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In the 1950s, the discovery of two new drugs sparked what would become a multibillion dollar market for antidepressants.
在20世纪50年代，两种新药的发现激发了日后价值数十亿美元的抗抑郁药市场。
Neither drug was intended to treat depression at all -- in fact, at the time, many doctors and scientists believed psychotherapy was the only approach to treating depression.
原来这两种药根本没有打算用来治疗抑郁症--事实上，当时许多医生和科学家都相信心理治疗是医治抑郁症的唯一方法。
The decades-long journey of discovery that followed revolutionized our understanding of depression -- and raised questions we hadn't considered before.
随后长达数十年的探索之旅彻底改变了我们对抑郁症的理解--并提出了我们未曾思考过的问题。
One of those first two antidepressant drugs was ipronaizid, which was intended to treat tuberculosis.
异烟酰异丙肼是最早的两种抗抑郁药之一，最初打算用来治疗结核病。
In a 1952 trial, it not only treated tuberculosis, it also improved the moods of patients who had previously been diagnosed with depression.
在1952年的一次试验中，它不仅治好了结核病，还改善了抑郁症患者的情绪。
In 1956, a Swiss clinician observed a similar effect when running a trial for imipramine, a drug for allergic reactions.
1956年，一名瑞士临床医生在对一种过敏药丙咪嗪进行试验时发现了类似的效果。
Both drugs affected a class of neurotransmitters called monoamines.
这两种药物都能影响一种叫做单胺类的神经递质。
The discovery of these antidepressant drugs gave rise to the chemical imbalance theory,
这些抗抑郁药物的发现催生了“化学物不平衡理论”，
the idea that depression is caused by having insufficient monoamines in the brain's synapses.
认为抑郁症是由于大脑的突触里缺乏足够的单胺类递质而造成的。
Ipronaizid, imipramine, and other drugs like them were thought to restore that balance by increasing the availability of monoamines in the brain.
异烟酰异丙肼、丙咪嗪和其它类似药物能通过增加大脑内单胺类递质的供应而恢复这个平衡。
These drugs targeted several different monoamines, each of which acted on a wide range of receptors in the brain.
这些药物能针对几种不同的单胺类递质，每种递质都能广泛作用于大脑里的各种受体。
This often meant a lot of side effects, including headaches, grogginess, and cognitive impairments including difficulty with memory, thinking, and judgment.
这通常意味着很多副作用，包括头痛、头晕，以及记忆、思考和判断困难等认知障碍。
Hoping to make the drugs more targeted and reduce side effects,
为了让药物更具针对性、减少副作用，
scientists began studying existing antidepressants to figure out which specific monoamines were most associated with improvements in depression.
科学家们开始研究现有的抗抑郁药，想要找出哪些特定的单胺类递质和抑郁症的改善最为密切相关。
In the 1970s, several different researchers converged on an answer: the most effective antidepressants all seemed to act on one monoamine called serotonin.
在20世纪70年代，几位研究者得出了一致的答案：最有效的抗抑郁药物似乎都作用于一种叫做血清素的单胺类递质。
This discovery led to the production of fluoxetine, or Prozac, in 1988.
这一发现使得氟西汀，即百忧解，于1988年问世。
It was the first of a new class of drugs called Selective Serotonin Reuptake Inhibitors, or SSRI's,
它是一类新药中的第一个--这类药物叫做选择性血清素再摄取抑制剂（SSRI），
which block the reabsorption of serotonin, leaving more available in the brain.
能阻止对血清素的再摄取，从而增加大脑中的血清素储备。
Prozac worked well and had fewer side effects than older, less targeted antidepressants.
百忧解效果很好，副作用也少于更早的、针对性更弱的抗抑郁药。
The makers of Prozac also worked to market the drug by raising awareness of the dangers of depression to both the public and the medical community.
为了推销这种药，百忧解的生产商也致力于提升公众和医疗群体对抑郁症危害的意识。
More people came to see depression as a disease caused by mechanisms beyond an individual's control,
更多人开始将抑郁症视为一种疾病，其发病机制不受个人控制，
which reduced the culture of blame and stigmatization surrounding depression, and more people sought help.
从而减少了围绕抑郁症的责备与污名化，也让越来越多人去寻求帮助。
In the 1990s, the number of people being treated for depression skyrocketed.
20世纪90年代，接受抑郁症治疗的人数迅速飞升。
Psychotherapy and other treatments fell by the wayside, and most people were treated solely with antidepressant drugs.
心理治疗和其它疗法纷纷旁落，大多数人只使用抗抑郁药物进行治疗。
Since then, we've developed a more nuanced view of how to treat depression -- and of what causes it.
从那之后，我们对抑郁症疗法和抑郁症成因的看法变得更加慎重细致。
Not everyone with depression responds to SSRIs like Prozac
百忧解等SSRI药物并不是对每一位抑郁症患者都有效果，
some respond better to drugs that act on other neurotransmitters, or don't respond to medication at all.
作用于其他神经递质的药物对有些人效果更好，有些人甚至任何药物都对他们无效。
For many, a combination of psychotherapy and antidepressant drugs is more effective than either alone.
对于很多人来说，心理治疗和抗抑郁药相结合比单独使用一种疗法更为有效。
We're also not sure why antidepressants work the way they do:
我们也不清楚抗抑郁药为何如此作用：
they change monoamine levels within a few hours of taking the medication, but patients usually don't feel the benefit until weeks later.
它们在服药后几小时内就能改变单胺类浓度，但患者通常要等到几个星期后才能感受到效益。
And after they stop taking antidepressants, some patients never experience depression again, while others relapse.
而在他们停止服用抗抑郁药后，有的患者再也不会经历抑郁症，而有人却会复发。
We now recognize that we don't know what causes depression, or why anti-depressants work.
我们现在认识到，我们不知道抑郁症的成因，也不知道抗抑郁药的原理。
The chemical imbalance theory is at best an incomplete explanation.
化学物不平衡理论最多是一个不完整的解释。
It can't be a coincidence that almost all the antidepressants happen to act on serotonin, but that doesn't mean serotonin deficiency is the cause of depression.
几乎所有抗抑郁药都恰好作用于血清素，这不可能是巧合，但也不意味着缺乏血清素就是抑郁症的成因。
If that sounds odd, consider a more straightforward example:
如果这听起来很奇怪，那就想象一个更直接的例子：
steroid creams can treat rashes caused by poison ivy -- the fact that they work doesn't mean steroid deficiency was the cause of the rash.
类固醇软膏可用于治疗毒漆藤引起的皮疹--但类固醇有效的事实并不代表类固醇缺乏是皮疹的原因。
We still have a ways to go in terms of understanding this disease. Fortunately, in the meantime, we have effective tools to treat it.
在理解抑郁症这一方面，我们还有很长的路要走。所幸的是，在此期间，我们有治疗它的有效工具。
