This study was designed to elucidate the role of depression symptoms in psychosocial treatments for cocaine dependence by reanalyzing the NIDA CCTS data using HLG models. A better understanding of the interrelations between cocaine use and depression severity during treatment may provide a powerful key to improve psychosocial interventions for cocaine use disorders.
In line with previous findings (Rounsaville, 2004
; Weiss et al., 1989
), treatment-seeking cocaine-dependent outpatients in the NIDA CCTS reported substantial depressive symptomatology when entering treatment and depression severity was positively associated to drug use severity at study entry. The subsequent, rapid reduction of drug use during psychosocial treatments for cocaine dependence was accompanied by a similarly rapid reduction of depression symptoms (Brown et al., 1998
; Husband et al., 1996
). At a first glance, this rapid decrease of depression severity during treatment might be seen as indication that depression symptoms were primarily substance-induced (Lesswing and Dougherty, 1993
). However, our findings from multidimensional HLG model analysis suggest that, at least during psychosocial treatments, drug use severity does not affect future depression severity but that severity of ongoing depressive symptoms positively predicts drug use severity for the upcoming month. Given the rapid reduction of drug use in our sample, the lack of effects of drug use on depression severity also appears to contradict clinical observations that depressive symptoms may follow cessation of drug use (Dackis and Gold, 1987
; Gawin, 1986
; Gawin et al., 1989
). However, elevated depression symptoms are typically most apparent in the first 3 to 5 days after cessation of cocaine use (Weddington et al., 1990
) and, thus, it is possible that the monthly assessments in the NIDA CCTS may have failed to capture a transient increase in symptoms. In any event, it appears that reduction of drug use is not necessarily followed by longstanding depressive mood in patients receiving psychosocial interventions. The lack of direct effects of drug use on depression severity in our study also suggests that the strong decline in depression symptoms early in the course of treatment is probably directly attributable to other effects rather than mediated through a reduction of drug use. Because treatment seeking may be increased during peaks in substance use and depressive symptoms, the relatively high motivation of treatment-seeking cocaine dependents, coupled with an increase in morale fostered by the counselor or therapist, might be important factors for the rapid reduction of depression symptoms. However, other natural recovery processes independent of treatment as well as regression to the mean are likely also contributing factors to the rapid remission of depression symptoms (Conner et al., 2008
The impact of depressive symptoms on next month drug use appears to be clinically meaningful. The statistical model indicated that a change from a BDI score of 5, a score that is in the middle of the normal, non-clinical range, to a BDI score of 25, a score that is in the middle of the moderate-severe depression range (Beck et al., 1988
), in the next month would be associated with an ASI–Drug Use Composite score increase of 0.020. To put this ASI–Drug Use change in context, it is worth noting that post-baseline estimated average ASI–Drug Use Composite scores for the treatment effects in the NIDA CCTS were IDC+GDC: 0.096, CT+GDC: 0.117, SE+GDC: 0.114, and GDC alone: 0.116 (Crits-Christoph et al., 1999
). Thus, the impact of depressive symptoms changing from a non-clinical level to a moderate depression level is roughly equivalent to the post-baseline differences between treatment modalities in the NIDA CCTS.
The effects of depression symptoms on future drug use during treatment are in line with several reports that have demonstrated depression to affect aspects of cocaine use which are likely to lead to greater severity of drug use (Rounsaville, 2004
). For example, studies have shown that depressed cocaine users experience greater euphoria associated with cocaine administration (Newton et al., 2003
; Uslander et al., 1999
) and higher levels of physiologic cocaine effects (Sofuoglu et al., 2001
) than non-depressed users. Also, depression may hinder cessation of cocaine use as depressed cocaine users seem to experience more severe craving (Elman et al., 2002
) and more severe withdrawal symptoms (Helmus et al., 2001
) than non-depressed individuals when discontinuing drug use. These findings may help to explain the effects of depression on drug use severity during psychosocial treatments found in our study. The latter are in accordance with some previous findings that also suggest effects of depression on drug use severity among treatment-seeking cocaine users (Carroll et al., 1993
). Accordingly, our data do not support contrary previous findings suggesting a positive effect of depression on substance use severity (McKay et al., 2002
). Thus, the hypothesis that the experience of painful depression symptoms provides a strong incentive to desist from drug use because these symptoms represent compelling negative consequences of continued cocaine use (Rounsaville, 2004
) is not supported by our findings.
Concerning differential treatment effects of the four psychosocial interventions under consideration (IDC, CT, SE, and GDC), there were no significant differences between the treatments, neither with respect to the development of drug use nor in terms of the progression of depression severity during treatment. Thus, interestingly, professional psychotherapies (CT and SE) did not perform better than drug counseling approaches (IDC and GDC) in terms of reducing depression symptoms, as had been previously reported using a different analysis approach (Crits-Christoph et al., 2001
). On the other hand, the superiority of IDC to the three other treatments under consideration in terms of reducing drug use, which has been reported by Crits-Christoph et al. (1999)
, was also not evident with the analysis techniques used here. This failure to replicate the superiority of IDC might arise from the fact that the HLG model used in our study did also consider AR effects in the analysis of change, as well as the fact that the previously reported superiority of IDC included analysis of data from intake to month 12 (Crits-Christoph et al., 1999
), not just intake to month 6.
However, our study also has some limitations: First, if available, weekly collected urine specimens were used to examine the validity of self-reported drug use as measured by the ASI. Only 10% of the urine tests indicated some drug use during a month when the patient denied use. Despite this good agreement between urine test results and self-reports of cocaine use, whether patients were using cocaine at times when no urine assessments were available is unknown. Second, because the analyses were post-hoc exploratory analyses and due to the correlational nature of the findings precluding mechanistic conclusions, further research is necessary to replicate our findings with independent datasets. Third, change was assessed only during the treatment period and not longer-term, so the results do not tell us if depression severity influences treatment maintenance over longer time periods. Fourth, monthly psychometric assessments performed in the NIDA CCTS could have missed relatively short-term fluctuations in depressive symptoms (e.g., dysphoric mood that is inherent in cocaine withdrawal, according to the DSM-IV). Fifth, the randomized controlled nature of the NIDA CCTS, which brings some limitations concerning external validity, calls for further research to examine whether our findings do also apply to naturalistic settings and routine care. Sixth, it remains unclear whether our findings also generalize to cocaine-dependent patients with more severe psychiatric comorbidity (in particular with more severe depression) as current psychotropic medication was an exclusion criterion in the CCTS. Accordingly, our patients reported somewhat lower levels of baseline depression severity as measured by the BDI compared to other studies of treatment-seeking cocaine dependent outpatients (Husband et al., 1996
; Weiss et al., 1989
), perhaps as a result of the specific exclusion criteria used in the CCTS. Seventh, future studies should also examine additional predictors as well as change in other (e.g., biomedical) outcome measures. And finally, another direction for future research would be to evaluate possible subtypes of cocaine dependents based on the interplay between drug use and depression as the population of cocaine dependents is large and likely heterogeneous not only with respect to drug use outcomes (Stulz et al., 2010
) but also in terms of the interplay between drug use and depression. Such identification of more homogeneous subgroups could facilitate the development or tailoring of interventions designed to meet the specific needs of each subgroup.
In summary, the moderate but statistically significant effects of depression symptoms on increased drug use found in our study suggest that depression symptoms are an important predictor of drug use outcomes during psychosocial treatments for cocaine dependence and, thus, should be taken seriously when occurring among cocaine-dependent patients. This may also have clinical implications for the sequence of treatments or treatment components being offered to cocaine-dependent patients with co-occurring depression symptoms (Carroll et al., 2004
; Nunes et al., 2006
). In particular, the present findings suggest that psychosocial treatments for cocaine dependence should take specific measures to target the frequently co-occurring depression symptoms among cocaine-dependent patients to improve drug use outcomes.