## 4 Discussion  
Research performed in recent years has allowed a better understanding of the etiology of psychosis, which is based on the vulnerability-stress model [10]. This model postulates a combination of molecular genetic variants together with environmental factors such as etiological factors of psychosis [14; 23]. Regarding the risk of acquiring the psychotic disorder, the authors all agree that cannabis is a trigger factor in the onset of psychosis [12]. Therefore, they argue that without the genetic variations of genes such as AKT1, COMT and DAT1, the debut of mental illness would be possible [18]. On the other hand, all studies agree that the AKT1 gene has various loci involved in the development of psychosis, such as rs11300233 and rs2494732 [18]. Likewise, the authors disagree about the alterations in the rs2494732 polymorphism of the AKT1 gene and its relationship with the appearance of the mental disorder [26; 27]. Based on this, the authors all affirm that in the presence of the rs2494732 locus, being homozygous T/T does not increase the risk of acquiring the disorder, while being homozygous C/C does increase the risk [10; 21; 24; 28; 29; 30; 31; 32]. In addition, all the investigations converge that carriers of one C and one T allele do not increase the probability of debut of the disease. This is unlike others who say yes, although not exponentially such as those with the two C alleles, which shows that this allele is the main one involved in the appearance of the mental disorder in terms of the gene that AKT1 refers. This finding is very revealing since it can shed light on treatments aimed at the intervention of this pathology, which currently does not have a curative treatment [25; 27; 29; 30; 31; 32]. Likewise, it is worth asking what is the minimum dose of cannabis necessary for schizophrenia to develop, since studies show that this disease can appear in very low percentages [34]. For this reason, it is important to make the population aware that low doses can cause the disease and intervening in the early stages of psychosis is essential to be able to stop the disease's progression. In addition, the nurse's work in this area is vital, carrying out primary prevention. A strongly emphasized fact in all the studies, and in which the various authors converge, is to focus on the biological plausibility of psychosis due to cannabis use in the presence of genetic variations [29; 31]. For this reason, the investigations coincide in the idea that the greater amount of dopamine released in the striatum is responsible for the appearance of mental illness [33]. Despite this, the direct mechanisms that cause the onset of the said illness are not shown exactly, with all the authors suggesting that the indirect mechanisms of GABAergic and glutamatergic signaling play a fundamental role [30; 33]. In another aspect, it is difficult to know exactly the action of the COMT gene with respect to the development of psychotic disorder [31]. Because of this, the authors begin to postulate that the COMT gene, in the presence of the amino acid Val in a specific position, increases the risk of acquiring the psychotic disorder, although others also suggest that the substitution for methionine contributes to its reduction, which reveals the importance that the presence of the amino acid Val has for the appearance of psychotic symptoms [27; 29; 30; 32; 33; 34]. Likewise, traumatic experiences such as child abuse contribute to the development of mental pathology, increasing the risk of the onset of psychotic disorder. This condition converges with consumption [21; 33]. Likewise, the exponential increase in the probability of acquiring the psychotic disorder is conditioned by the interaction of the G allele of AKT1 and being carried by allele 9 of tandem repeats in the 3\({}^{\prime}\) untranslated region, due to the greater amount of free dopamine in the striatum [23; 30; 42; 43; 44; 45].