Another model (Figure 2B) suggests that the various forms of impulsivity once again share a portion of their variance and mechanism with one another AND with addiction-related behaviors. It suggests that these tasks may well only share limited amounts of variance and mechanism but that this small similarity is exactly what links them each to addictions. In this case, the brain mechanisms they share in common should also be biomarkers often found in clinical drug addictions. It is notable, in this regard, that relatively low brain dopamine D2 receptor availability is both a biomarker for impulsive tendencies1, 31 and for substance use disorders.155, 266 Moreover, drug addictions have repeatedly been linked to structural and functional abnormalities in the same circuits implicated in impulsivity, namely the ventrolateral frontal cortex, ventromedial frontal cortex and limbic regions of the striatum.54, 266–271 From this perspective, a core set of neuroadaptations involving (perhaps) orbital and ventromedial frontal cortical dysfunction, reductions in brain dopamine D2 receptor signaling and/or altered serotonergic transmission that results from genetic or early environmental mechanisms OR from experience with the pharmacological effects
