Addiction is a brain disease characterized by craving for a drug, loss of control over consumption, development of tolerance and dependence, while simultaneously the repertoire of social functioning not related to intake behavior declines dramatically.
To understand the factors that compel some individuals to consume excessively, addiction research has focused on the identification of brain mechanisms that support reinforcing actions of addictive compounds and the progression of changes in neural function induced by chronic consumption.
In research on alcohol dependence, prospective studies on high-risk populations showed an increased vulnerability of subjects with a high tolerance for adverse effects of ethanol. Cellular and molecular mechanisms of tolerance, sensitization and dependence have been investigated intensively. Addiction has now been proven to be a chemically altering state of brain activity.
The ability of ethanol and other addictive compounds to enhance dopamine neurotransmission particularly within the dopamine (‘reward’) system was repeatedly demonstrated.
However, the past decade has placed the dopamine system within a broader context of neuronal circuitry involved in drug seeking, drug taking and recovery. The new emphasis on various neuropeptide systems has reemerged, including opioid peptides like beta-endorphin and the stress-related peptides of the hypothalamus–pituitary–adrenal axis.
Continued research is warranted to identify the various neurobiological-based components of the ‘spiraling distress-addiction cycle’ that underlie the transition from the first intake to addiction.