Maternal Weight, Child Mind: Is Poor Cognitive Development a Foregone Conclusion?

Global obesity rates continue to rise, doubling in the last 35 years. Obesity now affects approximately 16% of individuals worldwide, but rates vary dramatically across the globe. With roots in genetics, the environment and psychosocial factors, obesity is a complex chronic disease with numerous comorbidities. For individuals of childbearing age, prepregnancy obesity may be the most common problem in obstetrics and may be particularly concerning due to the risk for intergenerational transmission of chronic morbidity. There may be pregnancy, obstetrical and birth complications, as well as short- and long-term health consequences for both parent and child. Maternal obesity has been linked to gestational diabetes mellitus, hypertension, preeclampsia, and lifelong cardiometabolic disease risk [1]. In offspring, maternal obesity may indicate future obesity, diabetes, elevated blood pressure, fatty liver and behaviour changes that may affect health into adulthood [2]. In addition to these potential consequences, it has been hypothesised that maternal obesity may impair child neurodevelopment, including increased risk for autism spectrum disorder, attention-deficit hyperactivity disorder (ADHD) and poorer cognitive abilities [3]. In this issue of Paediatric and Perinatal Epidemiology, Dow et al. [4] report associations of maternal obesity with offspring cognitive outcomes at 5 years in 1100 children born at term and 2629 born preterm (24–34 weeks) in France. The authors reported a 2.8-point lower full-scale intelligence quotient (IQ) at 5 years in children born term and a 2.6-point lower IQ in children born preterm to people with obesity, compared to counterparts born to individuals with a body-mass index (BMI) in the normal weight category. These findings support the growing base of literature indicating a potential association of prepregnancy obesity with adverse cognitive outcomes in offspring. When examining the risk for lower intellectual functioning (IQ < 85), Dow and colleagues found that prepregnancy obesity was associated with higher risk in both cohorts—especially for children born preterm. Adjustments for confounders included location, maternal age, education, household SES, parity, singleton birth (preterm cohort), paternal BMI and pre-existing maternal psychological conditions. Fundamentally, pregnancy is a period of adaptation and resilience. The maternal-foetal literature indicates a unified symbiosis in which the dyad alters its developmental course in response to internal and external cues. Hence, exploring the relationship between maternal exposures and child cognition requires considering many other factors linked to children's cognitive outcomes, including gestational weight gain (GWG) [5], prenatal mental health [6], socioeconomic status (SES) [7] and the home environment [8, 9]. Maternal obesity itself is associated with inflammatory and hormonal disruptions that may affect foetal neurodevelopment, including alterations in neuron proliferation, myelination and synapse formation. Elevated adiposity increases proinflammatory cytokines that may cross the placenta and impact brain development, while hormone dysregulation (e.g., insulin and leptin) may disrupt neurogenesis and connectivity. GWG further complicates this relationship, as excessive weight gain during pregnancy has separately been linked to poorer cognition in the offspring. Poorer maternal mental health also predicts child cognitive outcomes. Specifically, maternal stress, depression and anxiety have been linked to offspring's general cognitive function, executive function, as well as risk for ADHD [10], potentially through foetal programming of the hypothalamic–pituitary–adrenal axis. SES also plays a critical role—children from lower SES backgrounds are more likely to experience environmental stressors, such as limited access to healthcare and nutrition, that may exacerbate cognitive challenges imposed by maternal obesity. The home environment, including parenting quality and early childhood stimulation, can also either mitigate or exacerbate these associations: some evidence indicates that a nurturing home environment may remediate adverse effects of reproductive exposures on child neurodevelopment [8, 9]. Notably, inadequate adjustment for maternal intelligence or stimulation at home, such as with the Home Observation for Measurement of the Environment (HOME) inventory, may have biased previous findings. These factors underscore the complex interplay of biological, environmental and socioeconomic influences on child development, highlighting the need for a comprehensive approach when studying the impact of maternal exposures on child cognition. Pregnancy is a sensitive window for both maternal and child health, and study after study cites prepregnancy obesity as a modifiable risk factor. Guidelines now recommend weight loss before pregnancy for individuals with excess adiposity to reduce the risk of pregnancy complications. But whether prepregnancy body size is truly modifiable remains unclear. Most prepregnancy weight loss trials have focused on fertility rather than long-term outcomes; hence, findings are limited to conception and live birth or miscarriage. No weight loss threshold that attenuates potential pregnancy risks has been established. Moreover, weight loss or dieting before pregnancy may confer specific prenatal risks associated with nutritional status, for example, micronutrient insufficiency, indicating the need for medical curricula rooted in the guidance of nutritional quality and balance. Consequently, how preconception weight loss affects long-term maternal and child outcomes and what potential harms exist is not known. Large multicenter trials examining sustained weight loss with long-term outcomes are warranted, and researchers must consider the broader scope of obesity prevention since not all pregnancies are planned. While Dow and colleagues make a compelling case for a modest link between prepregnancy obesity and child cognitive ability, it is still unclear if the potential effects of prepregnancy adiposity on child outcomes can be mitigated before, during or after pregnancy. It is plausible that prepregnancy interventions could assist individuals in reducing BMI through dietary changes, physical activity and even medical treatment, but weight loss interventions are not universally effective or accessible. Moreover, obesity may coexist with other risk factors, including poor mental health and inadequate access to health care that may complicate intervention efforts. However, positive influences, such as maternal well-being and exposure to a nurturing environment, may have salutary effects during pregnancy and postpartum; interventions that also address the pre- and postnatal environment have further promise for protecting the developing foetus and child. This requires not only individual lifestyle changes but also structural changes, such as improved access to nutritious food, healthcare and mental health support—particularly for marginalised individuals in the context of structural racism. Public health strategies to address obesity, particularly before pregnancy, through a multi-pronged approach may have an important role in improving maternal and child health outcomes. There is no sign that the obesity epidemic is slowing, and the potential impact of maternal obesity on child cognitive outcomes is only one piece of a much larger, complex puzzle. Further exploration is required to disentangle causation and direct intrauterine effects of reproductive morbidity. Likewise, more evidence from diverse populations, as well as early intervention, access to resources and a focus on holistic health (not just BMI) are essential considerations. So, is obesity a potentially modifiable risk factor that could attenuate child risk before pregnancy? Evidence points to this possibility, but the risk does not signify an inevitability. Developmental trajectories begin—but do not end—in utero. Amy R. Nichols is solely responsible for the content of this commentary. The author declares no conflicts of interest.