The association between maternal obesity and increased risks of stillbirth and infant mortality is well documented, but it has often been questioned whether the association is driven by obesity per se or by unmeasured factors such as insulin resistance or genes. In this issue of the Journal, Lindam et al. (Am J Epidemiol. 2016;184(2):98-105) present results from a sibling case-control study which strongly support that these tragic outcomes are independent of genetic and early environmental risk factors shared within families. By sampling sisters from the Swedish Medical Birth Register, Lindam et al. compared the body mass indices (weight (kg)/height (m)(2)) of women who had stillbirths and infant deaths with those of their sisters or of population controls. Significant excess risks of both outcomes were observed in obese women (body mass index ≥30), and associations were strongest when sister controls were used. Although this careful analysis adds to the existing evidence of a causal relationship between maternal obesity and impaired fetal and infant survival, a biological pathway has not yet been established. Additionally, we are in urgent need of effective tools to reduce obesity in childbearing women and to identify and treat high-risk pregnancies.