Cannabis and Adolescent Perceptions

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16th Dec 2019 Dissertation Reference this

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Introduction

The age of initiation of cannabis use is changing with younger children and adolescents

reporting daily cannabis use. According to the national institute on drug abuse (NIDA)

(2014), 16.4% of individuals age 12–17 and 51.9% of individuals’ ages 18–25 years have

used cannabis in their lifespan in the USA. While cannabis use appears to be increasingly

recognised as a ‘safe’ recreational drug (Camchong et al 2016), it is imperative to

comprehend what the consequences of chronic cannabis use are, during critical phases of

development such as adolescence. Researchers are still uncertain as to precisely how

cannabis use affects brain structure and function, but some studies indicate that long-term

chronic use leads to fluctuations in both neurological function and physical brain structure

(Battistella et al 2014). Further, cannabis’s relationship with psychological health remains

unclear. Researchers have established that cannabis use, significantly influences adolescent

psychosocial behavior, however, more research is required to corroborate accurately how

cannabis use correlates to mental health (Shrivastava et al 2011).

Previous studies exploring the impact of cannabis on development, advocate that there is a

tenacious effect on cognition and neuropsychological performance in individuals who initiate

cannabis use during adolescence (Jacobus and Tapert 2014). Longitudinal data demonstrate

that individuals with more persistent cannabis dependence have a distinct intelligence

quotient (IQ) deterioration, with substantial impact on complete IQ (full-scale IQ) ( Meier et

al 2012 ). Moreover, evidence proposes that overall IQ discrepancies do not completely

improve after cessation of use (1 year), particularly in adolescent-onset cannabis users (Meier

et al 2012). Further to its effects on intellectual aptitude, cannabis has been perceived to have

a negative influence on neuropsychological test performance in tasks that assess executive

function and psychomotor speed (Lane et al 2007). Even after 10 months of abstinence

Schweinsburg et al (2008) propose that individuals that commenced using cannabis during

adolescence have persistent neuropsychological deficits.

For the purpose of this assignment an overview of cannabis will be provided before focusing on more specific aspects of cannabis use pertinent to the adolescent population. This will include, gaining an insight into the perceptions and impact of legislative changes, among adolescents. Following on from this an overview of adolescent brain development will be discussed followed by an insight into the impact of cannabis use on the adolescent brain.

Finally the area of mental health and cannabis use among this cohort of society will be deliberated before concluding on the related points of the literature reviewed.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

What is Cannabis?

Cannabis is the preferred title of the plant Cannabis Sativa, Cannabis Indica, and of

minor significance, Cannabis Ruderalis (Gloss 2015). The usage of cannabis for medicinal,

ceremonial or recreational reasons is resultant from the activities of cannabinoids in the

cannabis plant and these compounds also produce the inadvertent adversarial consequences

of cannabis (Madras 2015). It is estimated that the plant comprises of at least 750 chemicals,

among which are some 104 different cannabinoids (Radwan et al 2015). Though cannabis

comprises many chemical substances, it is delta-9- tetrahydrocannabinol (THC) that has been

identified as the principal compound that creates the “high” that follows when smoking or

ingesting the plant materials (Radwan et al 2015).

 

Chemical structure of THC

Image result for cannabis structure

It is likely that other compounds in cannabis also contribute and interrelate with THC to

produce its innumerable  physical and psychological effects. Research has particularly

concentrated on better comprehending  the role of cannabidiol. Selected evidence proposes

that cannabidiol may moderate the effects of cannabis, diminishing the potential anxiolytic

and psychomimetic effects of THC, nevertheless other studies have not observed such effects

(Karschner et al 2011). However, THC levels are fluctuating, as propagation of different

strains are yielding plants and resins with striking growth in THC content over the previous

decade, from ~ 3% to 12-16% or higher  and differing in different countries (Swift et al

2013). THC levels in some cannabis preparations, have escalated even more drastically by

using a concentrating process (butane hash oil) that produces levels approaching 80% THC

(Stogner and Miller 2015).

Cannabis is consumed by numerous routes, with the most common route smoking, (Baggio et

al 2014) followed by vaporization, and then by the oral route. Azorlosa et al (1995) have

indicated that inhalation by smoking or vaporization discharges highest amounts of THC into

blood within minutes, attaining its peak at 15-30 minutes, and decreasing within 2-3.

The active chemical in cannabis tetrahydrocannabinol (THC) strongly resembles the structure

of cannabinoid chemicals that happen naturally in the body, called endogenous cannabinoids

(NIDA 2014). These chemicals are neurotransmitters that direct communications between

neurons in the brain and the rest of the nervous system (NIDA 2014). The areas of the brain

most connected with the receptors for endogenous cannabinoids are the hippocampus, basal

ganglia, amygdala, cerebellum, ventral striatum, neocortex, and the brain stem and spinal

cord; these are the principal regions accountable for pleasure, concentration, memory,

coordination, movement, and sensory and time perception (NIDA 2014).

Image result for The areas of the brain most associated with the receptors for  endogenous cannabinoids

The areas closely linked with cannabinoid receptors also manage pain inflection and prompt

higher-order processes (NIDA 2014). All of these areas feature in typical human brain

function and effect the ways that we behave and connect to other people and stimuli (NIDA

2014). Resultant from THC, closely resembling endogenous cannabinoids in structure, it

connects to the cannabinoid receptors in the brain and overwhelms the nervous system with

communications to that portion of the brain (NIDA 2014). This stimulates the areas of the

brain connected with endogenous cannabinoids, triggering instabilities to usual brain function

(NIDA 2014). This produces the effects that cannabis users recognise, such as feelings of

pleasure and relaxation, distorted perception of time, heightened sensory experiences, and

slow motor function (NIDA 2014).

 

Epidemiology of cannabis use

Patterns of drug use in Ireland have become increasingly diverse in terms of the type of drug

used, the availability of drugs and the demographics of users (van Hout 2009a). Service

providers consider that illicit drug and drug use has become a normal feature of society (van

Hout 2009a). UNICEF Ireland, Changing the Future (2011) surveyed a significant number of

16-20 year olds, and established that over a third of participants had taken an illegal drug and

that most had done so by the age of sixteen (UNICEF Ireland, Changing the Future 2011).

Widespread availability and ease of access to illegal substances has contributed to a degree of

acceptance in communities and has facilitated with the normalization of drug use. In recent

years Cannabis has become so obtainable and inexpensive, its use has amplified significantly

(Bellrose 2012). Cannabis is regarded among young people as a ‘safe drug’ and van Hout

(2010) argues that most young people estimate cannabis to be as safe as smoking cigarettes

and were not concerned with any future health impact associated with use.

The United Nations Office on Drugs and Crime (UNOCD) World Drug Report (2012)

identify that cannabis is the worlds’ most widely used substance with between 119 and 224

million users worldwide. The European Monitoring Centre for Drugs and Drug Addiction

(EMCDDA) (2011) lifetime prevalence figures for adult population (15-64 yr. old) show that

78 million European adults report using cannabis with Western Europe having the uppermost

frequency for cannabis in the world. In line with the aforesaid Global and European

statistics, it was observed that cannabis is the most extensively accessible and frequently used

drug in Ireland (Long and Horgan 2012). van Hout (2010) has indicated that the social

accommodation of recreational cannabis use is becoming more commonly established within

Irish society.

Similar to figures from other countries; 32.2 % of young Irish adults aged 15-34 years,

compared to 18% of older adults aged 35-64 years reported using cannabis with use more

common in males National Advisory Committee on Drugs (NACD) ( 2011). Lifetime

cannabis use was reported by 23.5%  of 15 year olds in the 2006 Irish HBSC survey (Currie

et al 2008). In 2006/07, cannabis was the most commonly used illegal drug with 21%

reporting lifetime use, which was also a significant increase on 2002/03 rates (12.0%).

Prevalence rates for lifetime cannabis usage amongst young adults (15-34 yrs) were at least

double those of older adults, 29.1% versus 14.5% respectively. Moreover, lifetime and

preceding month frequency of cannabis use among young adults had significantly increased

since 2002/03 (NACD 2008b).

However, Degenharth and Hall (2012) caution that since studies from different countries

often use various methods for estimating the prevalence of substance use, comparison of

results between countries could be misleading. The interpretations of reported estimates

should therefore be made with awareness of these methodological limitations

 

Perceived cannabis use norms and impact of legislative changes among adolescents

There is an emergent perception, predominantly in adolescents and young adults (Lopez-

Quintero and Neumark 2010), that cannabis is ‘harmless’ particularly when compared to

other abused substances such as nicotine and alcohol that are legal. Notwithstanding the

latent consequences, the levels of perceived risk and disapproval of cannabis amid adults and

adolescents are minimal and progressively diminishing ( Johnston et al 2012). Rationales

allude to, for this perception include, the deliberation that cannabis-associated mortality is

lower than tobacco and alcohol, which are linked with cancer and overdose/ vehicular

accidents, correspondingly (Hurd et al 2014).

Friese and Grube (22013) suggest that from an American perspective, changes in state laws

on medical or recreational cannabis use, may influence changes in adolescents’ access to

cannabis and cannabis use (CU) norms.  Information regarding medical cannabis legalization

or discrimination of cannabis use may indicate more liberal community norms in relation to

CU generally, and research data propose that CU norms in the community are related to

adolescent cannabis use (Friese and Grube 2013).

Perceived parental or friends’ approval of cannabis use is allied with an elevated cannabis use

prevalence among college students (Labrie et al 2011). Although cannabis use practices

among adolescents are less researched, preceding studies suggest that adolescent’ perceptions

of their parents’ or peers substance use or norms, may effect adolescents’ substance use

(Iannotti et al 1996). Cannabis use norms may be impacted by community’s drug use level or

norms, adolescents’ substance use, and the availability of cannabis (Bahr et al 2005). Drug

use norms of  close friends  can be associated with adolescents’ intention towards substance

use (Olds et al 2005). In a study comprising of 180 heavy CUs who participated in a

treatment trial, the perceived approval of close friends’ to cannabis use was positively

associated with cannabis use (Walker et al 2011). Therefore, when considered jointly,

adolescent’s perceived CU norms appear to be an important correlate of cannabis use (Wu et

al 2015).

With reference to the ‘Theory of planned behaviors’, a person’s attitudes, norms and

perceived control may influence the intention of CU and actual use (Malmberg et al 2012).

The opposite association between adolescent’s discontentment or apparent disapproval for

cannabis use by significant others, and lower CU, may be related to a higher level of

adolescent’s confidence, in being able to decline or avoid CU in tempting circumstances

(Malmberg et al 2012). Specifically, for those adolescents with negative attitudes towards

cannabis use and experience disapproval of CU from those within their social environments,

they may have a higher level of refusal or a lower intention of using cannabis, in comparison

to those within their peers who perceive a higher level of cannabis use acceptability

(Malmberg et al 2012).

In their critical review of the literature, Sznitman and Zolotov (2015) concluded that there

was insufficient evidence to support medical cannabis’s negative influence on public health.

Other studies support some concerning trends, predominantly as it relates to adolescents. One

American study found that adolescents had significantly higher rates of reported use in the

past 30 days and a lower perception of risk in states with legalized medical cannabis (Wall et

2011). Significant differences in past-year use and prevalence of dependence/misuse were

identified between states with medical cannabis laws and states without them (Cerda et al

2012). The probabilities of past-year use and dependence were virtually double for

individuals living in states with legalized medical cannabis (Cerda´ et al 2012).

The literature on adolescent use and perceptions of cannabis in relation to legislative changes

is in an embryonic state. Cerda´ et al (2012), hypothesize that ‘‘Future studies are needed . . .

on the particular impact of medical marijuana legalization on youth who bear a

disproportionate burden of marijuana-related disorders, and are vulnerable to the advertising

effects of other substances such as tobacco’’ (p. 26). The initial research appears to propose

that both cannabis laws and adolescent use are attributable to lenient normative approaches.

However, absent from this debate are the opinions of those who may have the greatest

perception into the individual and social consequences of cannabis use, substance misuse

treatment providers (Sorbesky and Gorgens 2016). ).

 

Cannabis as a ‘gateway drug’

Hurd et al (2014) deliberate that a chief characteristic of the debate concerning adolescent

cannabis use is whether there is a possibility that it increases the usage of other addictive

substances, such as heroin and cocaine later in life, a phenomenon recognised as the

‘Gateway Hypothesis’. However, epidemiological and clinical studies have chronicled an

important connection between continual early cannabis exposure and the increased

vulnerability to other illicit drug use (Fergusson and Boden 2008).

Overall, the data according to Hurd et al (2014) proposes, that use of ‘heavy’ drugs is

virtually systematically preceded by the use of cannabis, and that susceptibility is correlated

with the intensity of cannabis exposure. Moreover, the use of cannabis further emerges as

more destructive, when its commencement arises in younger versus older adolescents, with

regard to the adjustment for adolescent in transitioning to young adulthood, education

achievement, employment, misbehaviour and capacity to adapt to adult role (Fergusson and

Boden 2008). Notwithstanding these results, a principal warning regarding human studies, is

the complexity of indicating a contributory relationship between adolescent cannabis use and

consequent behavioural disturbances, particularly when considering the influence of genetic

and environmental features in conjunction with other characteristics such as polysubstance

use (Cleveland and Wiebe 2008).

Given these complexities, animal models are a respected method to attain direct

understandings about the relationship between early cannabis exposure and behavioral

disruptions (Bostwick 2012). Various rodent investigations discovering the latent gateway

consequences of cannabis, have primarily considered synthetic cannabinoid agonists,

however, these differ in pharmacological properties to THC (Fattore and Fratta 2011).

Nevertheless, studies exploring adolescent exposure to cannabinoid agonists or THC, deliver

indications of heightened consumption and sensitivity later in life to opiate drugs

(Tomasiewicz et al 2012).

Although animal studies demonstrate protracted behavioral and neurobiological

consequences of adolescent THC exposure into adulthood, Hurd et al (2014) observe that not

all adolescent cannabis users advance to future addictions or psychiatric disorders . In fact,

notwithstanding its commonplace usage, only a subsection of teens and young adults using

cannabis progress to abuse or dependence (SAMHSA 2011). Indeed, for the majority of

teenagers, cannabis is a terminus with no further use in relation to that or other illicit drugs,

as they mature into full adulthood, signifying that there are variances in individual

susceptibility and  there are remarkable differences in human beings in relation to their

environment, behavioral traits, genetics, and cultural norms (Hurd et al 2014). While these

and other influences contribute to substantial areas of  complex disorders such as addiction,

comprehension of the influence of particular factors is as equal a challenge as determining

their connections to risk (Hurd et al 2014)

 

Adolescent Brain Development: Overview

The term adolescent originates from the Latin verb ‘adolescere’, meaning “to grow” and is

understood  as a cycle of change and is often considered the most transformative phase in an

adolescents life. The period is more often said to extend from around 10 years of age to some

years over 20. The definition is, nevertheless, still largely dependent on culture and context

(Steinberg 2002). However, adolescence is a period of significant changes in the structure

and function of  the brain; other than the first three years of life, no other developmental

phase is characterized  by more intense transformations (Steinberg 2011).

While development of complete brain size is essentially complete by age five, explicit

structural and functional changes endure during adolescence and contribute to more

competent cognitive functioning (Tau and Peterson 2010). During adolescence, the brain

experiences significant developmental changes, with the frontal lobe maturing in later

adolescence and into early adulthood and both myelination and synaptic refinement

continuing throughout adolescence (Arain et al 2013)). Studies in typically developing teens

without heavy alcohol or drug use demonstrate that white matter volumes  increase

throughout the brain with continued myelination during adolescence (Jacobus and Tapert

2014.) Grey matter volumes peak around age 13 in males and age 11 in females and then

decline as unnecessary  neural connections are eliminated, resulting in a net volume loss

during this time (Giedd 2012). Increases in myelination, detected as increases in white matter

volumes, and in  pruning of grey matter, detected as decreases in cortical grey matter,

facilitate more effective  communication among neurons in the brain. These changes allow

specialized cognitive processing required for optimal cognition and performance (Brown &

Tapert 2004).

Image result for adolescent brain

During adolescence, the chief function of the brain is to generate effective neuronal pathways

through neuronal refinement (Tau and Peterson 2010). This process comprises substantial

loss of synapses in neocortical regions, transformation of the prefrontal cortex, maturational

changes in the hippocampus (Whitford et al 2007). Regions that experience significant

synaptic pruning in adolescence are temporal and frontal regions and striatal areas, with

prefrontal cortical areas being particularly late to mature (Casey et al 2008). Significantly,

circuits concerning the prefrontal cortex and the striatum are fundamental to complex order

cognitive skills which are reflective of decision making, risk and reward processing, and

cognitive control (Geier and Luna 2009).

 

 

Cannabis Use and the Adolescent Brain

Cannabis impact on brain development is remarkable in adolescent users, having intense

consequences on numerous regions of neurological and psychosocial growth (Volkow et al

2014). The human brain continues to experience rapid and dynamic expansion until

approximately 21 years of age, in which the brain experiences physical changes (Volkow et

al 2014). If the brain is subjected to cannabis during this development, particularly in

adolescent years, reward and pleasure centres can be “recalibrated”, signifying that cannabis

use throughout developmental years can create essential changes in learning and social

behavior (Volkow et al 2014).

Discoveries of intensified risk linked with adolescent cannabis use, combined with research

indicating a role of the endocannabinoid system in regulating neurodevelopmental processes,

have led to assumptions that adolescent cannabis use may interrupt the standard course of

neurodevelopmental processes and cause long-term changes in brain functioning (Viveros

et al 2012). Additionally, it seems there are a number of influences (e.g., female sex, early

trauma experience, genetics) that may decrease the consequences of adolescent cannabis use

on brain development (Lubman et al 2015).

Adolescent cannabis use might be connected with protracted changes in brain functioning in

part through the interruption of synaptic pruning processes in those regions that are

simultaneously growing (Lubman et al 2015). With regard to adolescence being a

predominantly significant period for the development of prefrontal brain areas, more recent

animal studies have revealed that altering endocannabinoid neurotransmission in adolescent

female rats causes enduring fluctuations in prefrontal brain regions reflective of disrupted

synaptic pruning (Rubino et al 2015). Therefore, research reinforces the suggestion that, at

some level, particular cognitive and behavioural deficiencies linked with early adolescent

cannabis use in the studies related to humans, may possibly be connected to the disturbance

of endocannabinoid-mediated neurodevelopmental procedures by cannabis (Albertella and

Copeland 2016). It is plausible to hypothesize that adolescent exposure to cannabinoids might

somehow interrupt these  maturational proceedings, thus leading to an adult brain with

transformed network connectivity in these  very brain areas (Rubino and Parolaro 2014)

 

  • Cognitive Impairment

Adolescents who use cannabis frequently, characteristically exhibit a number of non-acute

cognitive deficits in contrast to adolescents who do not use cannabis or use it occasionally

(Pardini et al 2015). For instance, a study by Hanson et al (2010) found enduring

discrepancies in the area of selective attention within a group of adolescent heavy cannabis

users, compared to a control group who had used cannabis less than 5 times in their lifetime.

Fluctuations in verbal learning and memory amongst this group, nonetheless, improved

following a period of abstinence (Schweinsburg et al 2008). Furthermore, some studies have

indicated that adults who started using cannabis early in adolescence display more substantial

cognitive impairment than adults who started using cannabis later (Koenders et al 2016).

Volkow (2014) has utilised the findings of non-acute cognitive deficits in adolescent cannabis

users, to support the idea that adolescence may be a particularly sensitive phase for the

adverse consequence of cannabis use. Albertella and Copeland (2016) contend that there is

also research, to suggest that pre-existing factors connected to cognition  may provide

justification for some of the differences found between adolescent cannabis users and non-

users. Some group differences in cognition may not be the consequence of cannabis use but

may be due to pre-existing group differences leading to earlier inception of cannabis use

(Jacobus and Tapert 2014). In particular, measures of selective attention undertaken in early

adolescence have been established to predict greater cannabis use by late adolescence

(Squeglia et al 2014). Correspondingly, impulsivity-related personality traits have also been

shown to predict regular adolescent cannabis use (van Leeuwen et al 2011)

Studies have also found differences in brain structure between those who commence cannabis

use in adolescence and non-users (Jacobus and Tapert 2014). These include differences in

orbitofrontal cortex volume which is a prefrontal brain area related to impulsivity, reward

processing, and cognitive control (Casey et al 2008) — at age 13, which predicted subsequent

onset of cannabis use by age 16 (Cheetham et al 2012). Thus, some of the cognitive deficits

seen in adolescent cannabis users as reported by Hanson et al (2010)  may in fact have

preceded cannabis use.

Long-term cannabis use has been connected with cognitive impairments in a diversity of

investigations, however, there is incongruity concerning the timeframe of the harmful effects.

Meier et al. (2012) undertook a 38-year follow up study using the 1,037 participants from the

‘Dunedin Longitudinal Study’. Participants were tracked from birth to age 38 and data on

cannabis use was established through interviews at ages 18, 21, 26, 32, and 38. Further to this

baseline neuropsychological testing was conducted at age 13, before cannabis use had been

commenced, and follow up neuropsychological testing was conducted at age 38. The

investigators established that persistent cannabis use was allied to comprehensive cognitive

declines, affecting multiple domains of neurocognitive functioning. Furthermore, participants

with adolescent onset of cannabis use had cognitive deficits that persisted more than a year

after cessation of cannabis use (Meier et al 2012). Results suggested that persistent use of

cannabis that is initiated while the brain is still developing might have a comprehensive

enduring influence on cognition even after end of cannabis use.

  • Executive functioning

Studies on adolescents with cannabis use histories identified worse performance on

perseverative responding and flexible thinking in contrast to controls (Lane et al 2007).

Inferior performance on executive functioning amid adolescent cannabis users was correlated

to more days of cannabis use in the preceding month (Harvey et al 2007). In a recent, large-

scale, longitudinal exploration, individuals with persistent cannabis dependence showed

decline in their intelligence quotient with time, predominantly in executive functioning

(Meier et al 2012).

Even after one month cannabinoids are measureable in the blood of chronic daily cannabis

smokers during continued abstinence (Bergamaschi et al 2013).  Cannabis continues to

impair executive functions, with the chronic, heavy cannabis users showing the most

enduring deficits (Shrivastava et al 2011). Decision-making, organization and concept

creating are the most prominent and robust deficits, but verbal fluency may or may not

persevere at this point (Madras 2015).

  • Learning and Memory.

Verbal and spatial working memory aptitudes develop throughout adolescence, with older

adolescents countering more accurately and more quickly (Brown et al 2009), and cannabis

use during this time appear to interfere with those improvements. Comparable to studies

examining the influence of alcohol on learning and memory, numerous studies have revealed

similar discrepancies among cannabis using youth. In one of the initial investigations of the

influence of cannabis on adolescent cognition, Schwartz et al (1989) identified that short-

term memory impairment persisted even after six weeks of abstinence in cannabis-dependent

adolescents (ages 14-16) compared to matched controls. Studies in the past two decades have

consistently recognised discrepancies in instant and delayed recall among adolescent and

young adult (ages 13-24) cannabis users (Gonzalez et al 2012). In a study of adolescent

cannabis users ages 16-18, cannabis users displayed inferior verbal learning and memory,

even after one month of abstinence (Medina et al 2007). However, memory deficits identified

among young adult ,(ages 20-24) cannabis users with recent use showed improvement with

abstinence over the course of eight years (Tait et al 2011). Notably, diminished performance

on learning and recall among adolescent cannabis users has been connected to severity,

frequency, and age of initiation of cannabis use (Solowij et al 2011).

  • Processing Speed and Attention

In the literature related to cannabis, deficits in attention and processing speed have also been

consistently recognised (Schweinsburg 2008). Adolescent cannabis users who smoke more

than once per week were found to have inferior performance on attention tasks (Harvey et al

2007). In a longitudinal study exploring neuropsychological performance amid heavy

cannabis using youth, compared to non-using youth, between-group differences in attention

were identified at baseline and across 3 weeks of observed abstinence, with attention

differences persevering with time (Hanson et al 2010). Reduced processing speed has also

been identified among heavy cannabis using youth (ages 16- 18), even after one month of

monitored abstinence (Medina et al 2007).

The neurological changes identified in long-term users that initiated use during adolescence

also factor into the lifetime education and achievements of users (Volkow et al 2014).

Dougherty et al (2012) report that adolescent-onset users are more likely to leave high

school and experience adulthood difficulties in achievement (Dougherty et al 2012).

Adolescents that regularly consume cannabis experience more learning problems due to

changes in brain structure and function, and are less likely to seek assistance in improving

poor school performance (Dougherty et al 2013). Cannabis use is a reliable and significant

gauge of poor grades in school, particularly as the age of first use decreases (Palamar et al

2014). Furthermore, long-term cannabis use correlates with unemployment, lack of higher

education, dependence on social welfare programs, and low socioeconomic status (Volkow et

al 2014).

 

Cannabis and Mental health issues in adolescents

The capacity of cannabis to induce paranoia was first noted in 1845 by French psychiatrist

Moreau de Tours. He was a personal user of cannabis however, he also who also studied the

impact of cannabis on his students. He observed “acute psychotic reactions, generally lasting

but a few hours, but occasionally as long as a week” (Moreau 1973). While the acute effects

of cannabis have been extensively observed, there are further long-term consequences that

can have  considerable impact on otherwise healthy controls (Renard et al 2014). Researchers

have been able to establish that it is practically impossible to overdose on THC to the point of

death, however, THC consumption can create erratic or psychotic behavior that in extreme

circumstances could lead to accidental death (NIDA 2014).

  • Psychotic disorders

Epidemiological studies advocate that cannabis use throughout adolescence presents an

amplified risk for the emergence of psychotic symptoms later in life (Evins et al 2012). In a 4

year study by Henquet et al (2005) of cannabis use in 2,437 14-24 year old participants,

identified as at risk and not at risk, for psychosis, a dose-response, with more frequent

cannabis use associated with a higher risk for psychosis was identified. However, the

converse was not ascertained in that, risk for psychosis was not found to be a predictor of

future cannabis use. Therefore, the results of Henquet et al (2005) study proposed that

cannabis usage was a risk factor for psychotic disorders, rather than psychotic disorders being

a risk factor for future cannabis use.

Bossong and Niesink (2010) undertook a literature search that comprised of various

neurobiological disciplines, which ultimately converged into a model that may clarify the

neurobiology of cannabis-induced schizophrenia. Bossong and Niesink (2010) contend that

cannabis use during adolescence intensifies the possibility of developing psychotic disorders

later in life. However, they acknowledge that the neurobiological processes underlying this

relationship are unidentified. Their model postulates that adolescent exposure to D9-

tetrahydrocannabinol (THC), the primary psychoactive substance in cannabis, transitorily

interrupts physiological control of the endogenous cannabinoid system over glutamate and

GABA release. As a result, THC may negatively have an impact on adolescent experience-

dependent development of neural circuitries contained within prefrontal cortical areas.

Contingent on the dose, precise time window and duration of exposure, the development of

psychosis or schizophrenia may be the consequence (Bossong and Niesink 2010).

Though particular cognitive deficits may be a fundamental characteristic of schizophrenia,

introducing cannabis use into the equation has stimulated remarkable findings. The

paramount findings have indicated that participants with schizophrenia and adolescent

cannabis use actually have better cognitive functioning than those without adolescent

cannabis use (Lesson et al 2012). However, only a minor amount of people who use cannabis

go on to develop psychotic symptoms.  This had directed Golgberger et al (2010) to suggest

that it is probable that both environmental factors and genetic predisposition feature

in influencing the psychotomimetic impact of cannabis, which is associated with early

cannabis exposure and a family history of psychosis. Furthermore, a recent study of a large

sample of students established that sensitivity to the psychotomimetic effects of cannabis

is suggestive of an inherent characteristic present subsequent to their first exposure to

cannabis (Krebs et al 2014).

  • Anxiety disorders

Anxiety disorders are the most common difficulties that result from chronic heavy cannabis

use (Renard et al 2014). Kedzior and Laeber (2014) report that the lifetime prevalence for

anxiety disorder within the general population is estimated around 6–17%, and this frequency

is increased in cannabis users with a prevalence up to 20% (Reilly et al 1998). A

comprehensive and recent meta-analysis (Kedzior and Laeber 2014) directs that anxiety is

significantly linked with the consumption and misuse of cannabis. However, only a few

studies have monitored the association concerning adolescent cannabis use and enduring

anxiety disorders. The use of cannabis throughout adolescence, can magnify the possibility of

creating anxiety-related symptoms in adulthood, predominantly if the inception of use was

initiated before the age of 15 (Renard et al 2014). Moreover, girls are at greater probability

than boys to for these symptoms to develop (Hayatbakhsh et al 2007).

A recent study by Degenhardt et al (2013) observed the relationship between cannabis use

and mental health of people between the ages of 15 and 29. The authors established that

substantial cannabis use throughout adolescence was associated with an augmented risk of

adulthood mental health challenges including anxiety disorders.

 

  • Depressive disorders

In many countries, an emergent body of evidence corroborates a correlation between

cannabis use and depression among young people (Renard et al 2014). Amongst people who

use cannabis the frequency of depressive disorders is twenty five per cent with approximately

half of these depressive disorders presenting as major depression, and the other half are

severe mood disorders (Chabrol et al 2008). A study conducted among Australians

adolescents, between 13 and 17 years of age established that those who use cannabis, have

three times the probability of encountering the criteria for depression in later life, in

comparison to adolescents who never used cannabis (Rey et al 2002). Similarly,

Hayatbakhsh et al (2007) established that those who frequently use cannabis are more likely

to display symptoms of anxiety and depression in early adulthood, predominantly when the

researchers took into account cumulative exposure to cannabis, and potentially considerable

confounding characteristics such as maternal smoking and alcohol consumption. Further to

this, a longitudinal study that was undertaken in young Norwegians and followed over a 13-

year period demonstrated a dose-dependent relationship between chronic cannabis

consumption and suicidal propensities later in life (Pedersen 2008). Taken together, these

longitudinal studies propose that early commencement and recurrent cannabis use, increases

the vulnerability to depression later in life (Renard et al 2014).

Among people with psychosis, van Gastel et al (2013) report elevated use of cannabis and it

has been further recognized by Ferdinand et al (2005), that psychotic symptoms are

established in people who have never used cannabis, before the onset of psychotic symptoms,

which also predicts future cannabis use. This proposes that existing cannabis-dependent

subjects may have underlying psychiatric disorders that contributed to self-medication and

that through repeated use, led to dependence (Renard et al 2014). Thus, while cannabis may

itself increase drug addiction and psychiatric vulnerability, preceding prodromal conditions

may initially promote the initiation and continuation of cannabis use (Hurd et al 2014).

Conclusion

The exposure of adolescent to cannabis is connected with a variety of enduring adverse

consequences, including heightened vulnerability to addiction, cognitive impairment, and

psychosis-related illness, which may be correlated to cannabis-induced interruptions in

neurodevelopmental processes. These effects are moderated by a number of influences, with

adolescents exposed to early life trauma and/or those who are exposed to certain genetic and

personality vulnerabilities being at a greater risk of experiencing adverse long term effects.

Further research is required to understand precisely the manner in which various risk

characteristics interact with the use of cannabis and how such interactions may influence

neurodevelopmental processes within susceptible individuals.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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