Thursday, November 24, 2005

Weed for What Ails You: Medical Marijuana

The medical marijuana case Gonzales vs. Raich has been remanded by the SCOTUS to the 9th circuit, reports Volkh Conspiracy. Along with Dispatches, I will leave it to the legal experts to comment on the constitutionality of Congress invoking the Commerce Clause to regulate an activity which is neither interstate nor commerce.

While I once agreed with those who asserted there was minimal evidence that marijuana causes lasting biological harm or addiction, there is new evidence not everyone may be aware of. In particular this large study documenting cannabis use associated with development of psychotic disorders (schizophrenia and schizoaffective disorder), this is a metanalysis showing increased risk for schizophrenia with cannabis use, and this review goes over some bench-science data and epidemiological data to the same effect.

I agree it's pretty inconsistant to argue that alcohol should be legal but cannabis illegal, given the overall burden of harm caused by each substance to society. But we shouldn't pretend there are no dangers to cannabis use at all.

However, the potential harms we've found for cannabis, so far, are unlikely to accrue to people with terminal diseases using marijuana to control nausea, for example. There are those who argue that we have not enough evidence that it is efficacious, or that we have other medicines that work. It is too easy though to succumb to the temptation to believe that average effects seen in studies of hundreds of people are directly translatable to every given patient. Just by chance, there will be some cancer patients for whom Anzemet is ineffective, and marijuana is effective. Those people deserve a chance to try marijuana.

The stickier case is the chronic migraineur or irritable bowel patient who wants to try marijuana. In these folks, I think that in general the potential harms--inducing mood disorders in particular--really do outweigh the short-term symptom relief marijuana can provide, especially in younger patients. Cannabinoid analogues like marinol may be a good choice, but smoked marijuana has too quick an onset, thus too much reward circuit activation, to be safe as a long-term treatment.

In the end though, if society trusts doctors to prescribe oxycontin with appropriate regulation (and I think it should), then it ought to trust doctors to prescribe marijuana.


At 2:29 PM, Anonymous Kevin McCulloch said...

I think your view here is quite reasonable.

Since you're a professional physician, maybe you can answer a question I always have with studies of this kind: given a correlation (such as that between marijuana use and schizophrenia), how do you determine cause and effect?

In other words, how do you know that marijuana makes people more likely to become schizophrenic, rather than schizophrenia making people more likely to abuse marijuana?

At 3:54 PM, Blogger fmodo said...

Great question.

There are two ways to establish exposure-disease associations. Cohort studies identify a group of exposed people and a group of unexposed people, watch them for years, and see who gets the disease.

The second classic study design is a case-control study. A group of people with a disease are compared with a group without the disease, and you compare the percent of people with the exposure of interest in each group--this is a retrospective design.

In both types, causality is inferred from timing--cause preceeds effect. Also, you try to to pick the subjects in each comparison group so you can match them by age, sex, or whatever categories you think important, to give you confidence that there really is no difference between the groups other than the exposure of interest, in order to decrease the possibilty of a third factor causing both exposure and disease. But you're right, by formal logic, a common cause of both exposure and disease would still be possible, though reversing causality in time would not.

The question you raise is whether there is a way to distinguish between prodromal schizophrenia as a risk factor for THC use and THC use as a risk factor for schizophrenia. This is another way of asking how to define which is exposure which is disease--more difficult in this case than in lung cancer and smoking. The answer comes only when we add genetics to classic epidemiological studies.

We think that cannabis use in fact both "self medicates" an underlying condition and feeds a degenerative process that leads to schizophrenia, in a particular vulnerable group of people.

1/4 of the population has a slow version of a gene called COMT, which is associated with a somewhat lower ability of your reward circuit to register pleasure. In this group, exposure to cannabis (especially as a teenager) can improve this mild 'pleasure deficiency' for brief periods, but overstimulation of other circuits causes neurodegeneration that predisposes these folks to tip into psychosis--that's been seen in one cohort study. In other words, slow COMT becomes the exposure leading to both cannabis use and psychosis; COMT must be considered the exposure because genotype preceeds both effects temporally.

With that info in hand, we need to do cohort studies on populations with different COMT types in order to better understand its effects--that's the state of the art in a nutshell.

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