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Prenatal Inflammation Linked To Autism Risk


According to new findings published online in the journal Molecular Psychiatry (22 January 2013) and supported by the National Institute of Environmental Health Sciences (NIEHS), maternal inflammation during early pregnancy may be related to an increased risk of autism in children. The study found elevated C-reactive protein (CRP) in mothers with children who have autism. CRP is a well-established marker of systemic inflammation. Results from the study indicated that the risk of autism among children in the study was increased by 43% among mothers with CRP levels in the top 20th percentile, and by 80% for maternal CRP in the top 10th percentile.) and add to mounting evidence that an overactive immune response can alter the development of the central nervous system in the fetus.


According to the authors, elevated CRP is a signal that the body is undergoing a response to inflammation from, for example, a viral or bacterial infection, and the higher the level of CRP in the mother, the greater the risk of autism in the child. However, the authors cautioned that the results should be viewed in perspective since the prevalence of inflammation during pregnancy is substantially higher than the prevalence of autism and that the vast majority of mothers with increased CRP levels will not give birth to children with autism.


The study capitalized on a unique national birth cohort known as the Finnish Maternity Cohort (FMC), which contains an archive of samples collected from pregnant women in Finland, where serum is systematically collected during the early part of pregnancy. The FMC consists of 1.6 million specimens from about 810,000 women, archived in a single, centralized biorepository. Finland also maintains diagnoses of virtually all childhood autism cases from national registries of both hospital admissions and outpatient treatment.


The study analyzed CRP in archived maternal serum corresponding to 677 childhood autism cases and an equal number of matched controls. The findings were not explained by maternal age, paternal age, gender, previous births, socioeconomic status, preterm birth, or birth weight.


This work is expected to stimulate further research on autism, which is complex and challenging to identify causes. Future studies may help define how infections, other inflammatory insults, and the body’s immune response interact with genes to elevate the risk for autism and other neurodevelopmental disorders. Preventative approaches addressing environmental causes of autism may also benefit from additional research.


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