Low birth weight (<2,500 g) and preterm birth (<37 weeks) were found to be associated with increased risk of autism spectrum disorder (ASD), however, the data regarding the entire birth weight (BW) and gestational age (GA) range are inconclusive. In this population nested case–control study, based on the Israeli National Insurance Institute records, we aimed to estimate the associations in the Israeli population. The study population included all children born between 2000 and 2012 and diagnosed with ASD (N = 12,635 cases), and a random 20% sample of children born in the same period who were not diagnosed with ASD (N = 369,548 controls). We used multiple logistic regression models to calculate the risk of ASD for each BW and GA category, adjusted for covariates (child sex, maternal age, paternal age, population group, maternal wage, paternal wage, having a sibling with ASD, multiple gestation and socioeconomic status). BW < 3,000 g and GA < 39 weeks were associated with higher risk of ASD, including BW of 2,500–3,000 g (adjusted odds ratio [AOR], 1.18; 95% CI, 1.12–1.24, in comparison to the 3,000–3,500 g category) and GA of 37 & 38 weeks (AOR, 1.35; 95% CI, 1.25–1.45 and AOR, 1.13; 95% CI 1.06–1.20, respectively; in comparison to GA of 40 weeks). To account for the high correlation between GA and BW, we modeled BW percentiles for gestational age and found that the BW < 20th percentile was associated with an increased risk of ASD (AOR, 1.10; 95% CI, 1.01–1.19). These results demonstrate that associations of ASD with BW and GA are not limited to commonly used clinical cutoffs. Autism Res 2020, 13: 655–665. © 2020 International Society for Autism Research, Wiley Periodicals, Inc.Lay SummaryAutism spectrum disorder (ASD) has been associated with low birth weight (<2,500 g) in prior research. Our study aims to describe the relationship between birth weight (BW) and ASD in the Israeli population. We found that BW<3,000 g was associated with a higher risk of ASD. These results demonstrate that an increased risk of ASD is not confined to clinically defined cutoffs such as BW < 2,500 g.

The objectives of our study were to (a) report how many children met an autism spectrum disorder (ASD) surveillance definition but had no clinical diagnosis of ASD in health or education records and (b) evaluate differences in demographic, individual, and service factors between children with and without a documented ASD diagnosis. ASD surveillance was conducted in selected areas of Arizona, Arkansas, Colorado, Georgia, Maryland, Minnesota, Missouri, New Jersey, North Carolina, Tennessee, and Wisconsin. Children were defined as having ASD if sufficient social and behavioral deficits and/or an ASD diagnosis were noted in health and/or education records. Among 4,498 children, 1,135 (25%) had ASD indicators without having an ASD diagnosis. Of those 1,135 children without a documented ASD diagnosis, 628 (55%) were not known to receive ASD services in public school. Factors associated with not having a clinical diagnosis of ASD were non‐White race, no intellectual disability, older age at first developmental concern, older age at first developmental evaluation, special education eligibility other than ASD, and need for fewer supports. These results highlight the importance of reducing disparities in the diagnosis of children with ASD characteristics so that appropriate interventions can be promoted across communities. Autism Res 2020, 13: 464–473. © 2019 International Society for AutismResearch,Wiley Periodicals, Inc.Lay SummaryChildren who did not have a clinical diagnosis of autism spectrum disorder (ASD) documented in health or education records were more likely to be non‐White and have fewer developmental problems than children with a clinical diagnosis of ASD. They were brought to the attention of healthcare providers at older ages and needed fewer supports than children with a clinical diagnosis of ASD. All children with ASD symptoms who meet diagnostic criteria should be given a clinical diagnosis so they can receive treatment specific to their needs.

Pre‐eclampsia is a leading cause of maternal death and maternal and perinatal morbidity. Whilst the clinical manifestations of pre‐eclampsia often occur in late pregnancy, the molecular events leading into the onset of this disease are thought to originate in early pregnancy and result in insufficient placentation. Although the causative molecular basis of pre‐eclampsia remains poorly understood, maternal inflammation is recognised as a core clinical feature. While the adverse effects of pre‐eclampsia on maternal and fetal health in pregnancy is well‐recognised, the long‐term impact of pre‐eclampsia exposure on the risk of autism spectrum disorder (ASD) in exposed offspring is a topic of on‐going debate. In particular, a recent systematic review has reported an association between exposure to pre‐eclampsia and increased risk of ASD, however the molecular basis of this association is unknown. Here we review recent evidence for; 1) maternal inflammation in pre‐eclampsia; 2) epidemiological evidence for alterations in neurodevelopmental outcomes in offspring exposed to pre‐eclampsia; 3) long‐term changes in the brains of offspring exposed to pre‐eclampsia; and 4) how maternal inflammation may lead to altered neurodevelopmental outcomes in pre‐eclampsia exposed offspring. Finally, we discuss the implications of this for the development of future studies in this field.