Longitudinal Effects of Prenatal Alcohol Exposure on Visual Neurodevelopment Over Infancy

Emma T. Margolis*, Lauren Davel, Niall J. Bourke, Cara Bosco, Michal R. Zieff, Alexa D. Monachino, Thandeka Mazubane, Simone R. Williams, Marlie Miles, Chloë A. Jacobs, Sadeeka Williams, Layla Bradford, Candice Knipe, Zamazimba Madi, Bokang Methola, Tembeka Mhlakwaphalwa, Nwabisa Mlandu, Khanyisa Nkubungu, Zayaan Goolam Nabi, Tracy PanReese Samuels, Nicolò Pini, Vanja Klepac-Ceraj, William P. Fifer, Daniel C. Alexander, Derek K. Jones, Steve C.R. Williams, Dima Amso, Kirsten A. Donald, Laurel J. Gabard-Durnam

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)


Prenatal alcohol exposure (PAE) affects neurodevelopment in over 59 million individuals globally. Prior studies using dichotomous categorization of alcohol use and comorbid substance exposures provide limited knowledge of how prenatal alcohol specifically impacts early human neurodevelopment. In this longitudinal cohort study from Cape Town, South Africa, PAE is measured continuously—characterizing timing, dose, and drinking patterns (i.e., binge drinking). High-density electroencephalography (EEG) during a visual-evoked potential (VEP) task was collected from infants aged 8 to 52 weeks with prenatal exposure exclusively to alcohol and matched on sociodemographic factors to infants with no substance exposure in utero. First trimester alcohol exposure related to altered timing of the P1 VEP component over the first 6 months postnatally, and first trimester binge drinking exposure altered timing of the P1 VEP components such that increased exposure was associated with longer VEP latencies while increasing age was related to shorter VEP latencies (n = 108). These results suggest alcohol exposure in the first trimester may alter visual neurodevelopmental timing in early infancy. Exploratory individual-difference analysis across infants with and without PAE tested the relation between VEP latencies and myelination for a subsample of infants with usable magnetic resonance imaging (MRI) T1w and T2w scans collected at the same time point as EEG (n = 47). Decreased MRI T1w/T2w ratios (an indicator of myelin) in the primary visual cortex (n = 47) were linked to longer P1 VEP latencies. Results from these two sets of analyses suggest that prenatal alcohol and postnatal myelination may both separately impact VEP latency over infancy.

Original languageEnglish
JournalDevelopmental Psychology
Publication statusAccepted/In press - 2024


  • fetal programming
  • infant neurodevelopment
  • myelination
  • prenatal alcohol exposure
  • visual-evoked potential event-related potential


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