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In 1970,

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marijuana was classified [br]as a schedule 1 drug in the United States:

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the strictest designation possible,

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meaning it was completely illegal [br]and had no recognized medical uses.

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For decades, this view persisted

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and set back research [br]on the drug's mechanisms and effects.

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Today, marijuana’s therapeutic benefits [br]are widely acknowledged,

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and some nations [br]have legalized medical use

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or are moving in that direction.

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But a growing recognition [br]for marijuana’s medical value

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doesn’t answer the question:

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is recreational marijuana use [br]bad for your brain?

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Marijuana acts [br]on the body’s cannabinoid system,

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which has receptors [br]all over the brain and body.

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Molecules native to the body, [br]called endocannabinoids,

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also act on these receptors.

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We don’t totally understand [br]the cannabinoid system,

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but it has one feature [br]that provides a big clue to its function.

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Most neurotransmitters [br]travel from one neuron to the next

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through a synapse to propagate a message.

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But endocannabinoids [br]travel in the opposite direction.

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When a message passes [br]from the one neuron to the next,

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the receiving neuron [br]releases endocannabinoids.

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Those endocannabinoids [br]travel backward

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to influence the sending neuron—

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essentially giving it feedback [br]from the receiving neuron.

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This leads scientists [br]to believe that the endocannabinoid system

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serves primarily [br]to modulate other kinds of signals—

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amplifying some and diminishing others.

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Feedback from endocannabinoids [br]slows down rates of neural signaling.

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That doesn’t necessarily mean

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it slows down behavior [br]or perception, though.

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For example, [br]slowing down a signal that inhibits smell

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could actually make smells more intense.

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Marijuana contains [br]two main active compounds,

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tetrahydrocannabinol or THC, [br]and cannabidiol, or CBD.

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THC is thought to be primarily responsible[br]for marijuana’s psychoactive effects

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on behavior, cognition, and perception,

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while CBD is responsible [br]for the non-psychoactive effects.

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Like endocannabinoids,

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THC slows down signaling [br]by binding to cannabinoid receptors.

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But it binds to receptors [br]all over this sprawling, diffuse system

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at once,

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whereas endocannabinoids [br]are released in a specific place

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in response to a specific stimulus.

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This widespread activity [br]coupled with the fact

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that the cannabinoid system[br]indirectly affects many other systems,

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means that each person’s [br]particular brain chemistry, genetics,

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and previous life experience

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largely determine [br]how they experience the drug.

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That’s true much more so with marijuana [br]than with other drugs

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that produce their effects [br]through one or a few specific pathways.

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So the harmful effects, if any, [br]vary considerably from person to person.

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And while we don’t know [br]how exactly how marijuana

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produces specific harmful effects,

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there are clear risk factors [br]that can increase peoples’ likelihood

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of experiencing them.

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The clearest risk factor is age.

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In people younger than 25,

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cannabinoid receptors [br]are more concentrated in the white matter

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than in people over 25.

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The white matter [br]is involved in communication,

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learning, memory, and emotions.

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Frequent marijuana use

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can disrupt the development [br]of white matter tracts,

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and also affect the brain’s ability [br]to grow new connections.

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This may damage long-term learning ability[br]and problem solving.

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For now, it’s unclear [br]how severe this damage can be

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or whether it’s reversible.

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And even among young people,

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the risk is higher the younger someone is—

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much higher for a 15 year old [br]than a 22 year old, for instance.

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Marijuana can also cause hallucinations [br]or paranoid delusions.

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Known as marijuana-induced psychosis,

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these symptoms usually subside [br]when a person stops using marijuana.

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But in rare cases, [br]psychosis doesn’t subside,

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instead unmasking [br]a persistent psychotic disorder.

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A family history of psychotic disorders, [br]like schizophrenia,

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is the clearest, though not the only, [br]risk factor for this effect.

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Marijuana-induced psychosis [br]is also more common among young adults,

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though it’s worth noting [br]that psychotic disorders

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usually surface in this age range anyway.

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What’s unclear in these cases [br]is whether the psychotic disorder

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would have appeared [br]without marijuana use—

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whether marijuana use triggers it early,

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is a catalyst for a tipping point [br]that wouldn’t have been crossed otherwise,

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or whether the reaction [br]to marijuana is merely an indication

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of an underlying disorder.

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In all likelihood, marijuana’s role [br]varies from person to person.

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At any age, as with many other drugs,

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the brain and body

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become less sensitive [br]to marijuana after repeated uses,

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meaning it takes more [br]to achieve the same effects.

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Fortunately, unlike many other drugs,

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there’s no risk of fatal overdose [br]from marijuana,

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and even heavy use [br]doesn’t lead to debilitating

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or life-threatening [br]withdrawal symptoms if use stops.

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There are more subtle forms [br]of marijuana withdrawal, though,

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including sleep disturbances, [br]irritability, and depressed mood,

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which pass [br]within a few weeks of stopping use.

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So is marijuana bad for your brain?

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It depends who you are.

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But while some risk factors [br]are easy to identify,

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others aren’t well understood—

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which means there’s still some possibility[br]of experiencing negative effects,

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even if you don’t have [br]any of the known risk factors.