Maternal lifestyle and environmental risk factors for autism spectrum disorders

Lyall, Kristen; Schmidt, Rebecca Jean; Hertz‐Picciotto, Irva

doi:10.1093/ije/dyt282

Cited by 344 publications

(253 citation statements)

References 156 publications

(167 reference statements)

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“…Recently, we demonstrated the efficacy of sulforaphane as an environmental detoxicant (36). Together with sulforaphane's capacity to activate the Keap1-Nrf2 cytoprotective signaling pathway (10), it may therefore protect against both environmental and endogenous risk factors that affect brain development in ASD (37). Given its favorable safety profile, future ABC and SRS total scores of participants who completed at least one postintervention measurement (n = 40).…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane treatment of autism spectrum disorder (ASD)

Singh

Connors

Macklin

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

362

261

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Autism spectrum disorder (ASD), characterized by both impaired communication and social interaction, and by stereotypic behavior, affects about 1 in 68, predominantly males. The medicoeconomic burdens of ASD are enormous, and no recognized treatment targets the core features of ASD. In a placebo-controlled, double-blind, randomized trial, young men (aged 13-27) with moderate to severe ASD received the phytochemical sulforaphane (n = 29)-derived from broccoli sprout extracts-or indistinguishable placebo (n = 15). The effects on behavior of daily oral doses of sulforaphane (50-150 μmol) for 18 wk, followed by 4 wk without treatment, were quantified by three widely accepted behavioral measures completed by parents/caregivers and physicians: the Aberrant Behavior Checklist (ABC), Social Responsiveness Scale (SRS), and Clinical Global Impression Improvement Scale (CGI-I). Initial scores for ABC and SRS were closely matched for participants assigned to placebo and sulforaphane. After 18 wk, participants receiving placebo experienced minimal change (<3.3%), whereas those receiving sulforaphane showed substantial declines (improvement of behavior): 34% for ABC (P < 0.001, comparing treatments) and 17% for SRS scores (P = 0.017). On CGI-I, a significantly greater number of participants receiving sulforaphane had improvement in social interaction, abnormal behavior, and verbal communication (P = 0.015-0.007). Upon discontinuation of sulforaphane, total scores on all scales rose toward pretreatment levels. Dietary sulforaphane, of recognized low toxicity, was selected for its capacity to reverse abnormalities that have been associated with ASD, including oxidative stress and lower antioxidant capacity, depressed glutathione synthesis, reduced mitochondrial function and oxidative phosphorylation, increased lipid peroxidation, and neuroinflammmation.

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Section: Discussionmentioning

confidence: 99%

Sulforaphane treatment of autism spectrum disorder (ASD)

Singh

Connors

Macklin

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

362

261

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“…60 This is relevant in the central nervous system, given that the oxidative stress threshold required for the p53-induced pro-oxidant effects in neurons is lower than those reported in any other cell type. 61 Taken together, instability in the p53 genomic region (haploinsufficiency, or altered CN) might set a background of heightened susceptibility for other detrimental triggers (environmental exposures, 33, 62 use of maternal medications and/or metabolic status, 63,64 other diseases [65][66][67][68] ) influencing the progeny outcome, especially during highly susceptible periods of development, such as perinatal stages.…”

Section: Discussionmentioning

confidence: 99%

Role ofp53, Mitochondrial DNA Deletions, and Paternal Age in Autism: A Case-Control Study

Wong¹,

Napoli²,

Krakowiak³

et al. 2016

Pediatrics

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The tumor suppressor p53 responds to a variety of environmental stressors by regulating cell cycle arrest, apoptosis, senescence, DNA repair, bioenergetics and mitochondrial DNA (mtDNA) copy number maintenance. Developmental abnormalities have been reported in p53-deficient mice, and altered p53 and p53-associated pathways in autism (AU). Furthermore, via the Pten-p53 crosstalk, Pten haploinsufficient-mice have autisticlike behavior accompanied by brain mitochondrial dysfunction with accumulation of mtDNA deletions.

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“…This study contributes to the ongoing debate about the long-term consequences of in utero exposure to nicotine on children's behavior [25]. Interestingly, studies examining the association between maternal prenatal smoking and ASD have generally reported no association [18], but given secular changes in diagnostic criteria of ASD and increased case recognition with time, this topic that requires additional research.…”

Section: Introductionmentioning

confidence: 86%

Commonalities and specificities between attention deficit/hyperactivity disorder and autism-spectrum disorders: can epidemiology contribute?

Melchior

Pryor²

2015

Eur Child Adolesc Psychiatry

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International audienceAttention deficit/hyperactivity disorder (ADHD) and autism spectrum disorders (ASD) are among the most frequent neurodevelopmental disorders in children and adolescents (5.9–7.1 % prevalence for ADHD [28] and approximately 0.62–0.70 % for ASD [17]). Core symptoms as well as treatment differ between these two disorders, yet some characteristics are shared, including symptoms of inattention, social dysfunction, and difficult behavior (e.g. tantrums, aggression) [2]. What is more, these two multifactorial disorders frequently co-occur [6] and have several risk factors in common (e.g. male sex, low birth weight, in utero neurotoxic exposures, low family socioeconomic position) [7, 8]. This raises questions regarding (1) the specificity of underlying etiological factors, (2) the degree of functional impairment across different profiles of comorbidity and (3) optimal treatment—particularly for children who have both ADHD and ASD [6]. Epidemiology can help gain a better understanding of the origins and consequences of ADHD and ASD, and several articles in this month’s issue of European Child and Adolescent Psychiatry provide a brilliant illustration. [...

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Maternal lifestyle and environmental risk factors for autism spectrum disorders

Cited by 344 publications

References 156 publications

Sulforaphane treatment of autism spectrum disorder (ASD)

Sulforaphane treatment of autism spectrum disorder (ASD)

Role ofp53, Mitochondrial DNA Deletions, and Paternal Age in Autism: A Case-Control Study

Commonalities and specificities between attention deficit/hyperactivity disorder and autism-spectrum disorders: can epidemiology contribute?

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