December 23, 2014
By Shelley M. White
Natural treatments potent enough to alleviate symptoms of psychosis and schizophrenia (whether it is induced by an infectious illness or microbe of some kind, severe nutrient imbalance, or any other origin) are scarce. However, various reports have surfaced claiming cannabis can successfully treat symptoms of psychosis and schizophrenia; and for each of these reports, multiple others have surfaced cautioning of cannabis induced psychosis.
While these reports exist on polar opposite ends of the spectrum, the validity of both are well-founded. Cannabis holds the power to either induce or reduce symptoms of psychosis and schizophrenia, as it contains compounds enabling it to do both. The key to treating psychosis and schizophrenia with cannabis lies in identifying and using the specific compounds able to alleviate symptoms.
Cannabis Induced Psychosis
Cannabis has long been linked to psychosis, believed to both induce symptoms of psychosis as well as exacerbate preexisting symptoms of psychosis, most notably those of schizophrenia. Clinical documentation of the validity of this belief dates back to 1848, when French psychiatrist Jacques-Joseph Moreau de Tour began studying the effects of cannabis on the brain and body, with his interest particularly fixated on its ability to induce psychosis in users. To nightmare-ghosttest his theory, Moreau used cannabis as an experimental psychotomimetic, a substance which mimics symptoms of psychosis, including but not limited to hallucinations, delusions and delirium. After observing behavioral changes similar to endogenous psychosis, or psychosis originating within rather than from external influences such as cannabis, Moreau concluded that THC worked as an excellent experimental psychotomimetic substance, indicating that the use, and definitely the abuse, of cannabis containing the psychoactive ingredient THC can initiate a symptom picture unparalleled to that of psychosis. Researchers who repeated the study in 2004 using more accurate measurements, scales and overall means of testing came to the same conclusion as Moreau.
Cannabidiol Reduces Symptoms and Progression of Schizophrenia and Psychotic Conditions by Enhancing Anandamide Signaling
Elevated levels of anandamide, a bioactive lipid that binds to cannabinoid receptors, in cerebrospinal fluid are linked to symptoms of psychosis and schizophrenia. More specifically, they are linked to the prognosis of schizophrenia and psychotic conditions, with the amount to which they are elevated determining the rate at which the psychosis will progress. When exploring anandamides role in the transitioning of schizophrenic patients from prodromal states of psychosis (early, initial stages proceeding full blown manifestation of psychotic symptoms) to advanced, final stages of psychosis, researchers measured anandamide levels in the cerebrospinal fluid and serum of subjects in initial prodromal states alongside individuals clinically deemed psychologically stable and healthy. On account of ensuring the most accurate results possible, high-performance liquid chromatograph/spectrometry was used for testing.
Schizophrenic patients displayed appreciably higher levels of anandamide compared to healthy test subjects. Schizophrenic patients who exhibited anandamide levels that were above average, yet were notably lower in comparison to other patients with schizophrenia and psychosis related conditions, were found to be at a greater risk for transitioning from initial prodromal states of psychosis to advanced states of psychosis. This may seem backwards, as the fact that elevated levels of anandamide are associated with schizophrenia, a fact which could easily lend to the false assumption that higher levels of anandamide correlate with higher levels of psychosis. On the contrary, the opposite holds true. Anandamidergic upregulation, or enhanced anandamide levels, in the initial prodromal stage of schizophrenia and psychotic conditions are a protective response of the endocannabinoid system activated early on, upon initial onset of symptoms of schizophrenia and psychosis.
That the cannabinoid Cannabidiol does not bind to cannabinoid receptors does not render it useless, especially in this case, considering its functioning in directly working to inhibit degradation of the endocannabinoid anandamide. Clearly, this is an exciting discovery for those afflicted with schizophrenia or conditions producing symptoms similar to schizophrenia, as it offers hope of a slower progression of the condition and the possibility of a living a longer, fuller life. In a study comparing the effectiveness of cannabidiol and amisulpride, a strong anti-psychotic, on schizophrenic symptoms, both medications performed successfully. However, the list of side effects of cannabidiol was significantly less in comparison to that of the prescription antipsychotic amisulpride. Essentially, not only did cannabidiol prove to be an effective treatment for reducing symptoms of schizophrenia and inhibiting progression of psychosis by greatly increasing anandamide serum levels, but it did so without simultaneously generating a cascade of more undesirable symptoms, as its use is not equipped with a stealthy list of side effects like amisulpride and other antipsychotic prescription drugs. In short, studies performed on human and animal test subjects using behavioral and neurochemical techniques indicate that the pharmacological profiles of cannabidiol and atypical antipsychotic drugs are strikingly similar.
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