Heterogeneity in the order of onset, on the other hand, would be consistent with (but again, not proof of) the existence of a third variable (e.g., shared genetic factors or pathophysiology)
serving as a common cause for both conditions. Further complicating
the picture, causal associations may manifest on an event level (e.g., alcohol use may disinhibit a wide range of inappropriate behaviors including problematic gambling [e.g., Smart and Ferris 1996]) or on a syndrome level (e.g., a new onset of PG occurring, ostensibly as a substitute for drinking, following alcoholism treatment [e.g., Ingram-Smith 1967; Lesieur and Heineman 1988]).
....
Dopamine may also play a major role in the regulation of this region’s functioning
(Kuhar et al. 1991; Self et al. 1996). In fact, researchers have theorized
that dysregulation in the systems supporting the activities of dopamine and the neurotransmitter serotonin may be central in both AUD and PG (Comings et al. 1996; Blum et al. 1995). Further, evidence suggests that specific genetic variations in the gene for the dopamine D2 receptor (a specific binding
molecule with which dopamine interacts) and the serotonin transporter gene may mediate, to some extent, individual differences in reward motivation
and responsiveness (Potenza 2001; Ibanez et al. 2001).
...
Researchers can estimate the extent of genetic versus environmental contributions
to specific behaviors and conditions
by contrasting their concordance between identical (i.e., monozygotic) and fraternal (i.e., dizygotic) twin pairs. In the only twin study that specifically examined these associations for PG and AUD, Slutske and colleagues (2000) reported that in a large male twin sample,
12 to 20 percent of the genetic variation in risk for PG and 3 percent to 8 percent of the nonshared environmental variation in the risk for PG was accounted for by risk for AUD
...
