Objectives: To examine alcohol use for mothers with and without an ADH1B*3 allele and the moderating effects of the maternal and child ADH1B*3 allele on a broad range of infant and 7.5-year outcomes.
Study Design: Blood samples from 263 black mother/child pairs (217 mothers and 239 children) were analyzed to determine incidence of the ADH1B allele and the relation of the maternal allele to pregnancy drinking assessed at every prenatal clinic visit. Moderating effects of ADH1B were examined by dichotomizing the moderator variable and performing regression analyses on the 2 groups.
Results: Pregnancy drinking at conception was less frequent in the presence of the ADH1B*3 allele, and virtually no adverse effects were found in children whose mothers had at least one ADH1B*3 allele. By contrast to the maternal allele, we found no consistent pattern of greater vulnerability in children lacking the ADH1B*3 allele.
Conclusions: These data are consistent with the hypothesis that the maternal ADH1B*3 allele provides some protection to the fetus from prenatal alcohol exposure.
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http://dx.doi.org/10.1016/j.jpeds.2005.08.023 | DOI Listing |
Chem Res Toxicol
July 2018
Department of Biochemistry , National Defense Medical Center, 161 Minchuan East Road Section 6 , Taipei 11490 , Taiwan.
Alcohol dehydrogenase (ADH) is the principal enzyme responsible for the metabolism of ethanol. Human ADH constitutes a complex family of isozymes and allozymes with striking variation in kinetic properties and tissue distribution. The liver and the gastrointestinal tract are the major sites for first-pass metabolism (FPM).
View Article and Find Full Text PDFPharmacogenetics
November 2004
Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan.
Alcohol dehydrogenase (ADH) catalyses the rate-determining reaction in ethanol metabolism. Genetic association studies of diverse ethnic groups have firmly demonstrated that the allelic variant ADH1B*2 significantly protects against alcoholism but that ADH1C*1, which is in linkage with ADH1B*2, produces a negligible protection. The influence of other potential candidate genes/alleles within the human ADH family, ADH1B*3 and ADH2, remains unclear or controversial.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!