Neuroscientific Grounds For Studying the Relationship Between Cannabis Use and Schizophrenia: Potential Therapeutic Applications

Thinking about my paper: So, clinical trials show that psychosis is exacerbated by marijuana use, but also that people who display schizophrenic symptoms naturally gravitate towards marijuana.

Perhaps, in its entirety, marijuana poses a risk to people that are already susceptible to schizophrenia. However, perhaps when it is broken into its constituent compounds, marijuana can be a useful remedy for these patients. For example, in one preliminary clinical trial, cannabidiol, which is posited as being responsible for weed's anxiety inducing effects, was found to treat schizophrenia as effectively as antipsychotics. The drug was devoid of THC, the active ingredient in marijuana, which is what imbues it with psychoactive properties.

Marijuana also has a wide range of effects that, given the neuroanatomy implicated in schizophrenic patients, might possess psychopharmacological potential when it is compartmental based on what properties of the plant are desired.

For example, cannabinoids have been shown to elicit anti-depressant behavior and activate serotonergic neurons through the medial prefrontal cortex. Additionally, several studies have indicated functional interactions between the cannabinoid and 5-HT (serotonin) systems in the brain. For example, the dorsal raphe, which is a significant source of serotonin in the forebrain, expresses the enzyme amide hydrolase, which catalyzes the inactivation of anandamide and 2-arachidonoylglycerol, the endogenous cannabinoid neurotransmitters that the brain naturally produces. Basically, anytime a neurotransmitter (chemical messenger) is present in the brain, they eventually need to be terminated by enzymes so that they aren't acting upon the brain for too long. So it is important to note that the same systems in the brain that mediate mood involve cannabinoids to come capacity-indeed, cannabinoid receptors are also abundantly expressed in the prefrontal cortex.

This is important because depression is a comorbid occurrence in many schizophrenic patients.

Studies have also suggested that marijuana can stimulate neurogenesis, or growth or new neurons, in the hippocampus. Not only is reduced hippocampal volume a common observation is depressed patients, but in one study, it was also bilaterally reduced in schizophrenic patients compared to controls.

Hence, marijuana, or at least some of its constituents, might be able to alleviate some of the symptoms experiences by a schizophrenic patient.s

Now, it has certainly been demonstrated that marijuana can worsen symptoms in this same population. But again, no conclusive statements can be made as to whether or not people with schizophrenia naturally gravitate towards marijuana, marijuana increases the onset of psychosis in people that are already vulnerable, or a combination of the two.

There is something to be said for vulnerability. Very few of us have an optimal genetic ancestry. Everyone's family history is riddled with dark spots. Specifically, a recent study isolates the NRG1 gene as a susceptibility gene for marijuana dependence. It is also found to be implicated in schizophrenia risk.

It is a correlation that requires further exploration. Currently, young people are taught to avoid marijuana like the plague due to the associated risk of developing schizophrenia. But as the evidence for any type of relationship remains correlation and also elucidates the role of prior susceptibility, advising every human being to stay far away from the drug is not practical. A recent statistical analysis that examined available data regarding cannabis users and schizophrenia found that it would be necessary to stop 2800 heavy cannabis users in young men and over 5000 heavy cannabis users in young women to prevent a single case of schizophrenia. Among light cannabis users, those numbers rise to over 10,000 young men and nearly 30,000 young women to prevent one case of schizophrenia.

Rather than condemning this mysterious and potent herb to scientific squalor, we must subject it to rigorous empirical study and be open to the idea that the connections between marijuana and psychosis, specifically schizophrenia, are not as simple as they may seem. Knowledge is power, and by perfecting pharmacodynamic parameters such as the ideal dosage and exactly how much exposure makes marijuana dangerous for these patients, we can increase the chances that this drug will be used in ways that are conducive to well being and while avoiding potential risks.

This, coupled with the fact that there aspects of the marijuana plant that demonstrate potential for therapeutic application for schizophrenic patients, demands that scientists investigate the matter further. Maximizing safety, reducing harm to vulnerable populations, and possibly improving the quality of life for the approximately 2.5 million Americans who suffer from this debilitating illness, makes the relationship between marijuana use and the schizophrenic brain worth studying.