Is marijuana bad for your brain?

In 1970,

marijuana was classified

as a schedule 1 drug in the United States:

the strictest designation possible,

meaning it was completely illegal

and had no recognized medical uses.

For decades, this view persisted

and set back research

on the drug's mechanisms and effects.

Today, marijuana’s therapeutic benefits

are widely acknowledged,

and some nations

have legalized medical use

or are moving in that direction.

But a growing recognition

for marijuana’s medical value

doesn’t answer the question:

is recreational marijuana use

bad for your brain?

Marijuana acts

on the body’s cannabinoid system,

which has receptors

all over the brain and body.

Molecules native to the body,

called endocannabinoids,

also act on these receptors.

We don’t totally understand

the cannabinoid system,

but it has one feature

that provides a big clue to its function.

Most neurotransmitters

travel from one neuron to the next

through a synapse to propagate a message.

But endocannabinoids

travel in the opposite direction.

When a message passes

from the one neuron to the next,

the receiving neuron

releases endocannabinoids.

Those endocannabinoids

travel backward

to influence the sending neuron—

essentially giving it feedback

from the receiving neuron.

This leads scientists

to believe that the endocannabinoid system

serves primarily

to modulate other kinds of signals—

amplifying some and diminishing others.

Feedback from endocannabinoids

slows down rates of neural signaling.

That doesn’t necessarily mean

it slows down behavior

or perception, though.

For example,

slowing down a signal that inhibits smell

could actually make smells more intense.

Marijuana contains

two main active compounds,

tetrahydrocannabinol or THC,

and cannabidiol, or CBD.

THC is thought to be primarily responsible

for marijuana’s psychoactive effects

on behavior, cognition, and perception,

while CBD is responsible

for the non-psychoactive effects.

Like endocannabinoids,

THC slows down signaling

by binding to cannabinoid receptors.

But it binds to receptors

all over this sprawling, diffuse system

at once,

whereas endocannabinoids

are released in a specific place

in response to a specific stimulus.

This widespread activity

coupled with the fact

that the cannabinoid system

indirectly affects many other systems,

means that each person’s

particular brain chemistry, genetics,

and previous life experience

largely determine

how they experience the drug.

That’s true much more so with marijuana

than with other drugs

that produce their effects

through one or a few specific pathways.

So the harmful effects, if any,

vary considerably from person to person.

And while we don’t know

how exactly how marijuana

produces specific harmful effects,

there are clear risk factors

that can increase peoples’ likelihood

of experiencing them.

The clearest risk factor is age.

In people younger than 25,

cannabinoid receptors

are more concentrated in the white matter

than in people over 25.

The white matter

is involved in communication,

learning, memory, and emotions.

Frequent marijuana use

can disrupt the development

of white matter tracts,

and also affect the brain’s ability

to grow new connections.

This may damage long-term learning ability

and problem solving.

For now, it’s unclear

how severe this damage can be

or whether it’s reversible.

And even among young people,

the risk is higher the younger someone is—

much higher for a 15 year old

than a 22 year old, for instance.

Marijuana can also cause hallucinations

or paranoid delusions.

Known as marijuana-induced psychosis,

these symptoms usually subside

when a person stops using marijuana.

But in rare cases,

psychosis doesn’t subside,

instead unmasking

a persistent psychotic disorder.

A family history of psychotic disorders,

like schizophrenia,

is the clearest, though not the only,

risk factor for this effect.

Marijuana-induced psychosis

is also more common among young adults,

though it’s worth noting

that psychotic disorders

usually surface in this age range anyway.

What’s unclear in these cases

is whether the psychotic disorder

would have appeared

without marijuana use—

whether marijuana use triggers it early,

is a catalyst for a tipping point

that wouldn’t have been crossed otherwise,

or whether the reaction

to marijuana is merely an indication

of an underlying disorder.

In all likelihood, marijuana’s role

varies from person to person.

At any age, as with many other drugs,

the brain and body

become less sensitive

to marijuana after repeated uses,

meaning it takes more

to achieve the same effects.

Fortunately, unlike many other drugs,

there’s no risk of fatal overdose

from marijuana,

and even heavy use

doesn’t lead to debilitating

or life-threatening

withdrawal symptoms if use stops.

There are more subtle forms

of marijuana withdrawal, though,