期刊
NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/ncomms15493
关键词
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资金
- Swedish Research Council
- Knut and Alice Wallenberg Foundation
- European Union [115300]
- Swedish Research Council [523-20097054, 521-2013-2531]
- Swedish Research Council for Health, Working Life and Welfare
- Formas
- VINNOVA [259-2012-24]
- Stockholm County Council [20100096, 20110602, 20120067, 20140134]
- Stiftelsen Frimurare Barnhuset
- Sunnerdahls
- Handikappfond
- Hjarnfonden
- National Institutes of Environmental Health Sciences [DP2ES025453, R00ES019597, P30ES023515]
- Mindich Child Health and Development Institute pilot grants
- Swedish Foundation for Strategic Research
- Jeanssons foundation
- National Institutes of Health
- Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institute of Environmental Health Sciences [HD073978]
- National Institute of Neurological Disorders and Stroke
- National Institute of Mental Health [MH097849]
- Beatrice and Samuel A. Seaver Foundation
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.
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