The Epidemiological Association Between Cannabis And Psychosis
The ideology of ‘cannabis psychosis’ has been deemed a controversy since cannabis’ association with psychosis had not been undoubtedly demonstrated. Early evidences implied that it was a precise entity, due to prolonged pharmacological effects suggested that the possibility that chronic psychosis could occur for the same reason. However, recent studies show no convincing argument directly linking psychosis and cannabis. These conflicting arguments raise a cause for concern as clinicians must distinguish between drug induced effects and patient other psychiatric issues in order to proceed upon prognosis.
An assessment of evidence shows that there is no convincing support for an exclusive clinical diagnosis of psychosis induced by the practise of cannabis usage. Cannabis, however, produce brief organic reactions which may exhibit psychotic episodes in clear awareness. Consumption in non-regular users or regular uses in habitual users can experience a temporary schizophreniform episode. Heavy users may have higher risks of developing schizophrenia in the next decade. For this to be explored, the uses of meticulous longitudinal reports are required to comprehend whether cannabis initiates the inauguration process for psychosis.
A longitudinal study of Swedish Conscripts in assessing the association between cannabis and schizophrenia was carried out by researchers in Sweden (Andréasson et al). The aim of study was to indicate whether cannabis consumption was directly proportional to the possibility of developing schizophrenia as a causation for psychosis. During a 15-year follow-up study, a cohort of 45,570 Swedish conscripts were closely followed to demonstrate the relative risk for schizophrenia among high consumers of cannabis compared with non-users. To take thse results researchers used a highly valid approach to endure extraneous variable did not affect the study’s result.
“The endocannabinoid system (ECS) is a widespread neuromodulator system that plays important roles in central nervous system (CNS) development, synaptic plasticity, and the response to endogenous and environmental insults”. The endocannabinoid system communicates its message in an alternate route to the normal transmission of neurochemicals. It functions in a rearward motion whereby the postsynaptic neurons are active; cannabinoids are made from lipid precursors present in the neuron. They are then are released from that cell and travel to the presynaptic neuron. This is where they attach to cannabinoid receptors. There are two types of cannabinoid receptors, the cannabinoid receptor 1 (CB1) receptors in the brain that deal with coordination and movement, pain, emotions, and mood, thinking, appetite, and memories, and other functions. CB2 receptors are more common in the immune system which affect inflammation and pain. Activation of neuronal CB1 receptors results in inhibition of adenylyl cyclase and decreased neurotransmitter release through blockade of voltage-operated calcium channels. This permits the cannabinoid to dictate subsequent activity by dimming its functionality.
The main component of cannabis is delta-9-tetrohydrocannibinol (THC), a chemical that stimulates the CB1 which are situated in high concentrations within the cerebellum, basal ganglia, amygdala, hippocampus, and regions of the cerebral cortex within the brain. THC overwhelms the endocannabinoid system quickly attaching itself to cannabinoid receptors throughout the brain interfering with the natural process of cannabinoids and cause an imbalance of communication between the system of neurones. The effect of cannabis exerts their influence by regulating how cells communicate. This could directly affect areas of the brain such as the hippocampus by disrupting the ability to recall the imminent occurrence of events. Anxiety can also be caused due to the occurrence of the disruption of neurochemicals within the amygdala. It is this which makes the user feel like they are in a state of panic and/or paranoia. It also can affect judgement through an imbalance of neurochemicals within regions of the neocortex. In turn users may have altered thinking which may lead to a psychotic frame of mind. Heavy users of cannabis may experience plasticity of neurone function in the brain, which can lead to permanent issues with mental health and memory. Mental health being deterred may also be a factor for a psychotic episode. Whether the amalgamation of the many effects of THC on the brain prompts the event of a psychotic episode is not definite. However, what is certain is that it may play a role in the convolution of fluidifying the explanation of psychosis.
Cannabidiol (CBD), another chemical existent within cannabis, however, seem to have antipsychotic properties. “Cannabidiol (CBD), a Cannabis sativa constituent, is a pharmacologically broad-spectrum drug that in recent years has drawn increasing interest as a treatment for a range of neuropsychiatric disorders”. Studies by Blessing et al show that the anxiolytic properties of CBD in humans were initially shown in the context of reversing the anxiety-causing effects of THC. CBD reduced THC-induced anxiety when consumption was simultaneous with this agent, but had no effect on baseline anxiety when taken alone. It is evident that CBD has an alternate effect on the brain and perhaps more beneficial than the psychotic effects an individual may experience when THC is present within the endocannabinoid system. “Cannabidiol (CBD) is a phytocannabinoid constituent of Cannabis sativa that lacks the psychoactive effects of Tetrahydrocannabinol (THC)”. It is crucial to note that CBD in fact displays antipsychotic effects which is the opposite of studies showing THC inducing psychosis. Therefore, the syllogism to affirm that cannabis is the root for psychosis to occur in an individual is controversial due to the many chemicals playing a role in affecting the mental stability of the user.
