Lastly, density measures, like dichotomous/other FH measures do not parse apart the effects of biological and psychosocial aspects in their measurement of FH. Although, Zucker et al. (1994) included the extended family in their computation of FEA scores, they reasoned that it mostly represented genetic risk, while Stoltenberg et al. (1998) included only parents and grandparents in their FHD measure, and reasoned that it represented biopsychosocial risk comprising biological effects (genes inherited from parents and grandparents) and psychosocial effects (rearing environment, with the assumption that individuals are most often reared by parents and grandparents). Yet, FH measures are not pure indices of genetic risk, but represent a complex combination of psychosocial family effects (rearing environment, family harmony, cohesion etc.) that interact with one’s molecular genetic risk. Therefore, the inclusion of more (vs. limited) relatives does not necessarily increase the genetic risk or undermine the psychosocial risk components in FH measures. Rather, including contributions from known family members into the measurement of FH, likely increases the informativeness of the role of FH for both aspects (biological and psychosocial). The COGA study has molecular genetic (polygenic risk scores for alcohol-related behaviors) as well as environmental measures (e.g., parental monitoring, family conflict etc.)
