Essentials: Understanding & Conquering Depression

Andrew Huberman

安德鲁·休伯曼

Welcome to Huberman Lab Essentials, where we revisit past episodes for the most potent and actionable science-based tools for mental health, physical health, and performance.

欢迎来到 Huberman Lab Essentials，在这里我们回顾过去的剧集，寻找针对心理健康、身体健康和表现的最有效、最可操作的基于科学的工具。

I'm , and I'm a professor of neurobiology and ophthalmology at Stanford School of Medicine.

我是，我是斯坦福大学医学院的神经生物学和眼科教授。

Today, we're discussing depression.

今天我们要讨论的是抑郁症。

In particular, we're going to talk about major depression.

特别是，我们要讨论重度抑郁症。

The phrase major depression is used to distinguish one form of depression from the other, the other one being bipolar depression.

重度抑郁症一词用于区分一种形式的抑郁症和另一种形式的抑郁症，另一种是双相抑郁症。

Major depression impacts 5% of the population.

重度抑郁症影响 5% 的人口。

That is an enormous number.

这是一个巨大的数字。

That means if you're in a class of a hundred people, five of them are dealing with major depression, or have at some point.

这意味着，如果你在一个一百人的班级中，其中有五个人患有严重抑郁症，或者在某个时候患有抑郁症。

Look around you in any environment, and you can be sure that a good portion of the people that you're surrounded by is impacted by depression or will be at some point.

在任何环境中环顾四周，您都可以确定您周围的人中有很大一部分受到抑郁症的影响或将在某个时候受到抑郁症的影响。

So, this is something we really have to take seriously, and that we want to understand.

所以，这是我们必须认真对待、我们想要理解的事情。

It is the number four cause of disability.

它是导致残疾的第四大原因。

A lot of people miss work, miss school, and before then, likely perform poorly in work or school due to major depression.

许多人错过了工作、错过了学校，在此之前，可能会因为重度抑郁症而在工作或学习中表现不佳。

So, let's talk about the things that are present in somebody that has major depression.

那么，让我们来谈谈患有重度抑郁症的人身上出现的事情。

First of all, there tends to be a lot of grief.

首先，往往会有很多悲伤。

There tends to be a lot of sadness.

往往会有很多悲伤。

That's no surprise.

这并不奇怪。

There's also this thing that we call anhedonia, a general lack of ability to enjoy things.

还有一种我们称之为快感缺失的现象，即普遍缺乏享受事物的能力。

For the time being, we want to frame up anhedonia, this lack of ability to achieve or experience pleasure, a kind of a flat effect, as it's called.

目前，我们想要构建快感缺失，即缺乏获得或体验快乐的能力，一种所谓的扁平效应。

Sometimes, even delusional thinking, negative delusional thinking, and in particular, anti-self confabulation.

有时甚至是妄想，消极的妄想，特别是反自我的虚构。

What is anti-self confabulation?

什么是反自我虚构？

Well, first of all, confabulation is an incredible aspect of our mind and our nervous system.

嗯，首先，虚构是我们的思想和神经系统的一个令人难以置信的方面。

You sometimes see other forms of confabulation in people who have memory deficits, either because they have brain damage, or they have age-related dementia.

有时你会在有记忆缺陷的人身上看到其他形式的虚构，要么是因为他们有脑损伤，要么是因为他们患有与年龄相关的痴呆症。

A good example of this would be, someone with age-related dementia sometimes will find themselves in a location in the house and not know how they got there.

一个很好的例子是，患有与年龄有关的痴呆症的人有时会发现自己处于房子的某个位置，但不知道自己是如何到达那里的。

And if you ask them, "Oh, what are you doing here?" they will create these elaborate stories.

如果你问他们：“哦，你在这里做什么？”他们将创造这些精心设计的故事。

"Oh, you know, I was thinking about going shopping today, and I was going to take the bus, and then I was going to do..." They create these elaborate stories.

“哦，你知道，我今天想去购物，我打算乘公共汽车，然后我要做……”他们创造了这些精心设计的故事。

They confabulate.

他们闲聊。

It's as if a brain circuit that writes stories just starts generating content.

就好像编写故事的大脑回路刚刚开始生成内容一样。

In major depression, there's often a state of delusional anti-self confabulation, where the confabulations are not directly or completely linked to reality, but they are ones that make the self, the person describing them, seem sick or in some way not well.

在重度抑郁症中，常常会出现一种妄想性的反自我虚构的状态，其中的虚构与现实没有直接或完全的联系，但它们会让自我、描述它们的人看起来生病或在某种程度上不太好。

A good example would be somebody who experiences a physical injury, perhaps.

一个很好的例子可能是遭受身体伤害的人。

Maybe they break their ankle, maybe it's an athlete, and they also happen to become depressed.

也许他们脚踝骨折了，也许是一名运动员，而且他们也恰好变得抑郁。

And you'll talk to them, you say, "How are things going?

你会和他们交谈，你说：“事情进展得怎么样？

How's your rehab?" And they'll go, "Oh, it's okay.

你的康复情况怎么样？”他们会说：“哦，没关系。

And I don't know, I'm just...

而且我不知道，我只是...

I feel like I'm getting weaker and weaker by the day.

我感觉自己一天天变得越来越虚弱。

I'm just not performing well." And then you'll talk to the person that they're working with, their kinesiologist or whoever the physical therapist is, and they'll say, "No, they're actually really improving.

我只是表现得不好。”然后你会和他们一起工作的人、他们的运动学家或物理治疗师交谈，他们会说：“不，他们实际上真的在进步。

And I tell them they're improving, but somehow, they're not seeing that improvement.

我告诉他们他们正在进步，但不知何故，他们没有看到这种进步。

They're not registering that improvement." They are viewing themselves and they are confabulating according to a view that is very self-deprecating, to the point where it doesn't match up with reality.

他们没有注意到这种改进。”他们以一种非常自嘲、甚至与现实不相符的观点来看待自己和谈论自己。

The other common symptomatology of major depression is what they call vegetative symptoms, okay?

重度抑郁症的另一个常见症状是所谓的植物人症状，好吗？

So, vegetative symptoms are symptoms that occur without any thinking, without any doing, or without any confabulation.

因此，植物人症状是在没有任何思考、没有任何行动或没有任何虚构的情况下出现的症状。

These are things that are related to our core physiology, things like constantly being exhausted.

这些都是与我们的核心生理机能相关的事情，比如不断疲惫不堪。

The person just feels exhausted.

这个人只是感到筋疲力尽。

They don't have the energy they once had.

他们不再拥有曾经拥有的能量。

So, it's not in their heads.

所以，这不在他们的脑子里。

Something is disrupted in the autonomic, or so-called vegetative nervous system.

自主神经系统或所谓的植物神经系统出现了紊乱。

And one of the most common symptoms of people with major depression, one of the signs of major depression, is early waking, and not being able to fall back asleep despite being exhausted.

重度抑郁症患者最常见的症状之一，重度抑郁症的症状之一，就是早醒，尽管精疲力尽却无法重新入睡。

So, waking up at 3:00 AM or 4:00 AM or 5:00 AM, just spontaneously, and not being able to go back to sleep.

因此，在凌晨 3:00 或 4:00 或 5:00 自发地醒来，并且无法再入睡。

It's well-known that the architecture of sleep is disrupted in depression.

众所周知，抑郁症会破坏睡眠结构。

What's the architecture of sleep?

睡眠的架构是怎样的？

Early in the night, you tend to have slow wave sleep more than REM sleep, or rapid eye movement sleep.

晚上早些时候，您的慢波睡眠往往多于快速眼动睡眠或快速眼动睡眠。

As the night goes on, you tend to have more rapid eye movement sleep.

随着夜晚的推移，您的眼动睡眠往往会更加快速。

That architecture of slow wave sleep preceding rapid eye movement sleep is radically disrupted in major depression.

在重度抑郁症中，快速眼动睡眠之前的慢波睡眠结构被彻底破坏。

In addition, the pattern of activity in the brain during particular phases of sleep is disrupted.

此外，大脑在特定睡眠阶段的活动模式也会被打乱。

And then there are some other things that relate to the autonomic nervous system, but that we normally think of as more voluntary in nature.

还有一些其他与自主神经系统有关的事情，但我们通常认为本质上更自愿。

And these are things like decreased appetite.

这些都是食欲下降之类的事情。

So, you could imagine that one could have decreased appetite because of the anhedonia, the lack of pleasure from food.

因此，你可以想象，一个人可能会因为快感缺乏（缺乏食物带来的乐趣）而导致食欲下降。

So, you can see that the symptomatology of major depression impacts us at multiple levels.

因此，您可以看到重度抑郁症的症状在多个层面上影响着我们。

There's the conscious level of how excited we are generally.

我们通常有多么兴奋是有意识的。

Well, that's reduced.

嗯，减少了。

There's grief, there's guilt, there's crying.

有悲伤，有愧疚，有哭泣。

But then there are also these vegetative things.

但也有这些植物性的东西。

There's disruptions in sleep, which of course make everything more challenging when we're awake.

睡眠受到干扰，这当然会让我们清醒时的一切变得更具挑战性。

We know that.

我们知道这一点。

Sleep is so vital for resetting.

睡眠对于恢复至关重要。

You're waking up early, you can't get back to sleep.

你早醒了，就再也睡不着了。

That's going to adjust your affect, your emotions in negative ways.

这将以消极的方式调整你的影响和情绪。

We know this.

我们知道这一点。

And appetite is off.

而且食欲不振。

And there are hormones that get disrupted.

还有一些荷尔蒙会受到干扰。

So, cortisol levels are increased.

因此，皮质醇水平升高。

In particular, there's a signature pattern of depression whereby cortisol, this stress hormone that normally is released in a healthy way only in the early part of the day, is shifted to late in the day.

特别是，抑郁症有一个标志性模式，即皮质醇（这种压力荷尔蒙）通常只在一天的早些时候以健康的方式释放，但会转移到一天的晚些时候。

In fact, a 9:00 PM peak in cortisol is one of the physiological signatures of depressive-like states.

事实上，皮质醇在晚上 9:00 达到峰值是类抑郁状态的生理特征之一。

It's not the only one, but it is an important one.

它不是唯一的一个，但却是一个重要的。

So, let's just take a few minutes, and talk about some of the underlying biology that creates this cloud, or this constellation of symptomology.

因此，让我们花几分钟时间来讨论一下产生这种云或一系列症状的一些基础生物学。

One of the most important early findings in the search for a biological basis of depression, was this finding that there are drugs that relieve some of the symptoms of depression.

在寻找抑郁症生物学基础的过程中，最重要的早期发现之一是发现有药物可以缓解抑郁症的某些症状。

Those drugs generally fall into three major categories.

这些药物通常分为三大类。

But the first set of ones that were discovered were the so-called tricyclic antidepressants, and the MAO inhibitors, the monoamine oxidase inhibitors.

但第一批被发现的是所谓的三环类抗抑郁药和 MAO 抑制剂，即单胺氧化酶抑制剂。

And these tricyclic antidepressants and the MAO inhibitors largely worked by increasing levels of norepinephrine in the brain, as well as in the body in some cases.

这些三环类抗抑郁药和单胺氧化酶抑制剂主要是通过增加大脑中去甲肾上腺素的水平来发挥作用，在某些情况下还可以增加体内的去甲肾上腺素水平。

They were discovered because of the exploration for drugs that alter blood pressure.

它们是在探索改变血压的药物时被发现的。

Norepinephrine impacts blood pressure, and drugs that lower blood pressure reduce levels of norepinephrine, and that, in many cases, was shown to lead to depression or depressive-like symptoms.

去甲肾上腺素会影响血压，而降低血压的药物会降低去甲肾上腺素的水平，在许多情况下，去甲肾上腺素会导致抑郁或抑郁样症状。

These tricyclic drugs and the MAO inhibitors actually increase norepinephrine, and frankly, they do quite a good job of relieving some, if not all of the symptoms of major depression.

这些三环类药物和 MAO 抑制剂实际上会增加去甲肾上腺素，坦率地说，它们在缓解重度抑郁症的部分（如果不是全部）症状方面做得相当好。

However, they carry with them many side effects.

然而，它们也带来许多副作用。

Some of those side effects are side effects related to blood pressure itself, by increasing noradrenaline, norepinephrine as it's called, you raise blood pressure.

其中一些副作用是与血压本身相关的副作用，通过增加去甲肾上腺素（所谓的去甲肾上腺素），你会升高血压。

That can be dangerous.

这可能很危险。

But they also have a lot of other side effects.

但它们也有很多其他副作用。

The reason they have other side effects is because they impact systems in the brain and in the body that impact things like libido, appetite, digestion, and others.

它们之所以有其他副作用，是因为它们会影响大脑和身体的系统，从而影响性欲、食欲、消化等。

They made some people so uncomfortable that they preferred not to take them, even though when they didn't take them, they had a worsening or a maintenance of their depressive symptoms.

它们让一些人感到非常不舒服，以至于他们宁愿不服用它们，即使当他们不服用它们时，他们的抑郁症状会恶化或持续。

A decade or so later, there was the discovery of the so-called pleasure pathways in the brain.

大约十年后，人们发现了大脑中所谓的快乐通路。

This pleasure pathway, as it's sometimes called, involves areas like the nucleus accumbens and the ventral tegmental area.

这种快乐通路有时被称为伏隔核和腹侧被盖区等区域。

These are areas of the brain that are rich with neurons that make dopamine.

这些大脑区域富含产生多巴胺的神经元。

And if you think to the symptoms of depression, of anhedonia, a lack of pleasure, a lack of ability to experience pleasure, well, that was a smoking gun that there's something wrong with the dopamine pathway in depression.

如果你想到抑郁症、快感缺乏、缺乏快乐、缺乏体验快乐的能力等症状，那么，这确实证明抑郁症的多巴胺通路出了问题。

So, it's not just norepinephrine, it's also the dopamine or pleasure pathway is somehow disrupted.

所以，不仅仅是去甲肾上腺素，多巴胺或快乐通路也受到了某种程度的破坏。

And then in the 1980s, there was the discovery of the so-called SSRIs.

然后在 20 世纪 80 年代，发现了所谓的 SSRI。

Most people are now familiar with the SSRIs, the selective serotonin reuptake inhibitors.

现在大多数人都熟悉 SSRIs，即选择性血清素再摄取抑制剂。

The SSRIs worked by distinct mechanisms from the tricyclic antidepressants and the MAO inhibitors.

SSRIs 的作用机制与三环类抗抑郁药和 MAO 抑制剂不同。

As their name suggests, SSRI, selective serotonin reuptake inhibitors, prevent serotonin from being wiped up from the synapse after two neurons talk to one another.

顾名思义，SSRI（选择性血清素再摄取抑制剂）可防止两个神经元相互交谈后突触中的血清素被清除。

What do I mean by that?

我这么说是什么意思？

Well, here's some very basic Neurobiology 101.

嗯，这是一些非常基础的神经生物学 101。

If you don't know any neurobiology, you're going to know some in about 15 seconds.

如果您不懂任何神经生物学，大约 15 秒后您就会了解一些。

Neurons communicate with one another by spitting out chemicals into the little gap between them.

神经元通过向它们之间的小间隙喷出化学物质来相互交流。

The little gap between them is called the synapse.

它们之间的小间隙称为突触。

Those chemicals bind to the neuron on the opposite side, and cause changes in the electrical activity of that neuron on the other side of the synapse.

这些化学物质与另一侧的神经元结合，并导致突触另一侧神经元的电活动发生变化。

Serotonin is one such neurotransmitter, or more specifically, it's a neuromodulator.

血清素就是这样一种神经递质，或更具体地说，它是一种神经调节剂。

It can change the activity of large groups of neurons in very meaningful ways.

它可以以非常有意义的方式改变大量神经元的活动。

Selective serotonin reuptake inhibitor means, when a person takes this drug, some of those drugs include things like Prozac or Zoloft, the more typical or generic names are things like Fluoxetine.

选择性血清素再摄取抑制剂意味着，当一个人服用这种药物时，其中一些药物包括百忧解或左洛复等药物，更典型或通用的名称是氟西汀等药物。

When people take those, more serotonin hangs out in the synapse and is able to be taken up by the neuron on the opposite side because of this selective reuptake inhibition.

当人们服用这些药物时，更多的血清素会滞留在突触中，并且由于这种选择性再摄取抑制，能够被另一侧的神经元吸收。

It prevents the clearance of serotonin from the synapse, and thereby, more serotonin can have an effect.

它阻止血清素从突触中清除，因此更多的血清素可以发挥作用。

So SSRIs don't increase the total amount of serotonin in the brain, they change how effective the serotonin that's already in the brain is at changing the activity of neurons.

因此，SSRI 不会增加大脑中血清素的总量，而是会改变大脑中已有的血清素改变神经元活动的效果。

About a third of people that take SSRIs don't derive any benefit.

大约三分之一服用 SSRI 的人没有获得任何益处。

It doesn't relieve their symptoms of depression.

它并不能缓解他们的抑郁症状。

However, for the other two thirds, there's often a relief of some, if not all of the symptoms of major depression.

然而，对于另外三分之二的人来说，重度抑郁症的部分症状（如果不是全部的话）通常会得到缓解。

The problem is the side effects that accompany those SSRIs.

问题是这些 SSRI 药物伴随而来的副作用。

And so these days, SSRIs are a complicated topic.

因此，如今，SSRIs 是一个复杂的话题。

It's sort of what I would call a barbed wire topic, but these drugs also have saved a lot of lives.

这有点像我所说的铁丝网话题，但这些药物也拯救了很多生命。

They've also improved a lot of lives.

他们还改善了很多生活。

The issue is that they tend to have varying effects on different individuals, and sometimes varying effects over time.

问题是它们往往对不同的人产生不同的影响，有时甚至随着时间的推移产生不同的影响。

So, they'll work for a while, then they won't work for a while.

所以，他们会工作一段时间，然后他们就不再工作一段时间。

There are also a lot of mysteries about the SSRIs, and those mysteries bother people.

SSRIs也有很多谜团，这些谜团让人们感到困扰。

SSRIs increase the amount of serotonin, or more specifically, they increase the efficacy of serotonin at the synapse.

SSRI 会增加血清素的量，或者更具体地说，它们会增加突触处血清素的功效。

That happens immediately, or very soon after people start taking SSRIs.

这种情况会立即发生，或者在人们开始服用 SSRI 后不久就会发生。

But people generally don't start experiencing any relief from their symptoms of depression, if they're going to experience them at all, until about two weeks after they start taking these drugs.

但人们通常要到开始服用这些药物大约两周后，他们的抑郁症状才会开始得到任何缓解（如果他们真的要经历的话）。

So, it's very clear that there are at least three major chemical systems in the brain, norepinephrine, dopamine, and serotonin, that relate to and can adjust the symptoms of depression.

因此，很明显，大脑中至少存在三种主要化学系统：去甲肾上腺素、多巴胺和血清素，它们与抑郁症症状相关并可以调节抑郁症症状。

And those actually can be divided into separate categories.

这些实际上可以分为不同的类别。

So, for instance, epinephrine, or norepinephrine, is thought to relate to the so-called psychomotor defects.

例如，肾上腺素或去甲肾上腺素被认为与所谓的精神运动缺陷有关。

This is the lethargy.

这就是昏睡。

This is the exhaustion.

这就是疲惫。

This is the inability to get out of bed in the morning.

这是早上起不来床的表现。

The lack of dopamine in depressive patients is thought to lead to the anhedonia, the lack of ability to experience pleasure.

抑郁症患者缺乏多巴胺被认为会导致快感缺乏，即缺乏体验快乐的能力。

And serotonin is thought to relate to the grief, the guilt, some of the more cognitive or more emotional aspects of depression.

血清素被认为与悲伤、内疚以及抑郁症的一些认知性或情感性方面有关。

So, we've got the norepinephrine system related to activity and alertness, the dopamine system relating to motivation, pleasure, and the ability to seek and experience pleasure, and then the serotonin system that's related to grief.

因此，我们有与活动和警觉性相关的去甲肾上腺素系统，与动机、快乐以及寻求和体验快乐的能力相关的多巴胺系统，以及与悲伤相关的血清素系统。

And unfortunately, brains and organisms don't work in a simple mathematical way where you just say, "Oh, well, this person's experiencing a lot of grief, but they don't have any problems with lethargy, and so let's just boost up their serotonin." On paper it works, but oftentimes it doesn't work clinically.

不幸的是，大脑和有机体并不是以简单的数学方式工作，你只需说：“哦，好吧，这个人正在经历很多悲伤，但他们没有任何嗜睡的问题，所以让我们增加他们的血清素。”在纸面上它是有效的，但在临床上通常不起作用。

A really good psychiatrist will work with someone to try and pull and push on these various systems to find the combination of drugs that may be or may not be correct for them.

一位真正优秀的精神科医生会与某人合作，尝试推动这些不同的系统，以找到可能适合或不适合他们的药物组合。

So, next I'd like to talk about hormones and how they relate to depression, and I'd also like to talk about stress and how it relates to depression, as well as talk about some of the genetics or the predispositions to depression.

因此，接下来我想谈谈激素以及它们与抑郁症的关系，我还想谈谈压力及其与抑郁症的关系，以及一些遗传学或抑郁症的倾向。

20% of people that have major depression have low thyroid hormone, and that leads to low energy, low metabolism in the brain and body.

20% 的重度抑郁症患者甲状腺激素水平较低，这会导致大脑和身体能量低下、新陈代谢低下。

Sometimes a psychiatrist will prescribe thyroid medication to increase thyroid output in people that are depressed, and that will work to relieve the symptoms.

有时，精神科医生会开甲状腺药物来增加抑郁症患者的甲状腺输出，这将有助于缓解症状。

So, there are certain situations or conditions that can impact the thyroid hormone system and make people more susceptible to depression, or make a preexisting depression worse.

因此，某些情况或条件可能会影响甲状腺激素系统，使人们更容易患抑郁症，或使已有的抑郁症恶化。

And those are things like childbirth.

这些都是像分娩这样的事情。

So, it's well-known that women who give birth can often undergo what's called postpartum depression, and that's thought to be hormonally related, either directly to the thyroid system, or perhaps to the cortisol system as well.

因此，众所周知，分娩的女性经常会患上所谓的产后抑郁症，这被认为与荷尔蒙有关，要么直接与甲状腺系统有关，要么也与皮质醇系统有关。

We'll talk about cortisol in a moment.

我们稍后会讨论皮质醇。

As well as certain women during certain phases of their menstrual cycle who experience symptoms that are very much like clinical depression, and oftentimes are diagnosed with clinical depression appropriately.

某些女性在月经周期的某些阶段会出现非常类似于临床抑郁症的症状，并且通常会被适当地诊断为临床抑郁症。

And of course, the menstrual cycle is associated with shifts in hormone levels.

当然，月经周期与激素水平的变化有关。

As well, menopausal and post-menopausal women are more susceptible to major depression, regardless of whether or not they've had that major depression earlier in their life.

此外，更年期和绝经后女性更容易患重度抑郁症，无论她们在生命早期是否患有重度抑郁症。

So, these are things to be on the lookout for, and to definitely talk to a doctor, and get a blood panel that hopefully includes measures of thyroid hormone and cortisol hormone.

因此，这些都是需要注意的事情，并且一定要咨询医生，并进行血液检查，希望包括甲状腺激素和皮质醇激素的测量。

Why cortisol hormone?

为什么是皮质醇激素？

Well, more stress is correlated with more bouts of major depression across the lifespan.

嗯，更大的压力与一生中更多的重度抑郁症相关。

How many bouts?

几回合？

Well, it turns out that as you go from having one to two to three, well, when you hit four to five bouts of really intense stressful episodes in life, these tend to be long-term stressful episodes, your risk for major depression goes way up.

好吧，事实证明，当你从一次到两次再到三次，好吧，当你在生活中遇到四到五次真正强烈的压力发作时，这些往往是长期的压力发作，你患重度抑郁症的风险就会上升。

And that's because the stress system is associated with the release of cortisol.

这是因为压力系统与皮质醇的释放有关。

The cortisol system can dramatically impact the way that these different neuromodulators, dopamine, norepinephrine, and serotonin function.

皮质醇系统可以极大地影响这些不同的神经调节剂、多巴胺、去甲肾上腺素和血清素的功能方式。

One of the more important reasons for learning how to counter stress in order to offset depression is that there is a genetic predisposition that certain people carry to become depressed.

学习如何应对压力以抵消抑郁症的更重要原因之一是，某些人具有抑郁的遗传倾向。

How do we know?

我们怎么知道？

Well, in what are called concordant monozygotic twins, so these would be identical twins, for which one of those twins goes on to have major depression, there's a 50% probability that the other one will have major depression.

嗯，在所谓的一致同卵双胞胎中，即同卵双胞胎，其中一个双胞胎患有重度抑郁症，则另一个将有 50% 的可能性患有重度抑郁症。

So, it's not 100%.

所以，这不是100%。

It's not 100% inherited.

并不是100%遗传的。

It's not 100% genetic, as you might say, but there's a much higher predisposition for depression.

正如你可能会说的，这并不是 100% 遗传，但抑郁症的易感性要高得多。

Whereas in fraternal twins, that number drops, and in siblings, that number drops to about 25%, and in half-siblings, it's about 10%.

而在异卵双胞胎中，这个数字下降了，在兄弟姐妹中，这个数字下降到 25% 左右，在同父异母的兄弟姐妹中，这个数字约为 10%。

Basically, the more closely related you are to somebody who has major depression, the more likely it is that you will also get major depression.

基本上，您与患有重度抑郁症的人关系越密切，您也患上重度抑郁症的可能性就越大。

And therefore, if you haven't gotten major depression, the more likely it is that you should take steps to learn to mitigate stress, because stress is the major factor that can trigger one of these depressive episodes.

因此，如果您没有患上重度抑郁症，您更有可能应该采取措施学习减轻压力，因为压力是引发这些抑郁发作的主要因素。

So, next, I'd like to talk about some of the tools that people who both have depression or who are prone to depression, as well as people who don't have depression and simply want to maintain a good mood, who want to maintain a positive affect and pursuit of things in life, what are the things that you can do?

那么，接下来我想谈谈一些工具，对于那些患有抑郁症或容易患抑郁症的人，以及那些没有抑郁症而只是想保持好心情的人，想要对生活中的事物保持积极的影响和追求，可以做哪些事情？

Any behavioral tool that adjusts the levels of a particular chemical ought to perhaps provide some relief for some of the symptoms of major depression.

任何调整特定化学物质水平的行为工具也许应该可以缓解重度抑郁症的某些症状。

Let's take an example that I've talked about before on the podcast, which is that if you get into a very cold shower or you take an ice bath, you will release norepinephrine and epinephrine in your brain and body.

举个我之前在播客上讲过的例子，如果你洗个很冷的澡或者洗个冰浴，你的大脑和身体就会释放去甲肾上腺素和肾上腺素。

There's no question about that.

毫无疑问。

If some aspects of depression are related to low levels of norepinephrine, will taking cold showers relieve your depression?

如果抑郁症的某些方面与去甲肾上腺素水平低有关，洗冷水澡会缓解抑郁症吗？

Perhaps.

也许。

It might even relieve certain aspects of that depression.

它甚至可能缓解抑郁症的某些方面。

Will exercise help?

运动会有帮助吗？

Well, if you go out for a run, you're going to increase the amount of norepinephrine in your body.

好吧，如果你出去跑步，你体内去甲肾上腺素的含量就会增加。

If you enjoy that run, it's likely that you'll increase the levels of dopamine, and probably serotonin in your brain and body as well.

如果您喜欢跑步，很可能会增加大脑和身体中多巴胺以及血清素的水平。

Will that cure your depression?

这能治愈你的抑郁症吗？

Well, there are a lot of studies exploring how exercise can impact depression, and indeed, regular exercise is known to be a protective behavior against depression, but it also can help relieve some of the symptoms of depression.

嗯，有很多研究探索运动如何影响抑郁症，事实上，众所周知，定期运动是对抗抑郁症的一种保护行为，但它也可以帮助缓解抑郁症的一些症状。

So, you may ask yourself, "Why would you need drugs at all?

因此，您可能会问自己：“为什么您需要药物？

Why would there be prescription drugs, or the need for supplementation, or other things to alleviate the symptoms of depression?"

为什么会有处方药，或者需要补充剂，或者其他东西来缓解抑郁症状？”

Ah, well, that's the diabolical nature of depression, which is, if people are far enough along in this thing, this sometimes called disease, sometimes called disorder, but major depression, oftentimes they can't get the energy to even get up and take a bath or a shower.

啊，好吧，这就是抑郁症的恶魔本质，也就是说，如果人们在这件事上走得足够远，这有时被称为疾病，有时被称为障碍，但重度抑郁症，通常他们甚至没有力气站起来洗澡或淋浴。

They have no motivation to do it.

他们没有动力这样做。

They have no desire to go for a run.

他们不想去跑步。

But it's very important to highlight the fact that these circuits that are accessible to some of us, the circuits for happiness, for pursuit of pleasure, for exercise, for getting in a cold shower, if that's your thing, that those circuits are present in all people, but for certain people that are experiencing major depression and are really in the depths of their depression, they can't really access those circuits in the same way that people who are not suffering from depression can.

但重要的是要强调这样一个事实，即我们中的一些人可以使用这些回路，这些回路是为了幸福、为了追求快乐、为了锻炼、为了洗冷水澡，如果这是你的事，那么这些回路存在于所有人身上，但对于某些正在经历严重抑郁症并且真正处于抑郁症深处的人来说，他们无法像没有患有抑郁症的人一样真正进入这些回路。

But let's look at depression from the standpoint of a deeper biological phenomenon, which is inflammation and the immune system.

但让我们从更深层次的生物现象——炎症和免疫系统——的角度来看待抑郁症。

There's growing evidence now that many forms of major depression, if not all of them, relate to excessive inflammation.

现在有越来越多的证据表明，许多形式的重度抑郁症（如果不是全部）都与过度炎症有关。

Now, inflammation plays an important role in wound healing, it is a positive aspect of our immune system.

现在，炎症在伤口愈合中发挥着重要作用，它是我们免疫系统的积极方面。

Our ability to combat wounds, combat illnesses, et cetera.

我们对抗伤口、对抗疾病等的能力。

But inflammation gone unchecked, inflammation that lasts too long, or is of too high amplitude, meaning too many cytokines and things of that sort in the body, is bad.

但如果炎症不受控制，炎症持续时间过长或强度过高，意味着体内有过多的细胞因子和此类物质，那就不好了。

And there's decent evidence now that inflammation can lead to or exacerbate depression, and that if we want to control depression, or limit or eliminate depression, that focusing on reducing inflammation and its associated pathways is a really good thing to do.

现在有充分的证据表明炎症会导致或加剧抑郁症，如果我们想控制抑郁症，或者限制或消除抑郁症，那么专注于减少炎症及其相关途径确实是一件好事。

And I think this is a really good thing for everybody to do, regardless of whether or not you suffer from depression, okay?

我认为这对每个人来说都是一件好事，无论你是否患有抑郁症，好吗？

So, first of all, who are the major players in creating chronic inflammation in the brain and body?

那么，首先，谁是造成大脑和身体慢性炎症的主要因素？

They are the inflammatory cytokines.

它们是炎症细胞因子。

Things like IL-6, interleukin-6, things like tumor necrosis alpha, TNF-alpha.

IL-6、白细胞介素 6 等，肿瘤坏死因子 α、TNF-α 等。

Things like C-reactive protein, all right?

像C反应蛋白这样的东西，好吗？

When we are stressed, chronically stressed, we get inflamed.

当我们承受压力，长期承受压力时，我们就会发炎。

Our brain and various locations in the brain become inflamed because certain classes of cells, in particular, those glial cells, the cells that are typically thought to just be support cells, those cells and their biochemistry, and their dialogue with the neurons of the brain and body, start to become disrupted.

我们的大脑和大脑中的各个部位会发炎，因为某些类型的细胞，特别是那些神经胶质细胞，通常被认为只是支持细胞的细胞，这些细胞及其生物化学以及它们与大脑和身体神经元的对话开始受到干扰。

It turns out that there is a set of actions that we can take in order to limit inflammation.

事实证明，我们可以采取一系列行动来限制炎症。

One of those approaches is to increase our intake of so-called EPAs, or essential fatty acids.

其中一种方法是增加我们所谓的 EPA（必需脂肪酸）的摄入量。

Increasing our intake of these essential fatty acids, and in particular, the EPA variety of omega-3s, can lower the effective dose of things like SSRIs.

增加这些必需脂肪酸的摄入量，特别是 EPA 中的 omega-3 脂肪酸，可以降低 SSRI 等物质的有效剂量。

The threshold level seems to be about one gram, a thousand milligrams of EPA.

阈值水平似乎约为一克、一千毫克 EPA。

So, you will sometimes see on a bottle of krill oil, or fish oil, or any other source, even a plant source or other source of EPA, that it's a thousand milligrams or 1,200 milligrams.

因此，有时您会在一瓶磷虾油、鱼油或任何其他来源（甚至植物来源或其他来源的 EPA）上看到 EPA 含量为 1000 毫克或 1,200 毫克。

But what's really important to look at is whether or not there's more than a thousand milligrams of EPA, because the EPA in particular is what's important here.

但真正重要的是要看 EPA 的含量是否超过 1000 毫克，因为 EPA 在这里尤其重要。

So, how would this work?

那么，这将如何运作呢？

These inflammatory cytokines act in a variety of different ways, but they mainly act to inhibit the release of serotonin, norepinephrine, and dopamine, or the synthesis of serotonin, norepinephrine, and dopamine.

这些炎性细胞因子以多种不同的方式发挥作用，但主要作用是抑制血清素、去甲肾上腺素和多巴胺的释放，或抑制血清素、去甲肾上腺素和多巴胺的合成。

Dopamine, also called 5-HT, essentially derives from a precursor called tryptophan.

多巴胺，也称为 5-HT，本质上源自一种称为色氨酸的前体。

Tryptophan arrives into our system through our diet, okay?

色氨酸通过我们的饮食进入我们的系统，好吗？

Tryptophan is an amino acid.

色氨酸是一种氨基酸。

Tryptophan is eventually converted into serotonin.

色氨酸最终转化为血清素。

However, if there's excessive amounts of inflammation, these inflammatory cytokines cause tryptophan to be diverted down a different pathway.

然而，如果炎症过多，这些炎症细胞因子会导致色氨酸转移到不同的途径。

The pathway involves something called IDO, indoleamine, which converts tryptophan into kynurenine.

该途径涉及一种叫做 IDO（吲哚胺）的物质，它将色氨酸转化为犬尿氨酸。

Kynurenine actually acts as a neurotoxin by way of converting into something called quinolinic acid, okay?

犬尿氨酸实际上通过转化为喹啉酸来充当神经毒素，好吗？

And quinolinic acid is pro-depressive.

喹啉酸具有促抑郁作用。

So, if that seems like a complicated biochemical pathway, what's basically happening here is that the tryptophan that normally would be made into serotonin, under conditions of inflammation is being diverted into a neurotoxic pathway.

因此，如果这看起来像是一个复杂的生化途径，那么这里基本上发生的事情是，在炎症条件下通常会被制成血清素的色氨酸被转移到神经毒性途径中。

An ingestion of EPAs, because it limits these inflammatory cytokines, things like IL-6, C-reactive protein, et cetera, can cause more of the tryptophan that one ingests or has in their body to be diverted towards the serotonergic pathway.

摄入 EPA，因为它限制了这些炎症细胞因子，如 IL-6、C 反应蛋白等，可能会导致摄入或体内含有的更多色氨酸转向血清素途径。

Exercise, it turns out, also has a positive effect on the tryptophan to serotonin conversion pathway.

事实证明，运动对色氨酸到血清素的转化途径也有积极的影响。

The activation of the muscles through rhythmic repeated use, in particular, aerobic exercise, but also resistance training has been shown to do this to some extent, tends to sequester or shuttle the kynurenine into the muscle so that it isn't converted into this neurotoxin that is pro-depression.

通过有节奏的重复使用来激活肌肉，特别是有氧运动，而且阻力训练已被证明可以在一定程度上做到这一点，往往会将犬尿氨酸隔离或输送到肌肉中，使其不会转化为这种促抑郁的神经毒素。

From the data that are published in quality peer review journals, it really appears that this inflammation pathway does function to increase depression through these pathways.

从高质量同行评审期刊上发表的数据来看，这种炎症途径确实可以通过这些途径增加抑郁症。

And so, knowing that there are behavioral steps and supplementation-based steps, or if you prefer, getting your EPAs from typical food, from nutritional approaches, I find that very reassuring that the mechanisms all converge on a common pathway, serotonin.

因此，知道有行为步骤和基于补充的步骤，或者如果您愿意，可以从典型食物、营养方法中获取 EPA，我发现这些机制都集中在一个共同的途径——血清素上，这非常令人放心。

There's a common biochemical pathway that can explain why these things not just work, but why they should work.

有一个常见的生化途径可以解释为什么这些东西不仅起作用，而且为什么它们应该起作用。

They should work because they operate in the very same biochemical pathways that antidepressants that are prescribed to people do.

它们应该有效，因为它们的生化途径与开给人们的抗抑郁药完全相同。

Now, I want to talk about something that, at least for me, was quite surprising when I first learned about it for sake of treatment of mood disorders, and that's creatine.

现在，我想谈谈一些东西，至少对我来说，当我第一次了解到它用于治疗情绪障碍时，它是相当令人惊讶的，那就是肌酸。

Creatine has a number of very important functions throughout the body.

肌酸在全身具有许多非常重要的功能。

For those of you that are into resistance training, and actually for those of you that are into endurance training as well, creatine has achieved a lot of popularity in recent years, because supplementation with creatine can draw more water into muscles and can increase power output from muscles.

对于那些热衷于阻力训练的人来说，实际上对于那些热衷于耐力训练的人来说，肌酸近年来非常受欢迎，因为补充肌酸可以将更多的水分吸入肌肉，并可以增加肌肉的功率输出。

However, there's also a so-called phosphocreatine system in the brain, and that phosphocreatine system has everything to do with the dialogue between neurons and these other cell types called glia.

然而，大脑中还有一个所谓的磷酸肌酸系统，该磷酸肌酸系统与神经元和称为神经胶质细胞的其他细胞类型之间的对话密切相关。

But the phosphocreatine system in the forebrain in particular, in the front of our brain, has been shown to be involved in regulation of mood and some of the reward pathways, as well as in depression.

但前脑中的磷酸肌酸系统，尤其是我们大脑前部的磷酸肌酸系统，已被证明参与情绪调节和一些奖励途径，以及抑郁症。

The American Journal of Psychiatry in 2012 published a study which was a randomized double-blind placebo-controlled trial of oral creatine monohydrate, and what it found is that it could augment or enhance the response to a selective serotonin reuptake inhibitor, in particular in women with major depressive disorder.

《美国精神病学杂志》于 2012 年发表了一项研究，这是一项口服一水肌酸的随机双盲安慰剂对照试验，结果发现它可以增强或增强对选择性血清素再摄取抑制剂的反应，特别是对于患有重度抑郁症的女性。

So, like EPA, creatine supplementation seems to either lower the required dose of SSRI that's required to treat depression, or it can improve the effectiveness of a given dose of SSRI.

因此，与 EPA 一样，补充肌酸似乎可以降低治疗抑郁症所需的 SSRI 剂量，或者可以提高给定剂量 SSRI 的有效性。

However, there are other studies that have looked directly at creatine supplementation in the absence of SSRIs, and those are interesting as well.

然而，还有其他研究直接研究了在不使用 SSRI 的情况下补充肌酸的情况，这些研究也很有趣。

So, let's talk a little bit more about novel therapeutic compounds for the treatment of major depression.

那么，让我们更多地讨论一下用于治疗重度抑郁症的新型治疗化合物。

One is ketamine, which is getting increasing interest in psychiatric clinics, in various experimental and clinical studies.

其中之一是氯胺酮，它在精神科诊所、各种实验和临床研究中越来越受到关注。

They create dissociative anesthetic states.

它们会产生解离性麻醉状态。

So, dissociative states are where people don't feel as closely meshed with their emotions and their perceptions.

因此，分离状态是人们感觉与自己的情绪和感知不紧密结合的状态。

Clinically, what's described in the trials for ketamine and things like it, that people who are depressed will take ketamine, will experience a kind of separateness from their grief and from their emotions, and that possibly there's plasticity, there are actually shifts in the neural circuitry such that their emotions don't weigh on them so heavily.

临床上，氯胺酮和类似药物的试验中所描述的，抑郁症患者服用氯胺酮，会体验到一种与悲伤和情绪的分离，而且可能存在可塑性，实际上神经回路发生了变化，这样他们的情绪就不会那么沉重地压在他们身上。

It's not always about just getting people peppy, and excited, and happy.

它并不总是只是让人们充满活力、兴奋和快乐。

There also seems to be a requirement for getting them distanced from their own grief.

似乎还需要让他们远离自己的悲伤。

And this brings us back to something that we talked about way back at the beginning of this episode, which was this particular feature of the anti-self confabulation.

这让我们回到了我们在本集开始时讨论过的事情，这就是反自我闲谈的一个特殊特征。

That everything that happens for the depressed person is a reflection of how life is bad, and their experiences just point to the fact that nothing is going to get better.

对于抑郁症患者来说，发生的一切都反映了生活的糟糕程度，他们的经历只是表明了一个事实：一切都不会好转。

This is the common language of depression.

这是抑郁症的共同语言。

If this is very depressing to hear me talk about, it is heavy, and that's what it's like to hear these things.

如果听我谈论这件事让人感到非常沮丧，那就很沉重，这就是听到这些事情的感觉。

It's even heavier, of course, for somebody to experience them.

当然，对于有人体验它们的人来说，它甚至更重。

And those beliefs, those patterns of guilt, and grief, and anhedonia, and delusional anti-self confabulations, those are the things that eventually, if they get severe enough, start to convert into things like self-harm, mutilation, and in the most tragic of cases, of course, suicide.

那些信念、那些内疚、悲伤、快感缺乏和妄想性反自我的胡言乱语，如果它们变得足够严重，最终会开始转化为自残、残害，当然，在最悲惨的情况下，会转化为自杀。

And so I think we can look to these treatments such as ketamine and its use in the clinic, as ways for people to get distanced from the negative affect that they feel isn't just inside them or overwhelms them, but that for the very severely depressed person, they feel is them.

因此，我认为我们可以关注氯胺酮等治疗方法及其在临床中的使用，作为人们远离负面影响的方法，他们认为这些负面影响不仅存在于他们内部或压倒他们，而且对于非常严重的抑郁症患者来说，他们觉得他们就是他们自己。

Another category of treatments that is being actively explored now in laboratories, and in the psychiatry realm are the psychedelics.

目前实验室和精神病学领域正在积极探索的另一类治疗方法是致幻剂。

And that's a huge category of compounds.

这是一大类化合物。

However, one in particular, psilocybin, is one that's being most intensely and actively pursued for its capacity to treat major depressive disorder.

然而，其中一种特别是裸盖菇素，因其治疗重度抑郁症的能力而受到最强烈和积极的研究。

But let's focus on psilocybin for its capacity to rewire neural circuits, and alleviate depression.

但让我们重点关注裸盖菇素，因为它能够重新连接神经回路并缓解抑郁症。

There have been anecdotal data or evidence over the years that psilocybin has this capacity.

多年来已有轶事数据或证据表明裸盖菇素具有这种能力。

How does psilocybin work?

裸盖菇素如何发挥作用？

Well, psilocybin engages or increases serotonin transmission, meaning it increases the amount of serotonin, mainly by acting at these 5-HT2A receptors.

裸盖菇素参与或增加血清素传输，这意味着它主要通过作用于这些 5-HT2A 受体来增加血清素的量。

But where in the brain does it happen, and what are the major effects?

但它发生在大脑的哪个部位，主要影响是什么？

First, let's talk about the major effects, because I think that's what people are interested in.

首先，我们来谈谈主要影响，因为我认为这是人们感兴趣的。

The study that I'd like to highlight is a fairly recent one.

我想强调的一项研究是最近的一项研究。

It was published in May of 2021 in Journal of the American Medical Association Psychiatry, so JAMA Psychiatry, and it's entitled, "Effects of Psilocybin-Assisted Therapy on Major Depressive Disorder: A Randomized Clinical Trial." Basically, what they did was they screened for patients to come into the clinic.

该研究于 2021 年 5 月发表在《美国医学会精神病学杂志》（JAMA Psychiatry）上，标题为“赛洛西宾辅助疗法对重度抑郁症的影响：一项随机临床试验”。基本上，他们所做的就是筛选进入诊所的患者。

These were people that suffered from major depressive disorder and administered either one or two rounds of psilocybin.

这些人患有重度抑郁症，接受了一轮或两轮裸盖菇素治疗。

Typically, it was 20 milligrams per kilogram of body weight, so it depends on body weight.

通常情况下，它是每公斤体重20毫克，所以这取决于体重。

What's really striking about this study, is that there was a very significant improvement in mood, and affect, and relief from depressive symptoms in anywhere from 50 to 70% of the people that were subjects in the study who received the psilocybin treatment.

这项研究的真正惊人之处在于，接受裸盖菇素治疗的研究对象中有 50% 至 70% 的人的情绪和情感得到了非常显着的改善，并且抑郁症状得到缓解。

These are really enormous and significant effects.

这些确实是巨大而显着的影响。

What's really interesting is there are some common themes to psilocybin administration and experience that lead to relief from depressive symptoms, but they are subjectively very varied.

真正有趣的是，裸盖菇素的给药和体验有一些共同的主题，可以缓解抑郁症状，但它们在主观上差异很大。

Meaning that whether or not people feel they had a good experience or a bad experience, whether or not people thought about their parents, or thought about the color of the ceiling, doesn't seem to have too much of an impact on whether or not they receive relief during these clinical studies.

这意味着，无论人们是否感觉自己有好的经历或不好的经历，人们是否想到了他们的父母，或者想到了天花板的颜色，似乎对他们在这些临床研究中是否得到缓解没有太大影响。

It seems like different people can have lots of different experiences and still receive benefit.

似乎不同的人可以有很多不同的经历，但仍然受益匪浅。

It's somehow rewiring associations between events, emotional events, past events, current events, and future events, in ways that allow people to get some sort of relief or distance from these narratives, these depressive stories about their past and present, and allow them to see new opportunity and optimism in the future.

它以某种方式重新连接了事件、情感事件、过去事件、当前事件和未来事件之间的关联，让人们从这些叙述、这些关于他们过去和现在的抑郁故事中获得某种解脱或距离，并让他们看到未来的新机会和乐观情绪。

One of the most common questions I get for this podcast is about different diets, different regimes, different nutritional plans, things like keto, ketogenic diet, or vegan diets, or intermittent fasting, or the all-meat diet, the so-called Lion Diet, et cetera.

我在这个播客中收到的最常见问题之一是关于不同的饮食、不同的生活方式、不同的营养计划，比如酮、生酮饮食或纯素饮食，或间歇性禁食，或全肉饮食，即所谓的狮子饮食，等等。

There are actually really interesting data relating nutrition and diet to major depressive disorder.

实际上有一些非常有趣的数据将营养和饮食与重度抑郁症相关。

There have been some explorations of whether or not a vegan diet can improve symptoms of depression.

关于纯素饮食是否可以改善抑郁症症状已经进行了一些探索。

Not a lot of data, not impressive data.

数据不多，也没有令人印象深刻的数据。

There have been very few controlled studies looking at the carnivore or all-meat diet.

针对肉食动物或全肉饮食的对照研究很少。

However, the ketogenic diet has been explored for its ability to relieve certain symptoms of depression, in particular to what's called maintained euthymia.

然而，生酮饮食因其缓解某些抑郁症症状的能力而被探索，特别是所谓的维持精神状态。

Euthymia is the kind of state of equilibrium between a manic episode and a depressive episode in a manic bipolar person.

情绪愉悦是躁狂双相情感障碍者躁狂发作和抑郁发作之间的一种平衡状态。

Euthymia is that kind of place in the middle where people feel neither too high nor too low.

Euthymia 是一种介于中间的位置，人们感觉既不太高也不太低。

And there are some interesting studies looking at the ketogenic diet for maintaining euthymia in manic depressives, but also in people with major depressive disorder.

还有一些有趣的研究着眼于生酮饮食对于躁狂抑郁症患者以及重度抑郁症患者维持正常情绪的作用。

The ketogenic diet, by way of increasing ketone metabolism or shifting brain's metabolism over to ketones, tends to modulate GABA, such that GABA is more active, and adjusts the so-called GABA glutamate balance.

生酮饮食通过增加酮代谢或将大脑代谢转向酮，倾向于调节GABA，使GABA更加活跃，并调节所谓的GABA谷氨酸平衡。

This is getting technical, but glutamate is an excitatory neurotransmitter, GABA is an inhibitory neurotransmitter, and their balance is vital for neuroplasticity, for maintaining healthy levels of activity in the brain, et cetera.

这越来越技术化了，但谷氨酸是一种兴奋性神经递质，GABA 是一种抑制性神经递质，它们的平衡对于神经可塑性、维持大脑活动的健康水平等至关重要。

And so there is decent evidence that people with major depressive disorders, in particular, the people with major depressive disorders that are refractory, meaning they don't respond to classical antidepressants, can benefit, it seems, from the ketogenic diet.

因此，有充分的证据表明，患有重度抑郁症的人，特别是患有难治性重度抑郁症的人，这意味着他们对经典抗抑郁药没有反应，似乎可以从生酮饮食中受益。

It's really interesting that eating in a particular way, lowering carbohydrates to the point where you rely on ketogenic metabolism in the brain, increases GABA, and can provide some relief for depressive symptoms, and that, in particular, seems to have positive effects in people that are refractory, or who don't respond to classic antidepressants.

非常有趣的是，以特定的方式饮食，将碳水化合物降低到依赖大脑生酮代谢的程度，增加 GABA，并可以在一定程度上缓解抑郁症状，尤其是，这似乎对难治性或对经典抗抑郁药没有反应的人有积极作用。

So, today we've covered what at least feels to me like a tremendous amount of material.

所以，今天我们讨论了至少在我看来是大量的材料。

This topic of depression is indeed an enormous topic to try and get our arms around.

抑郁症这个话题确实是一个值得我们尝试解决的巨大话题。

We talked about the symptomatology, we talked about some of the underlying neurochemistry and biology, and then we talked about approaches to deal with it that are really grounded in the neurochemistry and biology.

我们讨论了症状学，讨论了一些潜在的神经化学和生物学，然后我们讨论了真正基于神经化学和生物学的处理方法。

I just want to recap a few of those tools, and what those things are.

我只想回顾一下其中的一些工具，以及这些工具是什么。

So, number one, don't overwhelm your pleasure centers, either through activities or compounds.

所以，第一，不要通过活动或化合物压垮你的快乐中心。

It might seem counterintuitive, but you're setting yourself up for anhedonia and depression if you do that.

这可能看起来违反直觉，但如果你这样做，你就会让自己陷入快感缺失和抑郁症。

Second of all, we talked about the norepinephrine system, and how the norepinephrine system is really deficient in many forms of major depression, and in depression.

其次，我们讨论了去甲肾上腺素系统，以及去甲肾上腺素系统在许多形式的重度抑郁症和抑郁症中确实缺乏。

There is now more deliberate pursuit of norepinephrine-inducing activities that are healthy, that aren't adrenaline seeking per se, things like exercise that will increase our levels of noradrenaline.

现在，人们更加刻意地追求健康的、能诱发去甲肾上腺素的活动，这些活动本身并不是寻求肾上腺素，比如锻炼会增加我们去甲肾上腺素的水平。

I'd be remiss if I said that these activities could completely eliminate depressive symptoms in people with major depressive disorder.

如果我说这些活动可以完全消除重度抑郁症患者的抑郁症状，那我就失职了。

I don't think that's the case, and again, I want to acknowledge that people with major depressive symptoms often don't have the energy, the willingness, or the capacity to engage in some of these activities.

我认为情况并非如此，我想再次承认，患有严重抑郁症状的人通常没有精力、意愿或能力参与其中一些活动。

But things like deliberate cold showers, things like regular exercise, they aren't just feel-good activities.

但像刻意洗冷水澡、定期锻炼这样的事情，它们不仅仅是让人感觉良好的活动。

They actually engage the norepinephrine system, and keep that system tuned up, and allow us to increase our norepinephrine levels at will on a regular basis, and their mood-enhancing effects are real effects at the level of neurochemistry.

它们实际上参与去甲肾上腺素系统，并保持该系统的调节，并允许我们定期随意增加去甲肾上腺素水平，它们的情绪增强作用是神经化学水平上的真实作用。

Then, we talked about EPAs, these essential fatty acids, and it's clear that for most people, getting above a thousand milligrams, and probably even closer to 2,000 milligrams per day of EPAs, can be beneficial for mood, especially in attempts to treat or offset major depressive disorder.

然后，我们讨论了 EPA，这些必需脂肪酸，很明显，对于大多数人来说，每天摄入超过 1000 毫克，甚至可能接近 2,000 毫克的 EPA，可能对情绪有益，尤其是在尝试治疗或抵消重度抑郁症时。

We also talked about exercise, and how EPA and exercise on a regular basis can offset these inflammatory pathways.

我们还讨论了锻炼，以及 EPA 和定期锻炼如何抵消这些炎症途径。

And then we talked about the prescription compounds, and the compounds that are being used mainly in the course of studies of psychiatry and depression, things like ketamine, psilocybin, and related compounds.

然后我们讨论了处方化合物，以及主要在精神病学和抑郁症研究过程中使用的化合物，例如氯胺酮、裸盖菇素和相关化合物。

And then lastly, we talked about ketosis, which may not be right for everybody, but might be right for certain individuals out there who are grappling with this.

最后，我们讨论了酮症，它可能并不适合所有人，但可能适合某些正在努力解决这个问题的人。

I want to thank you for embarking on this journey of trying to understand what is depression, how does it work, and how to treat it.

我要感谢您踏上这段旅程，试图了解什么是抑郁症、它是如何运作的以及如何治疗它。

And thank you for your interest in science.

感谢您对科学的兴趣。