Research & Evidence

Evidence brief: Maternal obesity and prenatal alcohol exposure are associated with child development: Results from the Safe Passage Study

A sourced PLOS One study, published 2026-04-06. Read the researchers’ findings, methods and context, with links to connected African health evidence.

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Published in PLOS One on 2026-04-06, this study is presented as an attributed evidence briefing. The excerpts below are the original researchers’ words, reproduced under their Creative Commons Attribution licence. Health Signal has selected the abstract and, where needed, opening background paragraphs; the complete methods, results, limitations and references remain in the linked paper.

Original authors: Ayesha Sania, Shreya Rao, Nicolò Pini, Mandy Potter, Yael Rayport, Liana Eisler, Lucy Brink, Jyoti Angal, Michael M Myers, Hein Odendaal, Amy J Elliott, William P Fifer, Lauren C Shuffrey, Emma K Kalk

Source: PLOS One • DOI 10.1371/journal.pone.0345406

Read the complete primary study ↗ · Creative Commons Attribution licence

From the researchers

Abstract

A large body of evidence supports the role of the prenatal environment in shaping childhood development. The relative contributions of prenatal alcohol use (PAE), maternal socioeconomic, and nutritional status on child development vary in high- versus low-income settings. We analyzed data from a prospective cohort study among mother-infant dyads from Cape Town (CT), South Africa and the Northern Plains (NP), USA. The Mullen Scales of Early Learning were administered by trained assessors to evaluate cognitive, motor, and language development of 1-year old children. We used multiple linear regression models to assess standardized mean differences in development scores by (1) maternal prenatal factors, (2) delivery factors and (3) child factors within each study site. 1,728 infants from CT and 1,140 infants from the NP were included in the analyses. In CT, infants with moderate-to-high PAE had 0.17 SD (95% CI −0.30, −0.04) lower cognitive and 0.15 SD (−0.29, −0.2) lower expressive language scores compared to infants without PAE. In the NP, maternal obesity (BMI > 30 kg/m2) was significantly associated with −0.21 SD (−0.36, −0.06), and −0.13 SD (−0.27, −0.02) reductions in cognitive, and expressive language scores, respectively. Household crowding, lower levels of maternal educational attainment, prenatal maternal depression, low birthweight, admission to neonatal intensive care unit, and male sex had significant negative associations with cognitive and language development in both sites with effects ranging from −0.32 to −0.11 SDs. These results highlight the importance of assessing risk factors by populations across diverse social and cultural environments and emphasize the imperative to formulate intervention packages tailored to the local context.

Introduction

Understanding the predictors of early childhood development to support policy and intervention programs is a key priority worldwide, particularly in low-to-middle income countries (LMICs) where the majority of the world’s children reside. According to recent estimates, a third (80 million) of the 3 and 4-year-old children in LMICs do not attain their full developmental potential [1]. Early cognitive, language, and socioemotional development are key determinants of future educational and income achievement in adult life [2]. Suboptimal development in the early childhood period can have a lasting impact on the life course of individuals as well as the larger society. Therefore, understanding the independent contributions prenatal exposures on child developmental outcomes is a significant global public health priority.

The prenatal period is a critical developmental window that has the potential to shape long-term health outcomes for offspring through fetal programming mechanisms. A growing body of research within the developmental origins of health and disease (DOHaD) framework highlights how adverse in-utero environmental factors including poor maternal nutritional status, exposure to harmful chemicals, crowded living conditions, and socioeconomic challenges impact children’s cognitive, motor, and language development [3–6]. The impact of risk factors on child development varies between high- and low-income settings, reflecting important contextual differences in exposure patterns, socioeconomic status, and postnatal environments. For example, research from low-income settings consistently reports harmful effects of prenatal alcohol exposure (PAE) on both cognitive and motor skills [7–10], whereas the same patterns are not observed in high-income contexts [11–13], which suggests positive environmental factors in high-income settings might buffer the impact of PAE. Albeit, in high income settings, epidemiologic evidence demonstrates clear neurodevelopmental harm associated with prenatal alcohol exposure at moderate to higher levels [14,15]. Apparent protective effects of mild drinking are potentially explained by the confounding effects of maternal education and favorable socioeconomic conditions [16–18]. In addition, the null effects of PAE on child development in high income settings could be due to an enriched postnatal environment which acts as a buffer to the harmful effects of PAE on child development.

Reading this evidence

Use the full paper to check the study design, participant selection, comparator and outcome definitions before drawing a practical conclusion. An association does not by itself show cause and effect. A reported performance measure needs its denominator and uncertainty. A finding from a particular facility, sample or time period should retain that scope when it is discussed elsewhere.

This briefing makes the source accessible within the wider research & evidence desk. It does not assess an individual patient or certify a product. When considering relevance to another health system, examine the original authors’ account of context and limitations, then seek local implementation evidence. The related reporting below provides other studies to read alongside this one; it is a topic connection, rather than a claim that their results are directly comparable.

© 2026 Ayesha Sania, Shreya Rao, Nicolò Pini, Mandy Potter, Yael Rayport, Liana Eisler, Lucy Brink, Jyoti Angal, Michael M Myers, Hein Odendaal, Amy J Elliott, William P Fifer, Lauren C Shuffrey, Emma K Kalk. Excerpts reproduced under CC BY. Selection, formatting and contextual notes by Health Signal. The researchers are the authors of the source study, not members of Health Signal’s staff.

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Health Signal’s publication desk curates source-based health analysis and attributed research briefings. Study authors and originating institutions are credited within each article. Preparation used AI assistance; source and licence checks do not constitute independent replication or clinical endorsement.

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