"Recent research...has found that people who use marijuana and carry a specific variant of the AKT1 gene, which codes for an enzyme that affects dopamine signaling in the striatum, are at increased risk of developing psychosis. The striatum is an area of the brain that becomes activated and flooded with dopamine when certain stimuli are present. One study found that the risk of psychosis among those with this variant was seven times higher for those who used marijuana daily compared with those who used it infrequently or used none at all.
Another study found an increased risk of psychosis among adults who had used marijuana in adolescence and also carried a specific variant of the gene for catechol-O-methyltransferase (COMT), an enzyme that degrades neurotransmitters such as dopamine and norepinephrine...Marijuana use has also been shown to worsen the course of illness in patients who already have schizophrenia. As mentioned previously, marijuana can produce an acute psychotic reaction in non-schizophrenic people who use marijuana, especially at high doses, although this fades as the drug wears off.
Inconsistent and modest associations have been reported between marijuana use and suicidal thoughts and attempted suicide among teens. Marijuana has also been associated with an amotivational syndrome, defined as a diminished or absent drive to engage in typically rewarding activities. Because of the role of the endocannabinoid system in regulating mood and reward, it has been hypothesized that brain changes resulting from early use of marijuana may underlie these associations, but more research is needed to verify that such links exist and better understand them."
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"There’s consistent evidence showing a relationship over time between heavy or repeated cannabis use (or those diagnosed with cannabis use disorder) and an experience of psychosis for the first time...
The heaviest users of cannabis are around four times as likely to develop schizophrenia (a psychotic disorder that affects a person’s ability to think, feel and behave clearly) than non-users. Even the “average cannabis user” (for which the definition varies from study to study) is around twice as likely as a non-user to develop a psychotic disorder.
Furthermore, these studies found a causal link between tetrahydrocannabinol (THC - the plant chemical which elicits the “stoned” experience) and psychosis. This means the link is not coincidental, and one has actually caused the other...
Those with these genetic variants who have also experienced childhood trauma, or have a paranoid personality type, are even more at-risk. So too are adolescents and young adults, who have growing brains and are at an age where schizophrenia is more likely to manifest."
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"Findings show study participants who began using marijuana at the age of 16 or younger demonstrated brain variations that indicate arrested brain development in the prefrontal cortex, the part of the brain responsible for judgment, reasoning and complex thinking. Individuals who started using marijuana after age 16 showed the opposite effect and demonstrated signs of accelerated brain aging."
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"For one thing, recent studies show that cannabinoids manufactured by our own nerve cells play a crucial role in wiring the brain, both prenatally and during adolescence. Throughout life they regulate appetite, sleep, emotion, memory and movement—which makes sense when you consider the effects of marijuana. There are “huge changes” in the concentration of these endocannabinoids during the teenage years, according to neurologist Yasmin Hurd of the Icahn School of Medicine at Mount Sinai, which is why she and others who study this system worry about the impact of casually dosing it with weed.
Brain-imaging studies reinforce this concern. A number of smallish studies have seen differences in the brains of habitual weed smokers, including altered connectivity between the hemispheres, inefficient cognitive processing in adolescent users, and a smaller amygdala and hippocampus—structures involved in emotional regulation and memory, respectively.
More evidence comes from research in animals. Rats given THC, the chemical that puts the high in marijuana, show persistent cognitive difficulties if exposed around the time of puberty—but not if they are exposed as adults."
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"The literature not only suggests neurocognitive disadvantages to using marijuana in the domains of attention and memory that persist beyond abstinence, but suggest possible macrostructural brain alterations (e.g., morphometry changes in gray matter tissue), changes in white matter tract integrity (e.g., poorer coherence in white matter fibers), and abnormalities of neural functioning (e.g., increased brain activation, changes in neurovascular functioning). Earlier initiation of marijuana use (e.g., before age 17) and more frequent use has also been associated with poorer outcome."
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