A Review of the Effects of Maternal and Paternal Obesity on Neurodevelopmental Disorders and Related Neurobiology in Rodent and Human Offspring.

Obesity is one of the most prevalent health problems worldwide, and global obesity rates continue to rise. Consequently, rates of obesity in expecting mothers and fathers have also increased. The Developmental Origins of Health and Disease (DOHaD) hypothesis postulates that early-life exposure to adverse environmental conditions contributes to the increased risk of noncommunicable disease later in life. In this context, much work has been done to understand how parental obesity can affect the long-term health of offspring. In terms of offspring brain health and function, evidence suggests that elevated maternal body mass index (BMI) is associated with an increased risk of autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), and anxiety disorders, as well as deficits in learning and memory in offspring. Less well characterized is the impact of paternal obesity on the offspring brain. A limited number of studies have reported an association between paternal obesity and altered offspring neurodevelopment, including a higher risk of the offspring having neurodevelopmental disorders such as ASD and ADHD. Mechanisms proposed to underlie these effects include epigenetic modifications, placental changes, and alterations in neuronal protein expression. Here, we review the body of evidence supporting a neurodevelopmental impact of maternal and paternal obesity and associated biological mechanisms. Understanding how parental obesity influences offspring brain function has important implications for the advice given to people trying to get pregnant and expecting mothers, and provides vital insight into the contribution of parental health toward offspring brain health across the life course.