Abstract
The potentially deleterious effects on offspring health of excess maternal stress in pregnancy are important to understand-both whether observed associations are causal and through what mechanisms their effects may exert an influence. In this issue of the Journal, Räikkönen et al. (Am J Epidemiol. 2012;000(0):000-000) provide an ingenious test of a potential pathway through which maternal stress may influence offspring development. Licorice consumption is known to disrupt the ability of the placental enzyme 11β-hydroxysteroid dehydrogenase type 2 to inactivate cortisol before it reaches the fetus, leading to higher levels of cortisol exposure. Higher levels of cortisol exposure are also hypothesized to underlie the mechanism through which maternal stress may disrupt fetal development. Thus licorice consumption may serve, in some ways, to mimic maternal stress. The authors report associations between heavy licorice consumption during pregnancy and a wide range of offspring outcomes, including changes in pubertal timing, intelligence quotient, and mental health. In our view, these results should be considered preliminary; more work needs to be completed to determine the relationship of prenatal licorice consumption to these outcomes. Nonetheless, these intriguing and suggestive results demonstrate that this line of work should be given high priority, and they set the stage for additional research moving forward.