TY - JOUR T1 - Children born in the summer have increased risk for coeliac disease JF - Journal of Epidemiology and Community Health JO - J Epidemiol Community Health SP - 36 LP - 39 DO - 10.1136/jech.57.1.36 VL - 57 IS - 1 AU - A Ivarsson AU - O Hernell AU - L Nyström AU - L Å Persson Y1 - 2003/01/01 UR - http://jech.bmj.com/content/57/1/36.abstract N2 - Study objective: Coeliac disease, also called permanent gluten sensitive enteropathy, is being recognised as a widespread health problem. Defining the possible role of environmental factors in its aetiology might open doors to primary prevention. This study therefore analysed if the risk for coeliac disease varies with month of birth as a proxy for a seasonal pattern for possible causal environmental exposure(s). Design: A population based incidence register of coeliac disease in children below 15 years of age covering the period from 1973 to 1997. Incidence rates were calculated by month of birth, stratified for age at diagnosis. Poisson regression analyses were used to estimate the relative risk for coeliac disease for children below 2 years of age by season of birth, also taking into account gender and time period of diagnosis. Setting: Sweden. Participants: All 2151 children in the study base with verified coeliac disease. Main results: The risk for coeliac disease was significantly higher if born during the summer as compared with the winter (RR=1.4, 95% CI 1.2 to 1.7), but only in children below 2 years of age at diagnosis. This relative seasonal risk pattern prevailed during a 10 year epidemic of coeliac disease, although incidence rates varied threefold. The incidence was constantly higher among girls as compared with boys, but boys showed a more pronounced seasonal variation in risk than girls. Conclusions: An increased coeliac disease risk in children born in the summer compared with the winter reflects causal environmental exposure(s) with a seasonal pattern. Infections might be the exposure of importance, either by means of a direct causal role and/or through interaction with other exposures, for example, gluten intake. However, non-infectious exposures should also be explored as possible contributing causal factors. ER -