Senmao Zhang1,2, Xiaoying Liu1,2, Tubao Yang1,2, Tingting Wang1,3, Lizhang Chen4,5, Jiabi Qin6,7,8,9. 1. Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, Hunan, China. 2. Hunan Provincial Key Laboratory of Clinical Epidemiology, Changsha, Hunan, China. 3. National Health Commission Key Laboratory for Birth Defect Research and Prevention, Changsha, Hunan, China. 4. Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, Hunan, China. liche4005@126.com. 5. Hunan Provincial Key Laboratory of Clinical Epidemiology, Changsha, Hunan, China. liche4005@126.com. 6. Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, Hunan, China. qinjiabi123@163.com. 7. Hunan Provincial Key Laboratory of Clinical Epidemiology, Changsha, Hunan, China. qinjiabi123@163.com. 8. National Health Commission Key Laboratory for Birth Defect Research and Prevention, Changsha, Hunan, China. qinjiabi123@163.com. 9. Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China. qinjiabi123@163.com.
Abstract
OBJECTIVES: To estimate the association of maternal ADIPOQ gene, dietary habits in early pregnancy, and their interactions with the risk of congenital heart defects (CHDs) in offspring. METHODS: A case-control study of 464 mothers of CHDs children and 504 mothers of healthy children was included. Maternal dietary habits and genetic polymorphisms of ADIPOQ were the main exposure of interest. Their independent effects and interactions in the development of CHDs were analyzed in our study. RESULTS: The excessive consumption of pickled vegetables (aOR = 1.58, 95%CI: 1.17-2.12), smoked foods (aOR = 1.84, 95%CI:1.34-2.52), barbecued foods (aOR = 1.62, 95%CI: 1.09-2.39), fish and shrimp (aOR = 0.37, 95%CI: 0.27-50), and milk products (aOR = 0.64, 95%CI: 0.51-80) had a significant association with total CHDs risk. The polymorphisms of ADIPOQ gene at rs1501299 (T/T vs G/G: aOR = 0.27, 95%CI: 0.14-50; G/T vs G/G: aOR = 0.67, 95%CI: 0.46-98) and rs2241766 (G/G vs T/T: aOR = 4.35, 95%CI: 2.23-8.51; T/G vs T/T: aOR = 2.23, 95%CI: 1.51-3.28) showed a significant association with total CHDs risk. Likewise, our results found that maternal dietary habits and ADIPOQ genetic variants also were significantly related to the risk of specific CHDs phenotypes. In addition, gene-diet interaction revealed significant associations between the ADIPOQ gene and maternal dietary habits with total CHDs. CONCLUSIONS: Maternal dietary habits, ADIPOQ gene, and their interactions show a significant association with the risk of CHDs. However, our study has some limitations, thus our findings need to be taken with caution, which highlights that more studies are required to further corroborate our findings.
OBJECTIVES: To estimate the association of maternal ADIPOQ gene, dietary habits in early pregnancy, and their interactions with the risk of congenital heart defects (CHDs) in offspring. METHODS: A case-control study of 464 mothers of CHDs children and 504 mothers of healthy children was included. Maternal dietary habits and genetic polymorphisms of ADIPOQ were the main exposure of interest. Their independent effects and interactions in the development of CHDs were analyzed in our study. RESULTS: The excessive consumption of pickled vegetables (aOR = 1.58, 95%CI: 1.17-2.12), smoked foods (aOR = 1.84, 95%CI:1.34-2.52), barbecued foods (aOR = 1.62, 95%CI: 1.09-2.39), fish and shrimp (aOR = 0.37, 95%CI: 0.27-50), and milk products (aOR = 0.64, 95%CI: 0.51-80) had a significant association with total CHDs risk. The polymorphisms of ADIPOQ gene at rs1501299 (T/T vs G/G: aOR = 0.27, 95%CI: 0.14-50; G/T vs G/G: aOR = 0.67, 95%CI: 0.46-98) and rs2241766 (G/G vs T/T: aOR = 4.35, 95%CI: 2.23-8.51; T/G vs T/T: aOR = 2.23, 95%CI: 1.51-3.28) showed a significant association with total CHDs risk. Likewise, our results found that maternal dietary habits and ADIPOQ genetic variants also were significantly related to the risk of specific CHDs phenotypes. In addition, gene-diet interaction revealed significant associations between the ADIPOQ gene and maternal dietary habits with total CHDs. CONCLUSIONS: Maternal dietary habits, ADIPOQ gene, and their interactions show a significant association with the risk of CHDs. However, our study has some limitations, thus our findings need to be taken with caution, which highlights that more studies are required to further corroborate our findings.
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