Jianzhang Chen1, Kuolin Xin2, Junjie Wei3, Kangli Zhang4, Huajun Xiao5. 1. Faculty of Aerospace Medicine, Fourth Military Medical University, Xi'an, Shaanxi Province 710032, China; Department of Medical Psychology, General Hospital of Jinan Military Command, Jinan, Shandong Province 250031, China. Electronic address: chanjz@126.com. 2. Department of Medical Psychology, General Hospital of Jinan Military Command, Jinan, Shandong Province 250031, China. 3. Department of Outpatient, General Hospital of Jinan Military Command, Jinan, Shandong Province 250031, China. 4. Department of Medical Psychology, General Hospital of Jinan Military Command, Jinan, Shandong Province 250031, China. Electronic address: kanglizhang90@qq.com. 5. Department of Physiology, Institute of Aviation Medicine, Beijing 100142, China.
Abstract
OBJECTIVE: The aim of this study was to examine the association between maternal serum vitamin D status in first trimester and risk of ASD at age 3-7years in the offspring. METHODS: Using a case-control design, 68 children diagnosed with ASD and 68 sex and age matched typically-developing children were included. Archived maternal blood samples from the first trimester of pregnancy (11-13weeks gestational age) were identified for those participants. Maternal serum levels of 25 hydroxyvitamin D3 [25(OH) D], unmetabolized folic acid (FA), vitamin B12, homocysteine (HCY) and High Sensitivity C Reactive protein (CRP) were measured from those samples. We examined the associations between those factors in pregnancy and diagnosis of ASD with logistic regression using SPSS. RESULTS: Mothers in autistic group had significantly lower maternal serum levels of 25(OH) D than in typically-developing group [19.2(IQR: 15.8-22.9)ng/ml vs. 24.3(19.3-27.3)ng/ml, P<0.001], with 55.9% and 29.4% being vitamin D deficient, respectively (P<0.001). Levels of 25(OH) D increased with decreasing severity of ASD as defined by the CARS score (r=-0.302, P<0.001). Maternal first trimester serum levels of 25(OH) D in the lower 3 quartiles (quartile 1, 2, 3) (compared to the highest quartile) was associated with increased odds of ASD diagnosis in offspring [OR (95% CI) Q1: 1.36(0.84-2.58, P=0.25); Q2: 2.68(1.44-4.29, P=0.006); Q3:3.99(2.58-7.12, P<0.001)]. CONCLUSIONS: Lower first trimester maternal serum levels of 25(OH) D were associated with increased risk of developing autism in offspring. If these findings are confirmed, this may present an opportunity for prenatal intervention to reduce the risk for ASD.
OBJECTIVE: The aim of this study was to examine the association between maternal serum vitamin D status in first trimester and risk of ASD at age 3-7years in the offspring. METHODS: Using a case-control design, 68 children diagnosed with ASD and 68 sex and age matched typically-developing children were included. Archived maternal blood samples from the first trimester of pregnancy (11-13weeks gestational age) were identified for those participants. Maternal serum levels of 25 hydroxyvitamin D3 [25(OH) D], unmetabolized folic acid (FA), vitamin B12, homocysteine (HCY) and High Sensitivity C Reactive protein (CRP) were measured from those samples. We examined the associations between those factors in pregnancy and diagnosis of ASD with logistic regression using SPSS. RESULTS: Mothers in autistic group had significantly lower maternal serum levels of 25(OH) D than in typically-developing group [19.2(IQR: 15.8-22.9)ng/ml vs. 24.3(19.3-27.3)ng/ml, P<0.001], with 55.9% and 29.4% being vitamin D deficient, respectively (P<0.001). Levels of 25(OH) D increased with decreasing severity of ASD as defined by the CARS score (r=-0.302, P<0.001). Maternal first trimester serum levels of 25(OH) D in the lower 3 quartiles (quartile 1, 2, 3) (compared to the highest quartile) was associated with increased odds of ASD diagnosis in offspring [OR (95% CI) Q1: 1.36(0.84-2.58, P=0.25); Q2: 2.68(1.44-4.29, P=0.006); Q3:3.99(2.58-7.12, P<0.001)]. CONCLUSIONS: Lower first trimester maternal serum levels of 25(OH) D were associated with increased risk of developing autism in offspring. If these findings are confirmed, this may present an opportunity for prenatal intervention to reduce the risk for ASD.
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