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Letters to the EditorFull Access

The Role of Perinatal Risk in Neurodevelopmental Pathways to Early Childhood Disruptive Behavior: Response to Bell and Ajula

To the Editor: We thank Dr. Bell and Jessie Ajula for noting the critical role of adverse prenatal exposures in neurodevelopmental pathways and appreciate the opportunity to address their comments. Because of the focused nature of our Review and Overview article, space did not allow an in-depth discussion of the role of specific perinatal risk factors in neurodevelopmental pathways to disruptive behavior as well as the wider array of pediatric mental health issues. As Bell and Ajula note, a broad literature links fetal alcohol exposure as well as many other environmental exposures to developmental psychopathology. In fact, as we note in our discussion, these associations likely arise through interactions between the environment and neurodevelopment in multiple risk pathways, including the two targeted phenotypes in our review. Indeed, prenatal mechanisms of disruptive behavior and other early-onset psychopathologies are a critical area for future research and prevention. Our central point had been that progress might arise through a focus in such research on both broad behavioral tendencies as well as relatively narrow phenotypes and their associated pathways, which provide a bridge to neuroscience research.

The authors specifically inquire about the role of prenatal alcohol exposure in disruptive behavior, posing several potential mechanisms by which this exposure may amplify risk. This clearly raises important questions requiring in-depth examination beyond the scope of this letter to the editor. Moreover, the centrality of irritability in the phenotype of children with fetal alcohol syndrome is well documented. Nevertheless, extensive research also links this and other neurodevelopmental phenotypes to a diverse range of other exposures both in the perinatal period and at later points in development. These include various forms of psychosocial stress, cigarette smoke, illicit drugs, and other environmental toxins (16). Thus, research on the contribution of perinatal risk should be comprehensive and far reaching with an emphasis on unique and common pathways across diverse exposures at distinct points in development. Such consideration is of great importance for neuropsychiatric explication of the origins of mental disorders, which begin even before birth.

From the Department of Medical Social Sciences, Institute for Innovations in Developmental Sciences, and the Institute for Policy Research, Northwestern University, Chicago; and the National Institute of Mental Health, Bethesda, Md.
Address correspondence to Dr. Wakschlag ().

The authors’ disclosures accompany the original article.

References

1 Clark CA, Espy KA, Wakschlag L: Developmental pathways from prenatal tobacco and stress exposure to behavioral disinhibition. Neurotoxicol Teratol 2016; 53:64–74Crossref, MedlineGoogle Scholar

2 Demir-Lira ÖE, Voss JL, O’Neil JT, et al.: Early-life stress exposure associated with altered prefrontal resting-state fMRI connectivity in young children. Dev Cogn Neurosci 2016; 19:107–114Crossref, MedlineGoogle Scholar

3 Ericson JE, Crinella FM, Clarke-Stewart KA, et al.: Prenatal manganese levels linked to childhood behavioral disinhibition. Neurotoxicol Teratol 2007; 29:181–187Crossref, MedlineGoogle Scholar

4 Estabrook R, Massey SH, Clark CA, et al.: Separating family-level and direct exposure effects of smoking during pregnancy on offspring externalizing symptoms: bridging the behavior genetic and behavior teratologic divide. Behav Genet 2016; 46:389–402Crossref, MedlineGoogle Scholar

5 Fisher PA, Lester BM, DeGarmo DS, et al.: The combined effects of prenatal drug exposure and early adversity on neurobehavioral disinhibition in childhood and adolescence. Dev Psychopathol 2011; 23:777–788Crossref, MedlineGoogle Scholar

6 Massey SH, Hatcher AE, Clark CAC, et al.: Does MAOA increase susceptibility to prenatal stress in young children? Neurotoxicol Teratol 2017; 61:82–91Crossref, MedlineGoogle Scholar