The etiological explanations supporting the role of adolescent exposure to cannabis use on later occurrence of (a) – (c) are amongst the most controversial and elusive. There are other outcomes (e.g. educational achievement, cognition and working memory) that have been addressed to a limited degree with genetic methodologies and hence, are not included (some of that research and a significantly extended description of the research presented here is reviewed elsewhere (33)). Several prospective methodologies have been brought to bear on these hypotheses, however, the unequivocal demonstration of causality is a challenge even in well-crafted longitudinal studies that allow for the statistical control of multiple confounding factors (34). In particular, genetic influences that might contribute to, for instance, both early cannabis use and subsequent illicit hard drug use need to be accounted for.
