Marijuana: A Cause for Schizophrenia?
Nowadays, schizophrenia has gained much popularity because of researchers constantly trying to find the root cause for the neurodevelopmental disorder in order to reverse the chronic symptoms. However, several studies have indicated that gene polymorphism, environmental factors and developmental lesions can be the cause for Schizophrenia.(Insel, 2010). Additionally, marijuana has attracted the spotlight for etiological studies as percentage of patients using cannabis were significantly higher (Hasan). This calls for an overview for studies that have substantiated that marijuana has the causal effect on genomic structure variation and developmental lesions, which links us to schizophrenic population.
Psychosis generally springs up around the age of 18 – 25, hinging on that structural variation affect neurodevelopmental genes, which compromises neuronal proliferation, migration, or synapse formation in the prefrontal cortex while it’s still in its developmental phase until early adulthood. Scientists have found proof that identical genetic variation is associated with multiple neurodevelopmental disorders. Autism occurs at the age of three and schizophrenia at the age of eleven. Idiopathic syndrome, which is caused due to microdeletion of chromosome 22q11, is also responsible for schizophrenia in 30% of children. It is still a mystery how the very same genetic variant crusade into different mental disorders. According to researchers, a possible theory is that genomic modifiers or environmental influences are the instigating determinants. However, it is still unresolved (Allebeck, Adamsson & Engstrom, 2003, p. ).
Even though schizophrenia is detected or emerges later in life, its silent manifestation commence in uterus. During the second trimester, which is a focus area for fetal neurodevelopment undergoes through some disturbances, which has been directly associated with schizophrenia. A number of obstetric complications viz a viz low birth weight, gestational diabetes, asphyxia, emergency cesarean section bleeding during pregnancy, infections, excess stress levels can be these disturbances, which have been found in the studies to double the risk of developing schizophrenia. It is evident from research that there is approximately 10% higher risk for a first relative and 3% higher risk for a second relative and 40% higher risk if both parents have schizophrenia, whereas in case monozygotic twins and dizygotic twins, it 48 % and 12 -14 % higher risk for schizophrenia
Moreover, environmental and social factors may also play a role in the development of schizophrenia, especially in individuals who are vulnerable to the disorder.1 Environmental stressors linked to schizophrenia include childhood trauma, minority ethnicity, residence in an urban area, and social isolation.1 In addition, social stressors, such as discrimination or economic adversity, may predispose individuals toward delusional or paranoid thinking.1() It is a treatable disorder
The pathophysiology of schizophrenia involves several theories. One among them is linked with a neurochemical imbalance of aspartate, glycine and gamma-aminobutyric acid (GABA). Other centers on dysregulation of dopamine, glutamate and serotonin. Another one mentions about the endocannabinoid system within the human brain, which is capable of reversing the direction of synapses. All these neurotransmitters act on specific receptors and initiate the action.
The psychoactive compound that affects the brain through activating the CB1 receptors, which is found in cannabis is Δ9-tetrahydrocannabinol (Δ9-THC). The activated CB1 receptors reverse the synaptic messengers and suppress the release of neurotransmitters viz a viz dopamine.Further research explains, in the long term, usage of cannabis has shown to condition a desensitizing effect on dopamine receptors, which deforms neuronal functions. Additionally, animal studies also show that exposure to Δ9-tetrahydrocannabinol (Δ9-THC) during early-pubescent and pre-pubescent stages of life causes cognitive deficits in adulthood. Now it is not understood whether the cognitive impairment is independent or due to altered genetics in schizophrenics, but it is clear that cannabis exacerbates the risks of schizophrenia. (Onwuameze, Nam, Eipping, Wassink, Ziebell, Andreasen, Ho, 2012). Evidence demonstrates that there is a relationship between marijuana and schizophrenia, but the nature of the relationship is unclear. Further experiments on chronic cannabis users who lack genetic predisposition to schizophrenia would elucidate the relationship.
Another study done using single nucleotide polymorphisms (linked with DOT mutation)(Haney & Evans, 2016)., as markers, to identify onset of schizophrenia in human patients who were under the influence of marijuana testifies that gene sensitivity polymorphism was undergone. In this study, the sensitivity test explains that marijuana does in fact morph some nucleotides (Vaucher, 2018). There is enough correlating evidence to suggest a causal relationship between schizophrenia and marijuana use because it would involve exposing human patients to a degree of marijuana that might be harmful. Even though the short term effects did not seem to be saying, but the long term effects of the use were very consistent. It strengthens the causative relation hence, there is further need to investigate the causal relationship.
Therefore, further studies are required to have more insight on whether the gene polymorphism alone is responsible for schizophrenia, if so, it would clearly negate the causal effect of cannabis, but until then, scientists cannot rule out the possibility of a causal effect of cannabis on schizophrenia.
Abnormal activity at dopamine receptor sites (specifically D2) is thought to be associated with many of the symptoms of schizophrenia. Four dopaminergic pathways have been implicated (Figure 1).4,5 The nigrostriatal pathway originates in the substantia nigra and ends in the caudate nucleus. Low dopamine levels within this pathway are thought to affect the extrapyramidal system, leading to motor symptoms.1The mesolimbic pathway, extending from the ventral tegmental area (VTA) to limbic areas, may play a role in the positive symptoms of schizophrenia in the presence of excess dopamine.1 The mesocortical pathway extends from the VTA to the cortex. Negative symptoms and cognitive deficits in schizophrenia are thought to be caused by low mesocortical dopamine levels. The tuberoinfundibular pathway projects from the hypothalamus to the pituitary gland. A decrease or blockade of tuberoinfundibular dopamine results in elevated prolactin levels and, as a result, galactorrhea, amenorrhea, and reduced libido.
The serotonin hypothesis for the development of schizophrenia emerged as a result of the discovery that lysergic acid diethylamide (LSD) enhanced the effects of serotonin in the brain.1 Subsequent research led to the development of drug compounds that blocked both dopamine and serotonin receptors, in contrast to older medications, which affected only dopamine receptors. The newer compounds were found to be effective in alleviating both the positive and negative symptoms of schizophrenia.1
Another theory for the symptoms of schizophrenia involves the activity of glutamate, the major excitatory neurotransmitter in the brain. This theory arose in response to the finding that phenylciclidine and ketamine, two noncompetitive NMDA/glutamate antagonists, induce schizophrenia-like symptoms.6 This, in turn, suggested that NMDA receptors are inactive in the normal regulation of mesocortical dopamine neurons, and pointed to a possible explanation for why patients with schizophrenia exhibit negative, affective, and cognitive symptoms.7
The brain tissue itself appears to undergo detectable physical changes in patients with schizophrenia. For example, in addition to an increase in the size of the third and lateral ventricles, individuals at high risk of a schizophrenic episode have a smaller medial temporal lobe.
As statistical data can give a deeper insight on the subject matter, here mention are few studies that have prominent outcomes. One of the studies showed that any cannabis use in a lifetime was associated with a 1.4-fold increased risk of developing psychotic illness and a 3.4-fold increased risk for those with cannabis dependence. Other studies have demonstrated that psychoses develop earlier in cannabis users compared to non-users (Hasan et al., 2019). Many have found a dose-response relationship with increasing risk with more cannabis consumed, in which the risk for developing psychotic illness, specifically schizophrenia, was four times higher among heavy users compared to non-users (Marconi, Di Forti, Lewis, Murray, & Vassos, 2016). It is important to note the study by Manrique-Garcia et al. controlled for ‘disturbed behavior’ thus arguing against the point that those who develop psychosis and use marijuana are psychologically deviant (Manrique-Garcia et al., 2012).
Therefore, extra insights are called upon patients whose family members/parents are chronic users of cannabis but not schizophrenic, such definitive population for the studies can add on some more clarification.
In conclusion, there are not enough evidence to prove a direct causal relations. However, there are enough reasons to suspect a causal relationship. Therefore, there is a need for further studies with different control groups, which can better determine the nature of the relationship between schizophrenia and marijuana.
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