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6. CONCURRENT DISORDERS

antidepressant) had at least three consecutive cocaine-free weeks compared
with only 5% of those treated with placebo (Nunes et al., 1995). These results
suggest that psychostimulant users may consume psychostimulants in an
attempt to self-medicate an underlying negative affective state (Khantzian,
1997; Markou, Kosten & Koob, 1998).
In humans psychostimulant withdrawal is characterized by severe mood
disturbances including depressive symptoms combined with irritability and
anxiety (Gawin & Kleber, 1986; Weddington et al., 1990; Satel et al., 1991;
American Psychiatric Association, 1994). These symptoms last from several
hours to days, one of the most salient being anhedonia (i.e. diminished
interest or pleasure), which is also a core symptom of depression.This
anhedonia may be one of the motivating factors in the etiology and
maintenance of the cycle of psychostimulant dependence. Thus, the similarity
between a major depressive episode and psychostimulant withdrawal further
supports the hypothesis that there are overlapping neurobiological substrates
that mediate these depressive symptoms that are common to the two
disorders. Again, the mesolimbic dopamine system seems to be a likely
candidate that mediates both the reward of substance use, and the lack of
pleasure associated with substance withdrawal and depression. In the case
of psychostimulant dependence, it is clear that, at least in some cases, the
depressive symptoms are drug-induced. Substance use may also reflect an
attempt to self-medicate a pre-existing depression.

Alcohol use and depression
Studies in the United States over the past 20 years indicated that lifetime rates
of major depressive disorder were 38–44% in people with alcohol dependence
compared with only 7% in non-dependent individuals (Rounsaville et al.,
1982; Myers et al., 1984; Robins et al., 1984; Rounsaville, 1987; Robins & Reiger,
1991; Rounsaville et al., 1991; Kessler et al., 1994; Miller et al., 1996b; Schuckit
et al., 1997a, 1997b). Furthermore, approximately 80% of people with alcohol
dependence had symptoms of depression (Schuckit, 1985; Regier et al., 1990;
Roy et al., 1991; Kessler et al., 1996). Thus, there is substantial data indicating
that the rates of depression among people with alcohol dependence and the
rates of alcohol use among people with depression are substantially higher
than expected from the individual rates of these disorders.
Although not consistent, other evidence supporting the hypothesis that
depression and alcohol dependence are linked disorders comes from clinical
studies indicating that in some cases antidepressant treatment resulted in
both improvement in mood and reduction in alcohol use. People with
depression who are dependent on alcohol show lower rates of relapse to
alcohol use when treated with antidepressants (e.g. imipramine or fluoxetine),
compared with subjects who were given a placebo, either with or without
depression (Nunes et al., 1993; Cornelius et al., 1995; McGrath et al., 1996;
Mason et al., 1996). These observations in people with depression and alcohol

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