In agreement with previous studies (Saxon et al., 1993
; Budney et al., 1998
; Nirenberg et al., 1996
), cannabis use showed little relation to use of heroin or cocaine. Specifically, there was no linear dose-response relationship from nonuse to intermittent use to frequent use of cannabis, nor was there an inverted-U-shaped relationship (as in Church et al., 2001
). Obviously, it is not possible to prove the absence of an association between two variables. However, our analyses (with statistical power of .95 to detect an r2
as low as .11) indicate that cannabis use is unlikely to account for more than 11% of the variance in heroin or cocaine use in our population—and may account for much less, since in our sample it accounted for under 3%.
The statistical power of our analyses also indicates that if cannabis use predicts lapse to heroin use among patients who have become heroin-abstinent, the hazard ratio is unlikely to be greater than 2.22. A hazard ratio of that magnitude may be clinically significant, but the actual hazard ratio may be considerably lower; in our sample it was 1.54 at most and not statistically significant. This finding contradicts that of Wasserman et al. (1998)
. Interpretation of the discrepancy is complicated by a difference in the overall rate of lapse (more than 80% in our patients versus 41% in Wasserman et al.’s patients), which might have obscured any influence of cannabis use in our sample. The difference in overall rate of lapse may have been due to other sample differences (Wasserman et al.’s patients were given a wider, presumably more individualized range of methadone doses, and had generally been at their maintenance dose longer than our patients), and those differences themselves may have moderated any effect of cannabis use. It is also worth noting that our sample, though comparable to that of Wasserman et al. in terms of sex, age, education, and income, had a greater proportion of African-Americans, a slightly lower rate of unemployment, and, moreover, a far lower lifetime rate of psychiatric disorders (43% vs. 1% for Major Depressive Disorder, 49% vs. 6% for PTSD, and 43% vs. 13% for Antisocial Personality Disorder). Psychiatric diagnoses did not predict lapse in Wasserman et al.’s patients, but they did not test for an interaction of cannabis use with psychiatric diagnoses. Thus, it is possible that cannabis use differentially predicts lapse to heroin use in patients with psychiatric comorbidity. Finally, it is possible that the finding of Wasserman et al. (1998)
was due to chance; cannabis use was one of 20 predictors tested in that study, and with a Bonferroni correction, its p value increases from .004 to .08.
Our finding that cannabis use was not associated with treatment retention is consistent with others’ findings (Saxon et al., 1991
; Budney et al., 1998
; Church et al., 2001
). In fact, one report on 120 patients in a drug-free treatment program for heroin addiction suggested that marijuana use was a favorable prognostic factor for treatment retention (Ellner, 1977
Our findings could be taken to suggest that if cannabis use in methadone patients is to be discouraged, it should be for its own sake, not for the sake of a presumed causal relationship with treatment dropout or heroin or cocaine use. But even this interpretation may be too broad, because, in our posttreatment follow-ups, cannabis use during treatment failed to predict any of the psychosocial problems assessed by the ASI. Two of the psychosocial problems (number of recent days in jail and number of recent days of family conflict) were predicted, albeit weakly, by lifetime history of Cannabis Abuse or Dependence. Thus, the negative prognostic signs of interest may be symptoms of Cannabis Abuse or Dependence.
Counterintuitively, Cannabis Abuse or Dependence predicted less use of heroin and cocaine during treatment itself. This seems to replicate a prior finding among cocaine-dependent patients: durations of abstinence from cocaine were significantly longer in patients with comorbid Cannabis Dependence (Budney et al., 1996
). It is unlikely that this could be explained by patients’ substituting cannabis for heroin or cocaine; if substitution were occurring, one would expect to see an association with frequency of cannabis use, not with symptoms of Cannabis Abuse or Dependence. (In any case, behavioral-economic work has shown that cannabis is at best a weak substitute for heroin; Petry & Bickel, 1998
.) Since criteria were met through self-report via a structured interview, meeting criteria might be a marker of greater insight into drug-associated problems. This is consistent with our own recent finding that cocaine use during treatment was lower in methadone patients who had met criteria for Cocaine Dependence at intake (Epstein et al., in press
However, even if meeting DSM criteria for Cannabis Abuse or Dependence were a marker of greater insight, we found that patients who met criteria were continuing to use more cannabis than those who did not. This combination of findings—self-reported adverse consequences of cannabis use, plus continued use—is reason enough for cannabis use to be a focus of clinical attention within this subgroup of patients. In our sample, patients reported symptoms such as using more cannabis than intended and being high on cannabis when expected to perform role obligations or when hazardous. These self-reported symptoms seem to provide a good basis for encouraging the patient to reduce or discontinue cannabis use.
This finding is complicated by the fact that, in the 11 patients for whom recency data were available, eight reported that no symptoms had occurred within the past year. There is insufficient evidence to say what level of concern should be generated by continued cannabis use in a patient who endorses a past history of Cannabis Abuse or Dependence. Studies of the natural history of these disorders (Rosenberg & Anthony, 2001
; von Sydow et al., 2001
) have not addressed the issue, and have not been done in methadone-maintained heroin addicts. In clinical practice, changes in the number or severity of DSM-IV
symptoms of Cannabis Abuse or Dependence can be assessed through a semistructured interview (although reliability is not as good as for other diagnostic categories) (Miele et al., 2000
). Formal or informal use of such an instrument might serve as a barometer for reemergence of past symptoms.
The present study has limitations that should be considered. The most important is that, except when the DIS was given at study intake, we did not directly ask participants about the consequences of their cannabis use. We also limited the sensitivity of our analyses by categorizing cannabis use rather than treating it as a continuous variable. (However, it is our impression that most methadone-clinic staff and administrators view cannabis use as a behavior categorically distinct from abstinence. By categorizing levels of use, we struck a balance between having more sensitive analyses and having results expressible in terms that would be meaningful to most clinicians. Moreover, when we repeated some of our analyses after coding cannabis use as a continuous predictor, the results did not change.) After the first five weeks of treatment, all of our participants either underwent contingency management or a control condition (with vouchers given noncontingently); we do not have data from patients in more conventional long-term methadone maintenance. (This limitation carries one analytic advantage: our patients were not discharged for using heroin or cocaine, so rates of use were not artificially low.) Although we tried to enroll participants representative of the urban area our clinic serves, we excluded study applicants with symptoms of psychosis, mania, or active suicidal ideation, or with physical dependence on alcohol or sedatives; thus, our findings may not generalize to patients with such comorbidities. Due to the time-limited nature of our studies, no patient was enrolled in our clinic for more than 39 weeks, and our posttreatment follow-up for each patient was limited to three appointments in 12 months; therefore, we may have failed to detect long-term adverse outcomes. Our diagnoses of substance-use disorders were not based on the most recent edition of the DSM, and due to the archival nature of the data, we had only diagnostic summaries for most participants.
Another possible limitation is that our cannabinoid-positive participants did not test positive as frequently, on average, as those in other studies. Overall, 54% tested positive at least once. (For comparison, the corresponding figures from prior studies are 47% [Wasserman et al., 1998
], 55% [Saxon et al., 1993
], 65% [Budney, Bickel & Amass, 1998
] and 79 % [Nirenberg et al., 1996
].) However, among the subgroup who tested positive, only 11 (5%) of them tested positive every time. For comparison, the corresponding figure from another study is 41% (Saxon et al., 1993
). Similarly, if we use the classification chosen by Nirenberg et al. (1996)
, the percentages of intermittent, moderate, and consistent users (up to 1/3 positive, 1/3 to 2/3 positive, and 2/3 to all positive) among our users were 68%, 17%, and 15%; among the users described in Nirenberg et al. (1996)
, the percentages were 45%, 29%, and 25%. The percentage of our users who met DSM criteria for a cannabis-use disorder (15%) was similar to the 17% reported by Budney, Bickel & Amass (1998)
It might be argued that another limitation of the present study was the possibility of a ceiling effect: if patients’ drug problems were already at their maximum, it would be impossible to detect contributions from cannabis use. Mathematically, this was not the case. (For example, at posttreatment follow-up, participants reported having experienced drug-related problems on 13.5±0.9 out of the past 30 days, with a median of 5 and a range of 0–30.) It may be instructive to note that in another sample of methadone-maintained patients, ceiling effects did not
prevent detection of problems associated with smoking tobacco (McCarthy et al., 2002
The present findings add to the evidence that cannabinoid-positive urines in methadone-maintained patients need not be a major focus of clinical attention, unless the patient meets criteria for a cannabis-use disorder by reporting cannabis-associated problems. If the patient reports no such problems, our data (and most of the prior published data) offer little empirical justification for disbelieving the patient. Future work should address the question of long-term outcome in cannabinoid-positive patients who report only a past history of cannabis-associated problems. Future work should also determine whether interventions that decrease cannabis use in methadone-maintained patients (Calsyn & Saxon, 1999
) will be effective in patients who meet criteria for a cannabis-use disorder.