For example, investigations using oral alcohol challenges where alcohol is consumed in one continuous drink and paradigms giving alcohol in several servings with interspersed rest periods when alcohol plateaus, might not evaluate identical phenomena with identical genetic contributors. The same reservations apply to combining results from oral and IV alcohol paradigms, because in the latter BACs rise more rapidly, subjective responses tend to be more intense, and some IV paradigms included a phase where the BAC is maintained, with results that might reflect intrasession tolerance. Furthermore, alcohol challenges measure reactions over a relatively short laboratory session, but retrospective self-reports of drinks needed across effects relate to reactions during entire evenings of a real-life drinking. It might also be difficult to combine sensitivity results from studies of younger relatively alcohol-problem free modest drinkers (e.g., Schuckit et al., 2008) with the older heavy drinkers used to predict the escalation of baseline heavier drinking and binges (e.g., King et al., 2014). While it is possible that different methodologies to evaluate alcohol sensitivity might identify identical genes, researchers must consider that different combinations of
