The plausibility of maternal toxicant exposure and nutritional status as contributing factors to the risk of autism spectrum disorders

Nuttall, JR

HERO ID

5497933

Reference Type

Journal Article

Subtype

Review

Year

2017

Language

English

PMID

26613405

HERO ID 5497933
Material Type Review
In Press No
Year 2017
Title The plausibility of maternal toxicant exposure and nutritional status as contributing factors to the risk of autism spectrum disorders
Authors Nuttall, JR
Journal Nutritional Neuroscience
Volume 20
Issue 4
Page Numbers 209-218. [Nutritional neuroscience]
Abstract Recent research suggests the maternal environment may be especially important for the risk of developing autism spectrum disorders (ASD). In particular maternal infections, micronutrient deficiencies, obesity, and toxicant exposures are likely to interact with genetic risk factors to disrupt fetal brain development. OBJECTIVES: The goal of this paper is to investigate the plausibility of maternal toxicant exposure and nutritional status as causal factors in the development of ASD. METHODS: This paper reviews current research investigating the hypothesis that maternal toxicant exposure and prenatal micronutrient intake are important modifiable risk factors for ASD. RESULTS: Zinc, copper, iron, and vitamin B9 are identified as specific micronutrients with relevance to the etiology of ASD. Specific toxicants induce a maternal inflammatory response leading to fetal micronutrient deficiencies that disrupt early brain development. Importantly, maternal micronutrient supplementation is associated with reduced risk of ASD. Furthermore, animal studies show that micronutrient supplementation can prevent the teratogenicity and developmental neurotoxicity of specific toxicants. DISCUSSION: These findings lead to the hypothesis that maternal infection, obesity, and toxicant exposures (e.g. valproic acid, endocrine disrupting plasticizers, ethanol, and heavy metals) are all environmental risk factors for ASD that lead to fetal micronutrient deficiencies resulting from a maternal inflammatory response. It could be possible to use markers of inflammation and micronutrient status to identify women that would benefit from micronutrient supplementation or dietary interventions to reduce the risk of ASD. However, more research is needed to demonstrate a causal role of fetal micronutrient deficiencies and clarify the underlying mechanisms that contribute to ASD.
Doi 10.1080/1028415X.2015.1103437
Pmid 26613405
Wosid WOS:000399673200001
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword Animals; Autism Spectrum Disorder/etiology; Benzhydryl Compounds/blood/toxicity; Brain/drug effects/embryology; Diethylhexyl Phthalate/blood/toxicity; Disease Models, Animal; Ethanol/blood/toxicity; Fetal Development/drug effects; Homeostasis; Inflammation/blood/complications; Maternal Exposure/adverse effects; Metals, Heavy/blood/toxicity; Micronutrients/blood/deficiency; Nutritional Status; Obesity/blood/complications; Phenols/blood/toxicity; Pregnancy; Risk Factors; Valproic Acid/blood/toxicity; Developmental neurotoxicity; Inflammation; Maternal nutrition; Micronutrients; Risk factor; 3K9958V90M; 614OI1Z5WI; C42K0PH13C; MLT3645I99