LESSWRONG
LW

by Xodarap
3 min read
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This post summarizes The Long-term Effects of Cocaine Use on Cognitive Functioning: A Systematic Critical Review. The punchline is: 

The current evidence does not support the view that chronic cocaine use is associated with broad cognitive deficits. The view that cocaine users have broad cognitive deficits is inaccurate based upon current evidence, and the perpetuation of this view may have negative implications for treatment programs and development of public policies.

This is of interest to me, because cocaine may have short-term benefits as a stimulant, and may have fewer cognitive impacts than alcohol. I am not an expert in this field, and am mostly posting in the hopes that Cunningham’s Law will hold and someone will correct my misunderstandings.  

My Summary

  • Neurotoxicity
    • Cocaine may lead to increases in free radicals, oxidative stress, catalase activity etc. These precursors are used synonymously with “neurotoxicity” by e.g. this paper.
    • But cocaine use does not seem to lead to long-term depletion of relevant neurotransmitters. This is especially remarkable given that tests on nonhuman animals usually involve absurdly large dosages.
    • Normal human usage also has several differences with experimental procedures which make human use less likely to be neurotoxic: slow ramp-up (rather than having a huge dose the first time you use it) and dosing at will (rather than having a large dose forced on you when you aren’t feeling well).
    • Question: if cocaine was causing oxidative stress DNA damage (e.g. as suggested here), how likely is it that we would see a decrease in neurotransmitters large enough to be measurable in the usual study formats?
  • Changes in the prefrontal cortex
    • Under very large dosages, changes in the prefrontal cortex are observed in nonhuman animals: synaptic excitability, glucose metabolism, etc. These changes are accompanied by measurable differences in cognitive ability. 
    • Longitudinal studies in nonhuman primates showed decrease in cognitive performance after cocaine use, but differences had disappeared by three months of abstinence. After 20 months, cocaine-experienced monkeys had significantly greater metabolic activity in the cerebellum, but no difference in task performance.
    • “Considered together, converging evidence suggests that the compensatory neuroplastic changes associated with chronic cocaine exposure likely create conditions where cognitive performance is normalized during acute intoxication, declines during withdrawal, and recovers gradually over the course of abstinence”
  • Human studies
    • These generally suffer from methodological problems. Control subjects are not matched on age, sex, education, etc. They also are generally correlational and can’t determine causation.
    • Some research finds brain structure differences between cocaine using versus non-using participants. Authors usually conclude that this may explain claimed cognitive deficits in cocaine users, even if the authors did not test to see whether their participants actually had those cognitive deficits or differences could be explained by e.g. age of participants.
    • MRI
      • Cocaine abusers may have different concentrations of white and gray matter in various parts of the brain. Causality is unclear.
    • fMRI
      • 11/14 fMRI studies found no differences between groups based on cognitive measures, so based conclusions off of fMRI findings. The remaining three had methodological problems which could explain results (small sample sizes, age etc. differences between participants).
    • PET
      • Cocaine users have brain activation differences from nonusers, even after 25 days of abstinence. However, they do not show differences in task performance. These studies had methodological problems.
      • Better controlled studies found that cocaine dependent participants had mild cognitive impairment and structural differences; however, this was less than the cognitive impairment of alcohol dependent participants. Structural differences were less than psychopathological disorders such as schizophrenia.
  • My major uncertainties:
    • To what extent are the impacts of cocaine use nonlinear? Almost all research is on human or animal subjects with exceptionally high dosage.
    • If it is the case that moderate cocaine use causes, say, changes in gray matter volume in the basal ganglia, how likely is that change to be permanent?
    • If moderate cocaine use causes, say, changes in gray matter volume in the basal ganglia, how likely is that change to be detrimental?
    • How likely is oxidative stress to lead to neurotoxicity? Some research seems to assume they are synonymous, but this review thinks the first is a poor proxy for the second.
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Cognitive Impacts of Cocaine Use
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[-]frontier6460

Better controlled studies found that cocaine dependent participants had mild cognitive impairment and structural differences; however, this was less than the cognitive impairment of alcohol dependent participants. Structural differences were less than psychopathological disorders such as schizophrenia.

This sounds pretty bad? Especially so because there's other stimulants out there without studies showing they cause cognitive impairment. "Better than being an alcoholic or schizophrenic" is not much of an endorsement.

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[-]Xodarap10

Here's a longer quote from the article:

Out of the three PET studies summarized in Table 2, two studies not match groups
on age [111,112] and two did not find significant differences between groups on cognitive
measures [110,111]. The clinical importance of both Bolla et al. [111] and Goldstein et al. [112]
remains ambiguous. Both studies found that cocaine abusers exhibited a degree of cognitive
impairment. While Bolla et al. [111] based their conclusions on PET findings, those of Goldstein
et al. [112] were derived from a neuropsychological test battery. The studies also differed in
sample size, number of tasks administered, and use or non-use of demographically adjusted
scores. It is unclear what PET imaging tells us about the neurocognitive functioning of
individuals with cocaine use disorder, given that findings are open to debate and that doubts
persist as to whether metabolic changes in the brain are linked to a specific drug of abuse.

I interpret the authors as saying that it's unclear whether there's any difference at all, much less a "pretty bad" one.

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[-]supposedlyfun10

Agreed. Talk about damning with faint praise. Squinting gently at the research, chronic alcohol abuse looks to be worth -5 IQ points, about 1/3 of a standard deviation. 

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[-]rosyatrandom20

My observation: cocaine turns normal people into arseholes and arseholes into even bigger arseholes.

My conclusion: I would never recommend it to anyone, and certainly never try it again.

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[-]osten10

Are you sure about the imcreased sustained attention among cocaine users? The abstract in your link seems to suggest the opposite.

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[-]Xodarap10

I very well could be wrong, but I believe that slower response time indicates less impulsivity, which is "better" sustained attention. Here's how the review article I'm summarizing describes the findings:

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[-]Algernoq-20

Generally, people are biased toward doing what is easy and pleasurable, and making excuses to justify it.

Anecdotally, two programmers who might have occasionally used cocaine ended up quitting their programming jobs to become artists, and have been slowly spending their savings for a few years, working toward making a living through their art (unlikely, they're OK but not that great yet) and thinking the same tier of programming job will be available for them to go back to (doubtful). I strongly suggested that they should both go into AI programming, but they are too normie to listen. So my anecdotal evidence is that the cognitive impact of cocaine is that it makes people make irrational decisions. 

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