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Nat Commun. 2017 Jun 1;8:15493. doi: 10.1038/ncomms15493.

Fetal and postnatal metal dysregulation in autism.

Author information

1
Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, One Gustave L Levy Place, Box 1057, New York, New York 10029, USA.
2
Seaver Autism Center for Research and Treatment, Department of Psychiatry, Icahn School of Medicine at Mount Sinai, One Gustave L Levy Place, Box 1230, New York, New York 10029, USA.
3
Department of Women's and Children's Health, Center of Neurodevelopmental Disorders (KIND), Karolinska Institutet, Floor 8, Gävlegatan 22, SE-11330 Stockholm, Sweden.
4
Center for Psychiatry Research, Stockholm County Council, Norra Stationsgatan 69, Floor 7, SE-11364 Stockholm, Sweden.
5
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
6
Institute of Neuroscience and Physiology, University of Gothenburg, Box 430, SE-405 30 Göteborg, Sweden.

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.

PMID:
28569757
PMCID:
PMC5461492
DOI:
10.1038/ncomms15493
[Indexed for MEDLINE]
Free PMC Article

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