We still do not know if the `A', `C' and `E' in CU are the causal components in the relationship with CU or whether they index more distal phenotypic or broader genetic risks which predispose individuals to drug use which in turn mediates the risk of affiliating with deviant peers. However, we do know that the `A' and `C' risks are shared in common with the genetic and shared environmental risk for using and abusing cocaine, hallucinogens, sedatives, stimulants and opiates (81, 82), and that a number of other risks which CU might index have also been shown to elevate the risk of affiliating with deviant and drug using peers (5, 76, 78, 83). Environmental variables such as family structure (84–86) and adverse family environments (78) are predictive of PGD but the extent to which these are correlated with `A', `C' and `E' in CU remains unclear. Combined, our findings support the interpretation that the environmental and genetic risks explaining average cannabis use also mediate the risk of affiliating with deviant peers. This conclusion has implications for intervention and harm
