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Fetal and postnatal metal dysregulation in autism

Author

Listed:
  • Manish Arora

    (Icahn School of Medicine at Mount Sinai)

  • Abraham Reichenberg

    (Icahn School of Medicine at Mount Sinai
    Seaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai)

  • Charlotte Willfors

    (Center of Neurodevelopmental Disorders (KIND)
    Center for Psychiatry Research, Stockholm County Council)

  • Christine Austin

    (Icahn School of Medicine at Mount Sinai)

  • Chris Gennings

    (Icahn School of Medicine at Mount Sinai)

  • Steve Berggren

    (Center of Neurodevelopmental Disorders (KIND)
    Center for Psychiatry Research, Stockholm County Council)

  • Paul Lichtenstein

    (Karolinska Institutet)

  • Henrik Anckarsäter

    (Institute of Neuroscience and Physiology, University of Gothenburg)

  • Kristiina Tammimies

    (Center of Neurodevelopmental Disorders (KIND)
    Center for Psychiatry Research, Stockholm County Council)

  • Sven Bölte

    (Center of Neurodevelopmental Disorders (KIND)
    Center for Psychiatry Research, Stockholm County Council)

Abstract

Genetic and environmental factors contribute to the etiologies of autism spectrum disorder (ASD), but evidence of specific environmental exposures and susceptibility windows is limited. Here we study monozygotic and dizygotic twins discordant for ASD to test whether fetal and postnatal metal dysregulation increases ASD risk. Using validated tooth-matrix biomarkers, we estimate pre- and post-natal exposure profiles of essential and toxic elements. Significant divergences are apparent in metal uptake between ASD cases and their control siblings, but only during discrete developmental periods. Cases have reduced uptake of essential elements manganese and zinc, and higher uptake of the neurotoxin lead. Manganese and lead are also correlated with ASD severity and autistic traits. Our study suggests that metal toxicant uptake and essential element deficiency during specific developmental windows increases ASD risk and severity, supporting the hypothesis of systemic elemental dysregulation in ASD. Independent replication in population-based studies is needed to extend these findings.

Suggested Citation

  • Manish Arora & Abraham Reichenberg & Charlotte Willfors & Christine Austin & Chris Gennings & Steve Berggren & Paul Lichtenstein & Henrik Anckarsäter & Kristiina Tammimies & Sven Bölte, 2017. "Fetal and postnatal metal dysregulation in autism," Nature Communications, Nature, vol. 8(1), pages 1-10, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15493
    DOI: 10.1038/ncomms15493
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    Cited by:

    1. Paul Curtin & Austen Curtin & Christine Austin & Chris Gennings & Kristiina Tammimies & Sven Bölte & Manish Arora, 2017. "Recurrence quantification analysis to characterize cyclical components of environmental elemental exposures during fetal and postnatal development," PLOS ONE, Public Library of Science, vol. 12(11), pages 1-16, November.

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