In this issue of the IJE, Casas and colleagues 1 report associations of maternal pre-pregnancy obesity with lower infant cognitive development scores in two European cohorts, RHEA and INMA. This was observed after extensive confounder adjustment (in particular, multiple indicators of socioeconomic position) and results were replicated across the two cohorts, reflecting two important methodological strengths of the paper. This paper is timely as it contributes to a body of literature on maternal obesity and offspring cognitive ability that is currently sparse and relatively inconclusive. Although independent associations have been reported in several previous studies, inconsistent 2 and predominantly null 3 associations have also been observed when multiple cohorts have been investigated simultaneously. Nevertheless, the persisting associations observed independently of a comprehensive range of sociodemographic and postnatal factors, here and elsewhere, raise the question as to whether maternal obesity might adversely affect cognitive development in offspring via intrauterine mechanisms. In the presence of escalating rates of obesity worldwide, this association warrants further study since, if causal, this would clearly be an increasing public health concern. A crucial step in investigating the association of maternal obesity with offspring cognitive development, above and beyond replication of results, is to disentangle adjusted associations that are due to intrauterine mechanisms from those that reflect residual cofounding by postnatal, socioeconomic and familial factors not fully captured by the measured confounders. As can be seen from the results in the main paper and supplementary information, maternal obesity and lower infant cognitive scores were both associated with less favourable sociodemographic factors in this study (lower parental education, lower occupational social class, shorter breastfeeding duration etc.). Furthermore, confounder associations (namely, with infant cognitive scores) appeared stronger in RHEA, compared with INMA. Since the unadjusted association for maternal obesity and infant cognition was also substantially larger in RHEA (6.00, vs 3.37 in INMA), and this reduced markedly, resulting in similar effect sizes across the cohorts following confounder adjustment, confounding factors therefore appear to account for a substantial proportion of the observed relationship between maternal obesity and offspring cognition, at least at the unadjusted level. Given the known difficulties in fully capturing confounding, particularly socioeconomic,