting that environmental influences may be involved.
Cases doubled in a sample of 3,511 patients followed from 1974 to 1989, according to proteins measured in blood samples. This provides evidence that the condition doesn’t start in childhood, as doctors once thought it did, researchers said today in the Annals of Medicine.
The results may begin to explain why celiac disease has increased fivefold in the U.S. in the last 30 years, the authors wrote. The research suggests that the rise is not simply due to better diagnosis, and that the illness may be preventable, as people with a genetic disposition for it can live decades before getting sick, said Alessio Fasano, an author of the study.
“If we can understand what helps people lose gluten tolerance, we may develop tricks to retain tolerance, even if you’ve lost it already,” said Fasano, director of the University of Maryland’s Mucosal Biology Research Center in Baltimore and the celiac research center, in a telephone interview.
Celiac disease affects more than 2 million Americans, according to the National Institutes of Health, based in Bethesda, Maryland. The condition, which can be symptomless, is triggered when people ingest wheat or other foods containing gluten, such as bread or beer. The immune system attacks part of the small intestine, causing abdominal bloating, diarrhea, vomiting, constipation, weight loss and pain, the federal agency says on its website.
Because the illness is an autoimmune disease, the findings may also hold clues to other disorders, such as multiple sclerosis, that are caused by a malfunctioning immune system.
The report showing people may acquire celiac disease as they age time strengthens the idea that the environment may be crucial for developing the condition. Patients’ genes didn’t vary during the study, Fasano said.
The effects of environment may be described by thinking of the human genome as a piano, he said. As long as no one plays the instrument, the owner doesn’t notice that some keys are defective. If someone plays, suddenly the defect is obvious, Fasano said. Perhaps the player in celiac disease is a virus or bacterium, he said.
The study was done by testing blood samples taken in 1974 and 1989 from people in Washington County, Maryland, the authors wrote.
Fasano plans to study people who develop celiac disease at young ages and compare them with people who develop the disease later, to see if there can be some pattern, he said.
The research was funded by the University of Maryland School of Medicine, Madison, New Jersey-based Quest Diagnostics Inc., and other sources.