ArticleBirth defects research. Part A, Clinical and molecular teratology2010
Caffeine, selected metabolic gene variants, and risk for neural tube defects.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 34 citations in OpenAlex.
- Exome sequencing of family trios from the National Birth Defects Prevention Study: Tapping into a rich resource of genetic and environmental data.Birth defects research · 2019Article
- Interaction between maternal caffeine intake during pregnancy and CYP1A2 C164A polymorphism affects infant birth size in the Hokkaido study.Pediatric research · 2017Article
- Intake of Caffeinated Soft Drinks before and during Pregnancy, but Not Total Caffeine Intake, Is Associated with Increased Cerebral Palsy Risk in the Norwegian Mother and Child Cohort Study.The Journal of nutrition · 2016Article
- PharmGKB summary: caffeine pathway.Pharmacogenetics and genomics · 2012Article
- Exploring the caffeine-induced teratogenicity on neurodevelopment using early chick embryo.PloS one · 2012Article
- Caffeine intake and risk of neural tube defects.Birth defects research. Part A, Clinical and molecular teratology · 2011Article
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8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundInvestigations of maternal caffeine intake and neural tube defects (NTDs) have not considered genetic influences. Caffeine metabolism gene effects were examined in the National Birth Defects Prevention Study.
methodsAverage daily caffeine was summed from self-reported coffee, tea, soda, and chocolate intake for mothers of 768 NTD cases, and 4143 controls delivered from 1997 to 2002. A subset of 306 NTD and 669 control infants and their parents were genotyped for CYP1A2*1F, NAT2 481C>T, and NAT2 590G>A. CYP1A2*1F was classified by fast or slow oxidation status, and NAT2 variants were categorized into rapid or slow acetylation status. Case-control logistic regression analyses, family-based transmission/disequilibrium tests and log-linear analyses, and hybrid log-linear analyses were conducted to produce odds ratios (ORs) or relative risks (RRs) and 95% confidence intervals (CIs) for caffeine intake and maternal and infant gene variants, and to examine interaction effects.
resultsNTDs were independently associated with infant slow NAT2 acetylator status (RR, 2.00; 95% CI, 1.10-3.64) and maternal CYP1A2*1F fast oxidation status (OR, 1.49; 95% CI, 1.10-2.03). Mothers who consumed caffeine, oxidized CYP1A2*1F quickly, and acetylized NAT2 slowly had a nonsignificantly elevated estimated risk for an NTD-affected pregnancy (OR, 3.10; 95% CI, 0.86-11.21). Multiplicative interaction effects were observed between maternal caffeine and infant CYP1A2*1F fast oxidizer status (p(interaction) = 0.03).
conclusionsThe association identified between maternal CYP1A2*1F fast oxidation status and NTDs should be examined further in the context of the other substrates of CYP1A2. Maternal caffeine and its metabolites may be associated with increased risk for NTD-affected pregnancies in genetically susceptible subgroups.
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