Is marijuana bad for your brain Anees Bahji

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,

including sleep disturbances,
irritability, and depressed mood,

which pass
within a few weeks of stopping use.

So is marijuana bad for your brain?

It depends who you are.

But while some risk factors
are easy to identify,

others aren’t well understood—

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

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

1970 年,

大麻
在美国被列为附表 1 药物:

可能是最严格的指定,

这意味着它完全是非法的
,并且没有公认的医疗用途。

几十年来,这种观点一直存在,

并阻碍
了对药物机制和作用的研究。

今天,大麻的治疗益处
已得到广泛认可

,一些国家
已将医疗用途合法化

或正在朝这个方向发展。


对大麻的医疗价值的日益认可

并不能回答这个问题

:娱乐性大麻
对你的大脑有害吗?

大麻作用
于人体的大麻素系统,

该系统的受体
遍布大脑和身体。

体内的天然分子,
称为内源性大麻素,

也作用于这些受体。

我们并不完全
了解大麻素系统,

但它有一个特征
为其功能提供了重要线索。

大多数神经递质
通过突触从一个神经元传播到下一个神经元

以传播信息。

但内源性大麻素的
传播方向相反。

当信息
从一个神经元传递到下一个神经元时

,接收神经元
会释放内源性大麻素。

这些内源性大麻素
向后传播

以影响发送神经元——

本质上是
从接收神经元给它反馈。

这使科学家
们相信,内源性大麻素系统

主要
用于调节其他类型的信号——

放大一些信号并减弱另一些信号。

来自内源性大麻素的反馈
减慢了神经信号传导的速度。

但这并不一定意味着

它会减慢行为
或感知速度。

例如,
减慢抑制气味的信号

实际上可以使气味更强烈。

大麻含有
两种主要的活性化合物,

四氢大麻酚或 THC,
以及大麻二酚或 CBD。

THC 被认为主要
负责大麻

对行为、认知和感知的精神影响,

而 CBD
负责非精神影响。

与内源性大麻素一样,

THC
通过与大麻素受体结合来减缓信号传导。

但它同时与
这个庞大、扩散系统

中的受体结合,

而内源性大麻素
则在特定位置释放

以响应特定刺激。

这种广泛的活动
加上

大麻素系统
间接影响许多其他系统的事实,

意味着每个人
特定的大脑化学、遗传学

和以前的生活经历

在很大程度上决定
了他们如何体验药物。

通过一种或几种特定途径产生作用的其他药物相比,大麻更是如此。

因此,有害影响(如果有的话)
因人而异。

虽然我们不知道
大麻究竟如何

产生特定的有害影响,

但有明显的风险
因素可以增加人们

体验大麻的可能性。

最明显的风险因素是年龄。

在 25 岁以下的人中,大麻素受体比 25 岁以上的

人更集中在白质

。白
质参与交流、

学习、记忆和情绪。

频繁使用大麻

会破坏
白质束的发育

,也会影响大脑建立
新连接的能力。

这可能会损害长期的学习能力
和解决问题的能力。

目前,尚不清楚
这种损害有多严重

或是否可逆。

即使在年轻人中,

越年轻的人风险越高——

例如,15 岁的人
比 22 岁的人要高得多。

大麻还会引起幻觉
或偏执妄想。

被称为大麻诱发的精神病,

当一个人停止使用大麻时,这些症状通常会消退。

但在极少数情况下,
精神病并没有消退,

而是揭示
了持续性精神病。

精神疾病家族史,
如精神分裂症,

是这种影响最明显但不是唯一的
风险因素。

大麻引起的精神病
在年轻人中也更常见,

尽管值得注意的
是精神病

通常在这个年龄段出现。

在这些情况下尚不清楚的
是,精神病

是否会在
没有使用

大麻的情况下出现——大麻的使用是否会提前触发它,


不是否则不会跨越的临界点的催化剂,

或者
对大麻的反应是否仅仅是一个迹象

一种潜在的疾病。

很可能,大麻的作用
因人而异。

在任何年龄,与许多其他药物一样

,大脑和身体

在反复使用大麻后变得不那么敏感,

这意味着需要更多的时间
才能达到相同的效果。

幸运的是,与许多其他药物不同,大麻

没有致命过量的风险

即使停止使用,即使大量使用
也不会导致衰弱

或危及生命的
戒断症状。 然而,

还有更微妙
的大麻戒断形式,

包括睡眠障碍、
易怒和情绪低落,

这些都会
在停止使用后的几周内消失。

那么大麻对你的大脑有害吗?

这取决于你是谁。

但是,虽然一些风险因素
很容易识别,但

其他风险因素却没有得到很好的理解——

这意味着

即使您没有
任何已知的风险因素,仍然有可能经历负面影响。