WTH?!?!? (What the heck)

the pharmacy
the pharmacy (Photo credit: nirbhao)

I’m not, in any way, against efforts to develop pharmaceutical treatments for addiction. However, I’m of the opinion that there is a culture problem among researchers and some members of their universe.

Does any serious, knowledgeable person with an eye toward practice believe that a stimulant drug is going to be an effective treatment for alcoholism?

Yet, researchers are toiling away on this, finding that it actually worsened outcomes for some subjects and calling for more research:

Modafinil significantly improved self-report measures of state impulsivity, but had no effect on percentage of abstinent days or percentage of heavy drinking days, nor on the behavioral measures of impulsivity. However, subgroup analysis revealed that modafinil prolonged the time to relapse (p=.022) and tended to increase the percentage of abstinent days (p=.066) in ADP with poor response inhibition at baseline, whereas modafinil increased the percentage of heavy drinking days (p=.003) and reduced the percentage of abstinent days (p=.002) in patients with better baseline response inhibition. Overall results do not favor the use of modafinil in order to reduce relapse or relapse severity in ADP, and caution is required in prescribing modafinil to a non-selected sample of ADP. Further research on the effect of modafinil in ADP with poor baseline response inhibition is warranted.

All for a drug that no practitioner could believe will provide real treatment utility. Why? And, why do we have so much deference to them in our culture?

They’ve got hope for something. But, what?

Stimulant maintenance therapy did not work 😦

This study did not find a significant main effect of modafinil on the rate or duration of cocaine use among cocaine-dependent patients.

Now they decide to polish the turd:

Although these results are disappointing, we did find that modafinil-treated patients had nonsignificantly higher odds of attaining abstinence across all of the study time points, and those treated with 400 mg/day had significantly greater odds of attaining abstinence (p = .04) at the end of their 8-week medication trial (Visit 24). There was also a significant difference (p = .02) in the OR for abstinence at the final follow-up visit, suggesting the possibility that modafinil facilitated delayed clinical improvement that was not captured by our 8-week study design.

Back to reality:

Despite its ability to blunt cocaine-induced euphoria in three controlled human laboratory studies ( [Dackis et al., 2003][Hart et al., 2008] and [Malcolm et al., 2006]), modafinil did not show overall success in this outpatient clinical trial.

Maybe these people are just too tough:

It is important to note that all of the patients in this study tested positive for cocaine at baseline. It is well established that patients who test positive for cocaine at study start have extremely poor clinical outcomes when compared with those who are able to produce a cocaine-negative urine sample ( [Ahmadi et al., 2009],[Kampman et al., 2001][Patkar et al., 2002] and [Poling et al., 2007]). The reason for this finding is unclear, but it probably stems from greater addiction severity, less motivation for recovery, or both of these clinical features.

There will be evidence, dammit!

Despite our negative study, we believe it is premature to dismiss modafinil as a potential treatment for cocaine dependence.