While THC rich strains of pot can potentiate an already psychotic or prepsychotic state, CBD alone or CBD rich stains of weed, actually behave as antipsychotics. Yes, you heard correctly. CBD is emerging as a potent antipsychotic medication as seen below.
In 2012 an elegant, randomized, double-blinded trial headed by doctors Leweke, and Piomelli in a joint effort covering both Europe and the US respectively, found that a novel phytocannabinoid found in marijuana called CBD behaved as well as a powerful antipsychotic medication.
CBD MORE EFFECTIVE FOR PSYCHOSIS THAN PRESCRIPTION DRUGS
Surprisingly, CBD was found to be as efficacious as the European blockbuster antipsychotic drug amisulpride which was used in the study. Amisulpride, an atypical antipsychotic, is not available in the US but has a similar profile to many of the drugs currently used in America. Amisulpride is one of the most effective drugs currently in use for the treatment of schizophrenia.[ref]Am J Psychiatry 2002; 159: 180–190.[/ref]
Can it get better? Indeed, CBD was found to be as good as the potent antipsychotic used in the study, plus it turns out that the side effect profile of CBD was decidedly superior when compared to amisulpride.
I’m not surprised. As mentioned previously, the antipsychotics are dangerous drugs with some of the worst adverse drug effects of any pharmacologic category. For example, chronic use of the antipsychotics increases a patient’s risk for Parkinson’s disease, or technically Parkinsonism (identical in form and function but due to the drug not true Parkinson’s disease). I don’t have the space to discuss it here but these pharmaceuticals have several other grave adverse effects. That’s a great reason to look for less toxic medications such as CBD.
In fact, when you list the side effects of CBD next to the side effects and adverse drug effects of amisulpride, you immediately notice something remarkable. There basically are no side effects with CBD usage. That may not seem very important to you but trust me, all pharmaceuticals have side effects and many are disasters waiting to happen. So a “drug” (CBD) as powerful as a pharmaceutical antipsychotic without the disaster waiting in the wings is truly amazing.
THE OLD THEORY
Clinical investigators historically have suggested that hyperactivity of the endocannabinoid system may contribute to the psychotic state. This theory was based on previous studies which showed that potent THC preparations and other cannabinoid agonists can induce psychosis in healthy and schizophrenic patients. We discussed some of this research in my Reefer Madness series.
This proposed model of madness fueled two large-scale clinical trials using CB1 cannabinoid antagonists (blockers) in schizophrenic patients. Sadly, the study failed to demonstrate any positive results. Thus sinking the hypothesis that an overactive endocannabinoid system makes one as mad as a hatter.
In a brilliant move, Dr Leweke and his team decided to test a diametrically opposite theory based in part on studies that showed schizophrenic patient’s symptoms correlated inversely with cerebral spinal fluid (CSF) anandamide levels. That is, the higher the patient’s brain anandamide levels the less intense their symptoms were. A shopping list of compelling data also implicated CBD as a player.
The author’s state:
Furthermore, preliminary clinical case reports suggest that cannabidiol might exert antipsychotic effects in schizophrenic patients (three citations). In addition, experimental studies show that cannabidiol reduces psychosis-like effects of Δ9-tetrahydrocannabinol and synthetic analogs (two citations).[ref]Translational Psychiatry (2012) 2, e94; doi:10.1038/tp.2012.15 Published online 20 March 2012[/ref]
A RIDE WITH ANANDAMIDE
Anandamide is the human body’s native THC-like neurotransmitter acting on CB receptors. It is responsible for the regulation of pain, mood, and cognition. Running point on this topic, studies showed that pharmacologic blockade of anandamide degradation (metabolism) attenuates rather than enhances psychotic behavior clinically and in an animal model.
In other words using CBD (at 800 mg per day) blocks the activity of the enzyme (called FAAH) that normally eliminates anandamide at the synapse within the recesses of the brain. Very quickly scientists noted that psychotic symptoms in patients decreased markedly. It acted like an atypical antipsychotic but its mechanism of action was through a vastly different and novel brain pathway.
Dr Leweke comments on his study conclusions:
Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile. Moreover, cannabidiol treatment was accompanied by a significant increase in serum anandamide levels, which was significantly associated with clinical improvement. The results suggest that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.[ref]Translational Psychiatry (2012) 2, e94; doi:10.1038/tp.2012.15 Published online 20 March 2012[/ref]
In a previous publication I mentioned that CBD has numerous activities within the brain leading to complex end effects.
CBD itself is a weak, partial antagonist of CB1 receptors (THC is a weak agonist). Even though it weakly blocks CB1 receptors, its downstream effects appear to be the opposite of a blockade. That’s because CBD inhibits the enzyme responsible for the degradation of anandamide. That activity leads to an increase in the brain’s anandamide level which has a profound effect on the dampening of positive (voices) and negative (social withdrawal) aspects of madness. This feature plays a central role in our discussion of why CBD has such powerful antipsychotic activity.
Overall it appears that CBD’s effects are excitatory on the endocannabinoid system resulting in increased production of anandamide which is a very good thing for persons suffering from schizophrenia.
In concluding the author notes:
These results suggest that cannabidiol is as effective at improving psychotic symptoms as the standard antipsychotic amisulpride.
THIS SHOULD HAVE MADE HEADLINES
You didn’t read about this in the Times or USA Today but you should have. That’s because CBD is a natural compound and cannot be patented. Therefore, Big Pharma will not spend the time or money in its development. That means you will not see it promoted by the major news outlets. So we have to make sure patients know about this treatment all on our own.
I cannot emphasize enough on how important this finding is. What this study suggests is nothing short of a new paradigm in psychiatric research. It reveals that madness may have more to do with the recently discovered endocannabinoid system than with the classic model of insanity which predicates its theory on overexcited dopaminergic pathways in the brain.
Classically, the theory goes like this: madness has been viewed by the medical establishment as due to overactivity of dopamine (and several other neurotransmitters: serotonin being one of them) within special compartments in the central nervous system (CNS). Drugs which purportedly treat psychosis are designed to block dopamine (and serotonin with the atypicals). This helps to explain why the antipsychotics don’t work as well as they should. They may simply be active on the wrong system entirely.
The reason why this study is monu-“mental” is because number one, the antipsychotics both the classics (like Thorazine) and the atypicals (like amisulpride), provide more of a chemical lobotomy (Dr Peter Breggin Toxic Psychiatry); and number two, the antipsychotics are rife with a ledger of appalling side effects.
If further investigations prove CBD to be a prevailing antipsychotic it will usher in a golden age for psychiatry. It’s about time too. It will lift the specialty up and away from the medieval appurtenances it has so far relied upon. That’s of course if psychiatrists are willing to try a compound that will never be patented and will never appear in any of the glossy pages of their trade journals.