This paper examines the neurological and cognitive effects of marijuana use, tracing how delta-9-tetrahydrocannabinol (THC) binds to CB1 receptors distributed throughout the brain and disrupts normal neurotransmitter function. The paper discusses how cannabis impairs memory, attention, and judgment, and how it triggers learned drug-craving behaviors. It also addresses the psychiatric risks associated with regular use β including elevated schizotypy scores, depression, psychosis, and anxiety β as well as social consequences such as school failure and delinquency among adolescents. The paper concludes with recommendations for family-focused education and abstinence-based prevention strategies targeting young people most vulnerable to marijuana's long-term effects.
Mankind has used marijuana since prehistory for its psychoactive effect on the brain. The ancient Indians and Tibetans used it in Hindu religious ceremonies; the effect on the brain would often lead priests into a trance-like state that could be mistaken for a religious experience. Since then, marijuana has been increasing in popularity, until the modern 20th century, when the drug was made illegal in most countries.
In order to fully understand the effects of marijuana use on cognition and attention, one must look at how marijuana affects the physical brain itself. The brain is the center of the nervous system, and thus the center of all thought and cognition. Because a variety of studies have shown that marijuana use changes the way the brain works, it follows that smoking marijuana also changes the way thought and cognition function.
Cannabis enters the body through any number of routes β smoking, injection, or consumption β and then works its way through the blood vessels until it reaches the brain. The physical receptor in the brain that binds with delta-9-tetrahydrocannabinol (THC), the primary psychoactive ingredient of cannabis, is called CB1 (Moreira & Lutz, 2008, p. 197). CB1 receptors have been identified as interacting with or affecting "appetite, pain regulation, vegetative, and motor functions" (Gouzoulis-Mayfrank, 2006, p. 189). Such a widespread range of effects, spanning from appetite to motor functions, has a specific reason behind it: the body produces its own cannabinoids.
"The brain makes its own marijuana β natural compounds called endocannabinoids" (DeLuca, 2004). These endocannabinoids bind directly to CB1 receptors, which are located at the synapse. "This placement suggested that the cannabinoid receptor was somehow involved with signal transmission across GABA-using synapses" (Nicoll & Alger, 2004, p. 71).
As it turns out, endocannabinoids are used to generate a "retrograde" signaling system, in which a postsynaptic cell fires signals backward into a presynaptic cell rather than in the conventional forward direction. This places cannabinoids at a critically important position in brain function, as retrograde signaling is linked to an increase in long-term potentiation β the process by which synapses are strengthened in order to retain information.
"As researchers continued to study CB1, they learned that it was one of the most abundant G-protein coupled receptors in the brain" (Nicoll & Alger, 2004, p. 72). CB1 is the most widespread protein receptor, found around the cells of the "cerebral cortex, hippocampus, hypothalamus, cerebellum, basal ganglia, brain stem, spinal cord and amygdala" (Nicoll & Alger, 2004, p. 72). Because of CB1's widespread locations, and because cannabinoids affect the processes of every cell in which CB1 is present, exogenous cannabinoids such as THC β the kind derived from marijuana β can hijack these receptors and produce widely varying effects on brain processes.
For instance, the receptors in the hippocampus, which govern the creation of memories, can be altered by smoking marijuana. It is for this reason that memory is often impaired when a person consumes marijuana. The National Institute on Drug Abuse reported that marijuana intoxication's acute effects include "impairment in attention, judgment, and other cognitive functions" (National Institute on Drug Abuse, 2002), and that "long-term heavy use has been associated with memory impairment."
Smoking marijuana can also affect a person's craving for additional drugs, and a number of recent studies have established a connection between marijuana use and its interaction with other substances. "The most recent advances in cannabinoid-opioid cross-modulation have been made in the area of drug craving and relapse processes" (Robledo, Berrendero, Ozaita, & Maldonado, 2008, p. 214). Several of these studies have shown that the initial act of smoking marijuana can substantially increase the likelihood of further marijuana use through a learned process. Marijuana appears to transform neutral stimuli in the brain into stimuli that actively seek the high that drugs like marijuana can induce. One 2008 study concluded that "due to learning processes, originally neutral stimuli become drug-associated and can activate an implicit drug memory" (Wolfling, Flor, & Grusser, 2008, p. 976).
According to that study, this activation can "lead to a conditioned arousing 'drug-seeking' state" (Wolfling et al., 2008, p. 976). The individual ingesting marijuana is therefore accepting a risk from the very first use: that the brain will learn to crave the feelings generated by the drug. "Craving β as an emotional and motivational state β can persist for months or even years after the last consumption of the drug" (Wolfling et al., 2008, p. 978). In effect, by ingesting the drug, the individual is simultaneously teaching his or her brain to crave it, which is likely to lead to further use. Wolfling states that the drug "has a strong potency to motivate renewed drug intake in addicts" (p. 978), and that the experience of craving can be explained by increased emotional involvement based on the expected rewarding effects of drug use. The user learns to crave precisely that which produces the craving.
"Schizotypy, psychosis, anxiety, and psychiatric disorders"
"School failure, delinquency, and family disruption"
"Family education and abstinence-based prevention strategies"
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