IDEAS home Printed from https://ideas.repec.org/a/gam/jijerp/v17y2020i24p9190-d459168.html
   My bibliography  Save this article

Prenatal Multivitamin Use and MTHFR Genotype Are Associated with Newborn Cord Blood DNA Methylation

Author

Listed:
  • Kelly M. Bakulski

    (Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI 48109, USA)

  • John F. Dou

    (Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI 48109, USA)

  • Jason I. Feinberg

    (Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA)

  • Katharine K. Brieger

    (Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI 48109, USA)

  • Lisa A. Croen

    (Division of Research, Kaiser Permanente, Oakland, CA 94612, USA)

  • Irva Hertz-Picciotto

    (Department of Public Health Sciences and the M.I.N.D. Institute, School of Medicine, University of California, Davis, CA 95616, USA)

  • Craig J. Newschaffer

    (College of Health and Human Development, Penn State University, State College, PA 16802, USA)

  • Rebecca J. Schmidt

    (Department of Public Health Sciences and the M.I.N.D. Institute, School of Medicine, University of California, Davis, CA 95616, USA
    These authors contributed equally as co-senior authors.)

  • M. Daniele Fallin

    (Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA
    These authors contributed equally as co-senior authors.)

Abstract

Background: Fetal development involves cellular differentiation and epigenetic changes—complex processes that are sensitive to environmental factors. Maternal nutrient levels during pregnancy affect development, and methylene tetrahydrofolate reductase ( MTHFR ) is important for processing the nutrient folate. Hypothesis: We hypothesize that supplement intake before pregnancy and maternal genotype are associated with DNA methylation in newborns. Methods: In the pregnancy cohort, Early Autism Risk Longitudinal Investigation (EARLI), health history, and genotype information was obtained (n = 249 families). Cord blood DNA methylation (n = 130) was measured using the Illumina HumanMethylation450k array and global DNA methylation levels were computed over 455,698 sites. Supplement use preconception and during pregnancy were surveyed at visits during pregnancy. We evaluated associations between maternal preconception supplement intake and global DNA methylation or DNA methylation density distributions of newborn cord blood, stratified by the presence of a variant maternal MTHFR C677T allele. Results: Maternal preconceptional multivitamin intake was associated with cord blood methylation, dependent on maternal MTHFR genotype (interaction term p = 0.013). For mothers without the MTHFR variant allele, multivitamin intake was associated with 0.96% (95% CI: 0.09, 1.83) higher global cord blood methylation ( p = 0.04) and was also associated with the cumulative density distribution of methylation ( p = 0.03). For mothers with at least one variant allele, multivitamin intake had a null −0.06% (95% CI: −0.45, 0.33) association with global cord blood DNA methylation, and was not associated with the cumulative density distribution ( p = 0.37). Conclusions: We observed that cord blood DNA methylation was associated with maternal supplement exposure preconception and maternal genotype. Genetic context should be considered when assessing DNA methylation effects of modifiable risk factors around the time of pregnancy.

Suggested Citation

  • Kelly M. Bakulski & John F. Dou & Jason I. Feinberg & Katharine K. Brieger & Lisa A. Croen & Irva Hertz-Picciotto & Craig J. Newschaffer & Rebecca J. Schmidt & M. Daniele Fallin, 2020. "Prenatal Multivitamin Use and MTHFR Genotype Are Associated with Newborn Cord Blood DNA Methylation," IJERPH, MDPI, vol. 17(24), pages 1-16, December.
    • Handle: RePEc:gam:jijerp:v:17:y:2020:i:24:p:9190-:d:459168
    as

    Download full text from publisher

    File URL: https://www.mdpi.com/1660-4601/17/24/9190/pdf
    Download Restriction: no
    File URL: https://www.mdpi.com/1660-4601/17/24/9190/
    Download Restriction: no
    ---><---

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:gam:jijerp:v:17:y:2020:i:24:p:9190-:d:459168. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: MDPI Indexing Manager (email available below). General contact details of provider: https://www.mdpi.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.