Summary: Researchers have identified a link between low levels of vitamin D at birth and an increased risk of a child being diagnosed on the autism spectrum by the age of three.
Low vitamin D levels at birth were associated with an increased risk of autism spectrum disorders (ASDs) at the age of 3 years, researchers report in a recent Journal of Bone and Mineral Research study.
In the study of 27,940 newborns in China, 310 were diagnosed with ASDs at 3 years of age, with a prevalence of 1.11 percent. When the 310 children with ASDs were compared with 1,240 control subjects, the risk of ASDs was significantly increased in each of the three lower quartiles of vitamin D level at birth, when compared with the highest quartile: an increased risk of ASDs by 260 percent in the lowest quartile, 150 percent in the second quartile, and 90 percent in the third quartile.
“Neonatal vitamin D status was significantly associated with the risk of ASDs and intellectual disability,” said senior author Dr. Yuan-Lin Zheng.
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Relationship Between Neonatal Vitamin D at Birth and Risk of Autism Spectrum Disorders: the NBSIB Study” by Dong-Mei Wu, Xin Wen, Xin-Rui Han, Shan Wang, Yong-Jian Wang, Min Shen, Shao-Hua Fan, Juan Zhuang, Meng-Qiu Li, Bin Hu, Chun-Hui Sun, Ya-Xing Bao, Jing Yan, Jun Lu, and Yuan-Lin Zheng in Journal of Bone and Mineral Research. Published online November 27 2017 doi:10.1002/jbmr.3326
Relationship Between Neonatal Vitamin D at Birth and Risk of Autism Spectrum Disorders: the NBSIB Study
Previous studies suggested that lower vitamin D might be a risk factor for autism spectrum disorders (ASDs). The aim of this study was to estimate the prevalence of ASDs in 3-year-old Chinese children and to examine the association between neonatal vitamin D status and risk of ASDs. We conducted a study of live births who had taken part in expanded newborn screening (NBS), with outpatient follow-up when the children 3-year old. The children were confirmed for ASDs in outpatient by the Autism Diagnostic Interview-Revised and Diagnostic and Statistical Manual of Mental Disorders (DSM)-5 criteria. Intellectual disability (ID) status was defined by the intelligence quotient (IQ < 80) for all the participants. The study design included a 1:4 case to control design. The concentration of 25-hydroxyvitamin D3 [25(OH)D3] in children with ASD and controls were assessed from neonatal dried blood samples. A total of 310 children were diagnosed as having ASDs; thus, the prevalence was 1.11% (95% CI, 0.99% to 1.23%). The concentration of 25(OH)D3 in 310 ASD and 1240 controls were assessed. The median 25(OH)D3 level was significantly lower in children with ASD as compared to controls (p < 0.0001). Compared with the fourth quartiles, the relative risk (RR) of ASDs was significantly increased for neonates in each of the three lower quartiles of the distribution of 25(OH)D3, and increased risk of ASDs by 260% (RR for lowest quartile: 3.6; 95% CI, 1.8 to 7.2; p < 0.001), 150% (RR for second quartile: 2.5; 95% CI, 1.4 to 3.5; p = 0.024), and 90% (RR for third quartile: 1.9; 95% CI, 1.1 to 3.3; p = 0.08), respectively. Furthermore, the nonlinear nature of the ID-risk relationship was more prominent when the data were assessed in deciles. This model predicted the lowest relative risk of ID in the 72rd percentile (corresponding to 48.1 nmol/L of 25(OH)D3). Neonatal vitamin D status was significantly associated with the risk of ASDs and intellectual disability. The nature of those relationships was nonlinear. © 2017 American Society for Bone and Mineral Research.
“Relationship Between Neonatal Vitamin D at Birth and Risk of Autism Spectrum Disorders: the NBSIB Study” by Dong-Mei Wu, Xin Wen, Xin-Rui Han, Shan Wang, Yong-Jian Wang, Min Shen, Shao-Hua Fan, Juan Zhuang, Meng-Qiu Li, Bin Hu, Chun-Hui Sun, Ya-Xing Bao, Jing Yan, Jun Lu, and Yuan-Lin Zheng in Journal of Bone and Mineral Research. Published online November 27 2017 doi:10.1002/jbmr.3326