Therefore, these unshared individual-specific influences may be critical in understanding the link between EAU and SA. However, these findings also support the possibility of a causal pathway from EAU to SA. This is consistent with epidemiological research in multiple countries implicating EAU among boys and girls as a risk factor for SA (Kim and Kim 2010;Swahn et al. 2010;Swahn et al. 2012;Swahn and Bossarte 2007). All of these studies controlled for additional childhood risk factors, but importantly, did not control for shared familial influences. Thus, the current study enables the assertion that the link between EAU and SA is potentially independent from genetic or shared environmental factors.
