Population-based longitudinal studies showing an association between elevated concentrations of IL-6 or CRP at baseline and increased risk of depression at follow-up indicates reverse causality is an unlikely explanation for previously observed association between IL-6 and depression.8–11 Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort, we have reported that elevated concentrations of serum IL-6 in childhood are associated with increased risk of depression subsequently in early adulthood in a linear, dose–response fashion9 (figure 1A). This evidence concerns the gene CRP and depressive symptom measurement.