Anthropometric measurements in children with ASD point to genomic imprinting imbalance

Autism Spectrum Disorder (ASD) is a large set of neurodevelopmental disorders of complex aetiology. A mix of genetic and environmental factors are likely to cause ASD. Genetic risk for autism comes from common genetic variation. Genomic imprinting refers to genes that have different expression patterns according to the parent of origin - being silenced when imprinted. Paternally active genes increase resource extraction from the mother and reduce resource burden on the father. Children with ASD show consistent overgrowth during their first 1-2 years of life. Recently, it has been shown that children with higher birth weight and length have an increased risk of developing ASD. This overgrowth and apparent larger birth weight and length are consistent with the notion that a paternally biased genome might underlie the risk for ASD. The study compared height, weight, head circumference and thoracic circumference for age-matched (ages 4-8 years old) male children with ASD (n=30) with neurotypical children (n=33). No clinically significant differences were found among the two groups. After weaning, relative paternal contribution to a childs somatic development would increase, thus one would expect paternally active genes to start changing the childs behaviour, so as to make the child less demanding of resources (overall, and thus also on the father), with a counterweight represented by maternally active genes. A relative overabundance of paternally active genes would explain the data presented here, that shows children with ASD being no different from controls. Given the fact presented by other studies, that children with ASD seem to get a head start in growth, the lack of differences found in this 4-8 years old group indicates that children with ASD might actually fall behind in somatic growth, or at least stagnate by middle childhood.