One of the best things about my blogging gig over at Psychology Today is that I've now attracted the attention of more researchers in the field from all over the world. I'm a clinician doing my work in a suburb of Boston - I know some pretty cool and important people who make amazing research contributions, but I am certainly not among them. Most of my musings here at Evolutionary Psychiatry are theoretical - there are NO paleo 2.0 diet trials for any psychiatric condition, after all. If someone walks into my clinic with bipolar disorder, I can't say "oh, just try a ketogenic diet and a multimineral and you will be fine." There are no trials and case studies of ketogenic diets in the literature were failures.
That doesn't mean I don't push for elimination of food toxins, put in a little plug for pasture butter, demonstrate and encourage stress reduction techniques, focus on good sleep hygiene (and look for sleep disturbance and medical causes), and I do take people off statins when there is good clinical reason (primarily in folks with dementia, with good results, actually. Also, a couple of cases of resistant depression.) But I can't go full-blown evolutionary psychiatry with all my patients. Some aren't interested, and for others the data isn't there. Which is okay. EvPsych has reinvigorated my interest in the field and in research, and I feel the preventative potential of a paleo 2.0 diet is amazing - so for subclinical disease, I feel my blog and the diet are likely doing a lot of good, far more good than I could do in the time I have to see patients one by one. But I don't have any proof of that. Which is okay. I'll still keep looking for more evidence and more nutritional links.
But! Cannabis! I am honored that my twitter feed (warning - I might tweet about Crossfit, shampoo, and my children) is followed by Dr. Sanjuan in Spain, who sent me a link to this article, which among other articles will be the anchor for this post.
Cannabis. Evo Med is the province of rebels, and rebels love pot...
Pot might not love you.
Cannabis is the world's most popular recreational drug and its use has accelerated among adolescents in the United States.
There are two circumstances in which I tend to see heavy pot use - young people struggling with psychotic disorders, and older folks with lifetime heavy pot use struggling with cognitive function and anxiety problems. Such circumstances are weighted to bias my opinion against pot as the happy self-medication of choice. You are forewarned!
Cannabis use has a high comorbidity with populations with psychotic disorders. Its continued use is associated with poor outcomes in psychosis and with more frequent and earlier relapses (1). Use has been associated as a risk factor for emerging psychosis, and a young person with heavy use will have a two-fold risk of developing psychosis (2)(3). The earlier the age at which cannabis is first consumed, the greater the risk.
So, what might cannabis do that would cause psychosis in vulnerable individuals? THC will stimulate the cannabinoid receptors type 1 (CB1-R) , which are abundant in the cerebral cortex, particularly the frontal regions. basal ganglia, hippocampus, anterior cingular cortex and cerebellum. All of these areas can play a role in the neural circuitry of psychosis, and animal studies have implicated cannabis as a causative agent in the psychosis hotspot of the mesolimbic area.
Only a small proportion of cannabis users develop psychosis, suggesting there are genetic forces at play. The primary effect of endocannabinoid activation is the modulation of neurotransmitter release in the mesolimbic area. Animal studies also suggest that exogenous cannabinoids like THC affect dopaminergic transmission in the prefrontal cortex and the mesolimbic pathway (the areas affected by schizophrenia).
Let's examine COMT. This enzyme sits in the synapse and will break down dopamine, norepinephrine, and epinephrine. There is a common polymorphism of the COMT gene - folks with the valine allele of the COMT gene will have higher COMT function than those with the methionine allele. Increased COMT activity may result in a combination of reduced dopamine transmission in the prefrontal cortex and increased dopamine mesolimbic signaling - this combination is higher risk in schizophrenia, which presents with decreased executive functioning and working memory combined with risk of experiencing delusions and hallucinations.
Adolescents carrying the Val allele of the COMT gene are more at risk for schizophrenia in the Caspi research - the Sanjuan research found that those with the Met allele were more at risk. Other studies of cannabis use suggest that those with psychosis are more likely to use cannabis, and more likely to use the high-potency cannabis called "skunk."
That's all well and good. Repeated used of a cannabinoid agonist (POT) will produce prolonged and repeated use of the cannabinoid receptor. This will result in hunger, a bit of paranoia, psychosis, euphoria, cognitive impairment, and pain relief, and withdrawal effects of increased pain and anxiety.
So, does cannabis use increase the risk of schizophrenia use or what? Well, all the studies are observational, and it is pretty clear that those at risk for psychosis (with prodromal symptoms and high genetic risk) will tend to use more cannabis. However, the strongest evidence against a causative effect of cannabis is from native populations who regularly use cannabis, and in which there is no increased risk of psychosis. Your risk will depend upon your genes and experience- but I am not a fan.
No comments:
Post a Comment