| Maternal MTHFR genotype and haplotype predict deficits in early cognitive development in a lead-exposed birth cohort in Mexico City. | |
| | |
MedLine Citation:
|
PMID: 20504979 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
BACKGROUND: Maternal folate nutritional status and prenatal lead exposure can influence fetal development and subsequent health. The methylenetetrahydrofolate reductase (MTHFR) gene is important for folate metabolism, and 2 common polymorphisms, C677T and A1298C, reduce enzymatic activity; C677T is present at high penetrance in Mexican populations. OBJECTIVE: The objective of this study was to examine potential links between maternal and child MTHFR polymorphisms and child neurodevelopment in a lead-exposed population. DESIGN: Data regarding MTHFR polymorphisms C677T and A1298C, peri- and postnatal lead measures, and Bayley Mental Development Index at 24 mo of age (MDI-24) scores were available for 255 mother-child pairs who participated in the ELEMENT (Early Life Exposures in Mexico to Environmental Toxicants) study during 1994-1995. RESULTS: In covariate-adjusted regression models, maternal MTHFR 677 genotype predicted MDI-24 scores, in which each copy of the maternal MTHFR 677T variant allele was associated with lower MDI-24 scores (beta = -3.52; 95% CI: -6.12, -0.93; P = 0.004). Maternal MTHFR haplotype also predicted MDI-24 scores (mean +/- SE: 93.3 +/- 1.2 for 677C-1298A compared with 89.9 +/- 0.8 for 677T-1298A; P < 0.05). MDI-24 scores were not associated with maternal MTHFR 1298 genotype or child MTHFR genotypes. We did not observe significant MTHFR genotype x lead interactions with respect to any of the subject biomarkers of lead exposure. CONCLUSIONS: The maternal MTHFR 677T allele is an independent predictor of poorer child neurodevelopment at 24 mo. These results suggest that maternal genetic variations in folate metabolism during pregnancy may program offspring neurodevelopment trajectories. Further research is warranted to determine the generalizability of these results across other populations. |
| | |
Authors:
|
J Richard Pilsner; Howard Hu; Robert O Wright; Katarzyna Kordas; Adrienne S Ettinger; Brisa N Sánchez; David Cantonwine; Alicia L Lazarus; Alejandra Cantoral; Lourdes Schnaas; Martha Maria Téllez-Rojo; Mauricio Hernández-Avila |
Related Documents
:
|
19427969 - Lepr p.q223r polymorphism influences plasma leptin levels and body mass index in tunisi... 17519829 - The genetics of nonalcoholic fatty liver disease. 15331789 - Genetic and environmental contributions to carotid intima-media thickness and obesity p... 18628339 - Resistance to diet-induced obesity in mice with a single substituted chromosome. 17438019 - Abnormal folate metabolism in foetuses affected by neural tube defects. 16025839 - Insulin gene variable number of tandem repeats is associated with increased fat mass du... 2767679 - Autosomal dominant polycystic kidney disease and alpha -4.2 thalassemia in a caucasian ... 18445609 - Association of angiotensin-converting enzyme gene 2350g>a polymorphism with myocardial ... 16368709 - Mitochondrial and nuclear dna defects in saccharomyces cerevisiae with mutations in dna... |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2010-05-26 |
Journal Detail:
|
Title: The American journal of clinical nutrition Volume: 92 ISSN: 1938-3207 ISO Abbreviation: Am. J. Clin. Nutr. Publication Date: 2010 Jul |
Date Detail:
|
Created Date: 2010-06-21 Completed Date: 2010-07-07 Revised Date: 2011-08-01 |
Medline Journal Info:
|
Nlm Unique ID: 0376027 Medline TA: Am J Clin Nutr Country: United States |
Other Details:
|
Languages: eng Pagination: 226-34 Citation Subset: AIM; IM |
Affiliation:
|
Department of Epidemiology, University of Michigan, Ann Arbor, MI, USA. rpils@umich.edu |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Adolescent Adult Bone and Bones / metabolism Child, Preschool Cognition Disorders / chemically induced*, genetics* Developmental Disabilities / epidemiology, genetics* Dietary Supplements Energy Intake Female Genetic Linkage Genotype Haplotypes Humans Lead / metabolism Lead Poisoning / genetics* Methylenetetrahydrofolate Reductase (NADPH2) / genetics* Mexico Mothers Parity Polymorphism, Genetic* Polymorphism, Single Nucleotide Postpartum Period Pregnancy Regression Analysis |
| Grant Support | |
ID/Acronym/Agency:
|
K01 ES014907/ES/NIEHS NIH HHS; K01 ES014907-05/ES/NIEHS NIH HHS; K23 ES000381/ES/NIEHS NIH HHS; P01 ES012874/ES/NIEHS NIH HHS; P30 ES00002/ES/NIEHS NIH HHS; P42 ES05947/ES/NIEHS NIH HHS; R01 ES007821/ES/NIEHS NIH HHS; R01 ES013744/ES/NIEHS NIH HHS; R01 ES014930/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
|
7439-92-1/Lead; EC 1.5.1.20/Methylenetetrahydrofolate Reductase (NADPH2) |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Short-term effect of cocoa product consumption on lipid profile: a meta-analysis of randomized contr...
Next Document: Seven isolates of Actinomyces turicensis from patients with surgical infections of the anogenital ar...