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EFFECTS OF MARIJUANA USE ON THE BRAIN

Effects of Marijuana Use on the Adolescent Brain Abigail Sweeney Cleveland State University

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Today, cannabis has been considered as one of the predominantly abused drugs among teenagers. According to Lubman, Cheetham, and Yücel (2015), the popularity of cannabis in the past few years, especially among this age group, has resulted in the intensification of the attention placed on its potential benefits and harms. SAMHSA (2014) estimates that nearly 3-5% of the world population aged over 15 years has testified to have consumed marijuana. Also, more than 8.4% of individuals aged over 12 years use the drug in the US (SAMHSA, 2014). Additionally, about 20% of people aged 18 to 25 years old currently endorse marijuana smoking (Jacobus & Tapert, 2014). The development period referred to as adolescence has been considered to occur between 12 and 17 years. The adolescent time period characterizes a crucial stage in a person’s growth marked by unique social, emotional, physical, as well as cognitive changes. Also, several maturation processes in the central nervous system and healthy neurobehavioral plasticity occur, including volumetric growth, programming of neurotropic levels, myelination, changes in receptor distribution, and synaptic pruning. These changes mainly take place in the limbic region as well as the prefrontal cortex (PFC), and they are alleged to promote the advent of cognitive functions and people’s behavior (Jacobus and Tapert, 2014). Despite some speculations about there being “benefits” to marijuana, a vast majority of studies suggest that THC (tetrahydrocannabinol), the principal psychoactive component of marijuana, can cause adverse mental health effects. Many publications have underscored that adolescents consuming marijuana are at an elevated risk of experiencing various adverse psychological outcomes, including neurocognitive impairments and psychotic outcomes (Yücel et al. 2010). Until recently, the biochemical process by which marijuana produces its implications of behavior was enigmatic when its constituents were isolated, and Δ9 tetrahydrocannabinol (THC) was found to epitomize its psychoactive

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elements (Yücel, 2010). Consequently, many studies have found proof of changes in the brain in both young adults and teens who smoke marijuana. Pedersen (2008) did a review of forty-three research studies of the brain and chronic cannabis use. His findings were consistent with changed neural functioning and structural brain anomalies in marijuana users. Only eight of these studies were concentrated on teens although the results demonstrated that both functional and structural brain changes occur immediately after the adolescents begin smoking the drug. Research has also shown that these modifications may still be evident after a month of abstinence (Pederson, 2008). Overall, marijuana use through puberty has been shown to cause irreparable damage to the brain (Pederson, 2008). Cognition Investigations on adult marijuana users often report a somewhat noticeable reduction in performance in comparison to the control subject in cognitive domains such as processing speed, retention, and attention (Pederson, 2008; Gonzalez et al., 2012). Adolescence is associated with ongoing perceptive development in the spheres of executive functioning and retention. Also, this development stage is predominantly specialized in functions such as cognitive control. In turn, these are associated with neocortical tissue maturation, which consequently leads to adverse implications for engagement in reward and risk behavior and school performance. Horwood et al. (2012) examined young adults who used cannabis and found memory deficits. In this study, it was found that the cessation of usage was linked to improved performance with abstinence in a period of a minimum of eight years. This means that after cessation of marijuana usage for at least eight years, memory deficits were found to have decreased in severity. Additionally, Yücel et al. (2010) found that marijuana smokers performed

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worse in measures of delayed and immediate verbal memory in comparison to the community controls. In a subsequent similar study, the authors found that no variances between the cannabis community control and the consumers on measures of perceptive activities. Gonzalez et al. (2012) had similar results as they found disparities on delayed and immediate recall among young adult marijuana smokers at the age of twenty as compared to the control subjects who were not using marijuana. However, no variances were detected on measures of impulsivity. The findings of these researchers indicate that using marijuana affects the decision-making tasks of the brain. Crean, Crane, and Mason (2011) reviewed existing knowledge of both short-term and long-term implications on executive perceptive tasks such as working memory, decision-making and risk-taking, attention and concentration, verbal fluency, as well as inhibition and impulsivity after using cannabis. They found that there were mixed results of acute effects of marijuana on executive function. Their findings indicate that the damaging effects of cannabis consumption on concentration and attention were stronger in regular smokers that had developed a drug tolerance than the inexperienced ones. Abstinence disrupted these cognitive functions. Instead of the acute administration of cannabis was also found to impair aspects of decision-making, planning, and impulsivity. Verbal fluency seemed to be intact although impairments in working memory were observed. Solowij and Battisti (2008) carried out a clinical study on 181 adolescents aged between 16 and 20 years. Their findings demonstrate that marijuana users performe poorly on recall and learning, that was related to the age of initiating cannabis, frequency, and severity. They conducted a study on prospective memory, whereby they evaluated undergraduates from 18 to 24 years of age (Solowij & Battisti, 2008). They found no difference in self-reported prospective mind, although cannabis users only recalled few location-action combinations during the

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objective video-based potential memory task. Other research studies also demonstrate a decrease in intelligence quotient, especially processing speed and executive functioning, associated with persistent use of marijuana consumption in adolescents. Structural Neuroimaging Dynamic changes occur in the grey matter structures of adolescents as they go through development. Grey matter within the brain is a part of the brain that contains neurons and axon terminals. This means that grey matter in the brain contains the synapses that carry and send messages to other parts of the brain (Merriam-Webster, 2018). For instance, the elimination of synapse and dendritic pruning probably lead to decreased cerebral volume and cortical thinning, while subcortical structures such as amygdala and hippocampus have been found to increase with age. Several studies have proven that the consumption of marijuana is related to changes in the brain. Gilman et al. (2014) used an MRI to observe the brain modifications in youths between 18 and 25 years who used cannabis at least once a week but were not depended on it. When comparisons between the non-users and users were carried out, the latter showed changes in shape, size, and mass of the gray matter of the regions linked to addiction. These include the amygdala, which is involved in decision-making, emotions, and memory, as well as the nucleus accumbens that has a role in reward pleasure, processing, and motivation. More significant disparities were observed in participants who smoked this drug. A study was carried out by Malone, Hill and Rubino in 2010 among adolescent marijuana users between the age of 16 and 19 years. It found that the right medial orbital prefrontal cortex volume of smokers had decreased when compared to the non-users. Additionally, the findings also indicated that the size was positively related to the age of marijuana initiation in the study population. This means that the young individuals who had started using the drug had a reduced orbital prefrontal cortex volume.

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However, Weiland et al. (2015) tried to replicate Gilman et al.’s (2014) investigations in young adults and adolescents who smoked marijuana daily, and their findings did not match those of the initial study. They argued that previous investigations failed to sufficiently control the participants’ use of alcohol. Therefore, after Weiland et al. (2015) carefully matched the intake of liquor in both the experiments and control subjects, they did not find any physical differences in the amygdala or the accumbens of daily cannabis users. On the other hand, the white matter tissue integrity such as coherence of fiber tracts and myelination is considered essential for effective cortical connectivity in the growing brain. Various studies have concluded that there is a linear increase in the white matter tissue during early development (Crean et al., 2011). As the fiber bundles mature from childhood and the brain becomes increasingly myelinated, diffusion of water molecules is restricted on the central axis of the common axon (Crean et al., 2011). This happens because the fibers gradually become compact and limited in intracellular space. In their research, Crean et al. (2011) found alterations of the white matter in the adolescent marijuana users from the age of 16 to 19 years. They also found more reduced white matter integrity as well as increased MD and decreased FA in cannabis smokers who also used alcohol. Weiland et al. (2015) additionally found that cannabis enhanced white matter diffusivity in the prefrontal cortex in comparison to alcohol consumers. Relation to Mental Illnesses: Anxiety and Depression According to Volkow et al. (2016), continuous cannabis use is linked to increased risk of depressions and anxiety, although the causality is yet to be well established. Malone, Hill, and Rubino (2010) also argued that it aggravates the progression of illness in patients with schizophrenia. More massive use of cannabis, exposure at a younger age, and higher drug

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potency can all adversely influence the disease course (Volkow et al., 2016). Research shows that it progresses the onset of a psychotic incident by 2-6 years. Volkow et al. (2016) further argue that it is difficult to determine causality in such investigations since other elements apart from cannabis use may be directly linked to the increased risk of mental illness. This, in turn, makes it challenging to confidently attribute the risk of psychological conditions to marijuana consumption. However, Malone et al. (2010) and Lubman et al. (2015) provide substantial evidence that the use of cannabis is highly linked to mental illnesses such as anxiety disorder, depression, and schizophrenia. Considerable changes in social, psychological, and physical domains characterize the critical stage in human development referred to as adolescence. These alterations are reinforced by the remodeling of part of the brain involved in sensorimotor, emotional, cognitive, and motivational systems (Malone et al., 2010; Lubman et al., 2015). Specifically, they encompass broad thinning of cortical synapses that increase myelination and decrease the cortical grey matter (Malone et al., 2010; Lubman et al., 2015). Endocannabinoid System Relations to Depression, Schizophrenia, and Anxiety Disorder Considerable changes in social, psychological, and physical domains characterize the critical stage in human development referred to as adolescence. These alterations are reinforced by the remodeling of part of the brains involved in sensorimotor, emotional, cognitive, and motivational systems (Malone et al., 2010; Lubman et al., 2015). Specifically, they encompass broad thinning of cortical synapses that lead to increased myelination and a decline in the cortical grey matter. Anxiety disorders make up the most commonly known impediments that emerge from the massive chronic consumption of marijuana. While the prevalence of anxiety disorder in general

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population has been estimated to be approximately between 6 and 17 percent, it is more common in marijuana users with levels of up to 20 percent (Renard et al., 2014). According to Renard et al. (2014), anxiety is substantially positively linked to the misuse and consumption of marijuana. Nevertheless, there is hardly any study that has focused on the link between the consumption of marijuana and long-standing anxiety disorders. Smoking marijuana as an adolescent has been linked to increased risk of having symptoms related to anxiety in later stages of life, especially if the individual began using the drug before the age of fifteen. Furthermore, boys are less likely to develop these symptoms. Degenhardt et al. (2013), explored the link between the cannabis intoxication and psychological health in their participants whose age ranged from 15 to 29 years. They found that heavy marijuana smoking during the formative teen years was linked to an enhanced possibility of developing an apprehension illness in adult years, even if the person did not use cannabis in the later stages of life. Numerous researchers support the relationship between depressive disorders among young cannabis users (Lubman et al., 2015; Renard et al., 2014; Pedersen, 2008). In this group, the prevalence of depressive disorders is 25 percent (Lubman et al., 2015). Nearly half of these cases account for severe mood disorders, while the rest are primarily depression. According to Malone et al. (2010), the risk can surge approximately five times depending on the onset of cannabis use and gender since men are less susceptible as compared to their female counterparts. Research has found that adolescents who consume marijuana have a higher probability of meeting the criteria for depression in adulthood than those who have never used the drug (Renard et al., 2014; Lubman et al., 2015). Additionally, approximately 30 percent of adolescents between 15 and 17 years of age who are heavy marijuana users often develop depressive symptoms by 21 years. Therefore, teens who smoke cannabis have a higher probability of

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reporting symptoms of depression and anxiety as young adults. Pedersen’s (2008) longitudinal study that followed young Norwegians from their early to late teenage over a period of 13 years demonstrated a dose-dependent association between suicidal tendencies in adulthood and massive consumption of marijuana. All these studies suggest that the use of this drug on a regular basis during the adolescence phase increases the chances of contracting depressive disorders in adulthood. Nevertheless, a few researchers propose that hereditary predisposition and ecological factors are linked to the causality (Lubman et al., 2015). Additionally, Crean et al. (2011) established that depressive symptoms in teen cannabis users were linked to smaller white matter volume. This implies that the consumption of this drug as an adolescent may affect the white matter connections in the region of the brain that are involved in mood control. Although these studies highlight the relationship between cannabis consumption and depression as well as preexisting genetic elements, additional research is required to illuminate on the neurobiological processes that reinforce the long-term implications of marijuana intoxication on the subsequent inception of depressive syndromes. The Endocannabinoid System In the last few years, research has established that the endocannabinoid structure has a vital function in the neuro-developmental progressions that occur in adolescence. It is comprised of “two G-protein-coupled cannabinoid receptors, also referred to as CB2 and CB1 enzymes, responsible for degradation and synthesis, and endocannabinoid ligands (endocannabinoids; mainly 2-aeachidonoyl ethanolamide [2-AG] and anandamide [AEA])” (Lubman et al., 2015). In the brain, a primarily extracted “G-protein–coupled receptors” is the CB1 receptor. It is reported to facilitate the majority of effects of cannabinoid intoxications on the CNS (central nervous system), while the CB2 is copious in the exterior tissues, especially the immunity system.

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According to Renard, Krebs, Le Pen, and Jay (2014), CB1 receptors are principally presynaptically positioned, whereby, when endocannabinoids activate them, transmission in both glutaminergic synapses and GABA-ergic is inhibited. Therefore, the endocannabinoid system has an essential part in the regulation of the equilibrium between excitatory and inhibitory neuronal actions. Undeniably, it has been shown that cannabinoids exert neural effects through inhibiting glutaminergic neurotransmission and controlling glutamate-induced excitotoxicity (Lubman et al., 2015). Cannabis consumption and psychosis: Schizophrenia Some of the psychotic symptoms linked to marijuana include feeling of unreality, depersonalization, hallucinations, loss of control, concentration difficulties, paranoia and fear, thought disturbances, dysphoria, apprehension, as well as other perceptual modifications (Malone et al., 2010). Research has established that marijuana consumption is linked to schizophrenia. This mainly manifests itself in the later years of life. According to Malone et al. (2010), the exposure of cannabinoid to teens has been established to exert a long-term reduction on the expression of CB1 receptors and G-protein coupling in some regions of the brain in a similar manner used to induce schizophrenic-like symptoms in animal models. Furthermore, this has also been reported to trigger several molecular and cellular incidents in the brain, which can be potentially attributed to the progression of various schizophrenia signs (Malone et al., 2010). However, concrete evidence is yet to be reported of the mechanisms by which the components of marijuana cause this illness. This has raised queries regarding whether teen marijuana consumption prompts the development of schizophrenic symptoms in genetically susceptible individuals. Also, there are researchers who still investigate whether people with prevailing susceptibility to psychosis have a higher probability of using this drug in self-medicating

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treatment to relieve certain psychotic signs. Malone et al. (2010) argue that this explanation of self-medicating does not consider the relationship between teen marijuana smoking and the onset of mental illness in adulthood, as this association is often detected in nonexistent conditions of psychological distress. Consequently, the latter is not inherently a predictor of cannabis consumption. Cannabinoid Receptors Research regarding the human intellect supports the CB1R (cannabinoid receptor type 1) dysfunction in particular regions of the brain of schizophrenic patients. According to Lubman et al. (2015), this is precisely the cortical areas that are involved in the functioning of the memory and cognition which take place in the dorsolateral PFC as well as posterior and anterior cingulate cortices. Consequently, these are the two brain tasks in schizophrenia which are compromised. In conclusion, various researchers indicate that marijuana consumption adversely affects the brain functions and structures, especially in adolescent users. Marijuana has become one of the most common drugs that teenagers use. Cannabis consumption has been linked to various beneficial and harmful effects. The chronic use of cannabis in the adolescent phase has been reported to increase the risks of developing cognitive impairment and mental illness,...