Occurrence of Congenital Heart Defects in Relation to Maternal Multivitamin Use

The purpose of this study was to assess the relation between maternal multivitamin use and risk for cardiac defects in the offspring, using a population-based approach. The Atlanta Birth Defects Case-Control study is a population-based case-control study of infants born between 1968 and 1980 to moth...

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Bibliographic Details
Published inAmerican journal of epidemiology Vol. 151; no. 9; pp. 878 - 884
Main Authors Botto, Lorenzo D., Mulinare, Joseph, Erickson, J. David
Format Journal Article
LanguageEnglish
Published Cary, NC Oxford University Press 01.05.2000
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Summary:The purpose of this study was to assess the relation between maternal multivitamin use and risk for cardiac defects in the offspring, using a population-based approach. The Atlanta Birth Defects Case-Control study is a population-based case-control study of infants born between 1968 and 1980 to mothers residing in metropolitan Atlanta, Georgia. The 958 case infants with nonsyndromic cardiac defects were actively ascertained from multiple sources. The 3, 029 infants without birth defects (control infants) were selected from birth certificates by stratified random sampling. Periconceptional multivitamin use, defined as reported regular use of multivitamins from 3 months before pregnancy through the first 3 months of pregnancy, was contrasted with no use during the same time period. Periconceptional multivitamin use was associated with a reduced risk for nonsyndromic cardiac defects in the offspring (odds ratio (OR) = 0.76; 95% confidence interval (Cl): 0.60, 0.97). The risk reduction was strongest for outflow tract defects (OR = 0.46; 95% Cl: 0.24, 0.86) and ventricular septal defects (OR = 0.61; 95% Cl: 0.38, 0.99). No risk reduction was evident when multivitamin use was begun after the first month of pregnancy. If these associations are causal, the results suggest that approximately one in four major cardiac defects could be prevented by periconceptional multivitamin use. Am J Epidemiol 2000A 51: 878-84.
Bibliography:ArticleID:151.9.878
ark:/67375/HXZ-ZFFTFFDD-W
istex:624B8EDCCA5C203FCC6E09511ACF6E465121D5A1
ISSN:0002-9262
1476-6256
DOI:10.1093/oxfordjournals.aje.a010291