Antenatal antioxidants to avert autism?
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COMMENTARY
Antenatal antioxidants to avert autism? Alexander M. Quaas 1,2
&
William G. Kearns 3,4
Received: 12 October 2020 / Accepted: 13 October 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Paternally derived de novo mutations (DNMs) caused by oxidative stress (OS) have been implicated in the development of autism spectrum disorders (ASDs). Whether preconception antioxidant supplementation can reduce the incidence of ASDs by reducing OS is an area of uncertainty and potentially important future scientific investigation. Keywords Autism spectrum disorder . De novo mutations . Preconception counseling . Antioxidants
In this month’s issue, Staley explores the role of antioxidant supplementation for males to lower the risk of autism spectrum disorders (ASD) arising from de novo mutations (DNM) [1]. Autism is a multifactorial complex heterogeneous disorder diagnosed clinically based on a child’s developmental history and behavior [2]. As such it can be challenging to detect, and misdiagnosis is common. The severity of the disorder can vary greatly, and related developmental disabilities that used to be classified separately, such as Asperger syndrome, are now included in the diagnosis, hence the term “autism spectrum disorder” (ASD). In her opinion paper, Staley remarks that according to the Centers of Disease Control (CDC), ASD is the “fastest growing developmental disability” in the USA, with a prevalence increase of 1 in 468 in the 1990s to 1 in 54 currently. No genetic disorder in history has increased in prevalence over such a short period of time, suggesting that changes in diagnostic criteria as well as increased awareness and detection may at least be partly responsible for this staggering increase. From a molecular perspective, an autism-related genetic change can be identified in 25% of children [3], and an estimated 400–1,000 genes are likely involved in autism * Alexander M. Quaas [email protected] 1
Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of California, CA San Diego, USA
2
Reproductive Partners San Diego, 9850 Genesee Avenue, Suite # 800, La Jolla, San Diego, CA 92037, USA
3
Johns Hopkins University School of Medicine, Baltimore, MD, USA
4
AdvaGenix, Rockville, MD, USA
susceptibility [4]. Identified genetic causes of autism include chromosomal abnormalities, copy number variants (CNVs), and single-gene disorders [3]. Several hypotheses regarding the etiology of ASD exist. Advanced paternal age is one of the proposed potential primary causes. As males increase in age, more mutations accumulate during spermatogenesis. However, a simplistic pathophysiologic construct with paternal age as the sole etiology is inconsistent with the observed 4:1 male to female ratio of individuals with ASD. Staley succinctly summarizes the economic burden and proposed etiologies, with special focus on paternally derived de novo mutations (DNMs), the “single largest contributor” to autism risk. She provide
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