Giving Genes Their Due, But Not More
正视基因的功劳，但不要过誉
A review of Behaving: What’s Genetic, What’s Not, and Why Should We Care? by Kenneth B. Schaffner. Oxford: Oxford University Press (2016), 304 pages.
对牛津大学出版社出版的Kenneth B. Schaffner的《行为：什么是遗传的，什么不是，以及我们为何要在意这些》的书评。
No one gets anxious about using genetics to help explain a medical disease like cancer or heart disease. But using genetics to help explain a normal behavior like aggression, or a psychiatric disorder like depression, can be an entirely different story. At first blush, this difference in response to using genetics to explain different features of the same animal seems odd.
没有人会担心用遗传学来帮助解释疾病，如癌症或心脏疾病。但是用遗传学来帮助解释普通的行为，例如攻击行为，或精神障碍，如抑郁，则是一个完全不同的故事。对于用遗传学来解释同一动物的不同特征却有不同的反应，乍一看这似乎很奇怪。
After all, it’s not as if medical geneticists, on the one hand, and behavioral and psychiatric geneticists, on the other, employ different research methods. The difference, of course, is that the behavioral and psychiatric geneticists investigate features of ourselves that we take to be central to our humanity: our ways of acting and being in the world. To use genetics to try to explain those features elicits the anxious question, is human behavior genetically determined?
毕竟，这并不是说医疗遗传学家与另—边的行为和精神遗传学家，采用的是不同的研究方法。所不同的当然是，行为和精神遗传学家研究我们自己的特征，我们认为这些特征是我们人性的核心：我们行动和存在于世界的方式。试图用遗传学解释这些特征引起了一个令人焦虑的问题，人的行为是不是遗传决定的？
Few people have been thinking about that question for as long, or with as much devotion to the scientific facts and philosophical subtleties, as the philosopher of science, Kenneth Schaffner. In his magisterial, wise, and succinct new book,Behaving, he disentangles its two separate but related components. The first, which he devotes the lion’s share of the book to illuminating, concerns reductionism: specifically, can behavior be reduced to genes? No, it can’t.
没几个人像科学哲学家Kenneth Schaffner这样，长期思考这一问题，并大量精力投入科学事实和深奥哲理。在他的权威，智慧，简洁的新书《行为》中，他理顺了行为的两个独立但相关的成分。第一，他用本书的大部分篇幅，做了关于还原论的阐释：具体而言，行为可以被简化为基因吗？不，不能。
But it can, at least in principle, be reduced to, or explained in terms of, a mind-bogglingly large number of variables — including genes — which interact over time. The second concerns determinism: even if genes alone don’t determine behavior, does the fact that behavior is determined mean that freedom is an illusion? No. But it does mean that we have to jettison the sort of freedom that children sometimes imagine — freedom untethered to our bodies and histories.
但它可以，至少在原则上，可以简化或被解释成，包括基因在内的一大堆变量，数量多到令人发狂，且这些变量一直交互作用。第二点则关于决定论：即使基因并不能单独决定行为，行为是被决定的这一事实是否意味着自由是一种错觉？不。但它确实意味着我们必须抛弃那种自由，即有时孩子们会想象的那种——不受我们的身体和历史羁绊的自由。
In the course of decreasing the anxiety associated with genetic determinism, Schaffner’s book also decreases the anxiety associated with the fantasy of “designer babies” — a fantasy which depends on the notion that just by “editing” genes we can produce any trait we want, from great athleticism to great intelligence.
在试图减少遗传决定论所带来的焦虑时，Schaffner的书也降低了与“设计婴儿”狂想有关的焦虑——这一狂想基于以下概念：仅通过“编辑”基因，我们便可以创造任何我们想要的特质，从强大的运动能力到极高的智力。
By dispelling this wildly simplistic notion, Schaffner’s book serves not only as an anxiety reducer — or “anxiolytic” — but also as a “mood stabilizer”: it helps stabilize the mania that can afflict those who envision the Human Genome Project as the key to the future of medicine.
通过打消这种疯狂简单化的概念，Schaffner的书不仅可充当一种焦虑缓和剂——或“抗焦虑药”——而且可充当一种“情绪稳定剂” ：它有助于稳定一种狂热，这狂热让那些把人类基因组计划当成开启医学未来的金钥匙的人备受折磨。
Schaffner provides a balanced account while never losing sight of what has been and will be achieved by using genetics to explain medical, behavioral, and psychiatric traits — especially if integrated with insights at myriad other levels of analysis, from the genetic and neuronal to the psychological and social.
Schaffner提供了一个平衡的描述，他从未忽视在用遗传学解释医疗、行为和精神特质的方面，已经和将会实现的成就—— 特别展望了若把这些成就和遗传学、神经科学、心理、社会等诸多其他层面的分析相结合所能带来的前景。
A Judge and a Behavioral Geneticist Have a Conversation
一个法官和一个行为遗传学家的对话
Schaffner begins with three Socratic dialogues (minus any Socratic snarkyness or dead ends) that elegantly introduce the basic concepts and methods of behavioral genetics. They are worth rehearsing here. The dialogues feature a Behavioral Geneticist and a fictional Judge. Based on the breathless headlines she’s read over the years, the Judge anticipates that she will increasingly confront the results of behavioral genetics research in her courtroom.
Schaffner以三个苏格拉底式对话开始。（没有任何苏格拉底的反讽或死结）这些对话优雅的介绍了行为遗传学的基本概念和方法。他们值得在此被回溯。这些对话的主角是一个行为遗传学家和一个虚构的法官。根据她多年来读到的那些令人喘不过气的头条新闻，法官预计，她将在她的法庭面对越来越多的行为遗传学研究结果。
This provides the Behavioral Geneticist with a pretext for explaining how such results can — and cannot — help explain human behavior, and how such results are — and are not — relevant to everyday understandings of behaviors like aggression, traits like performance on IQ tests, and disorders like ADHD. (Because there is no difference between the concepts and methods of behavioral genetics and psychiatric genetics, from here on out I will use “behavioral genetics” to include the use of genetics to illuminate behaviors and traits, whether or not they are associated with a psychiatric diagnosis.)
这为行为遗传学家提供了理由，来解释这些结果可以或者不可以帮助解释人类行为，以及这些结果和一些对行为，特质，或者疾病的日常理解怎样关联或不相关。例如攻击性人格的行为，智商测试的表现，以及多动症。（因为行为遗传学的概念和方法与精神病遗传学之间没有区别，在此我将使用“行为遗传学”，以包括遗传学在解释的行为和特征上的应用，无论其是否与精神病诊断相关。）
Two radically different sorts of investigation are undertaken by behavioral geneticists, and the dialogues introduce a basic but crucial distinction between them. The first uses “classical” methods to demonstrate that genes help explain observed differences in human traits and behaviors, whereas the second uses “molecular” methods to determine which genes or genetic differences are generating those observed differences.
行为遗传学家进行了两种截然不同的调查，而对话介绍了它们之间基本但关键的一个区别。第一种是使用“经典”方法来阐明基因有助于解释人的特征和行为上可见的差异，而第二个则使用“分子层面”方法，以确定哪些基因或遗传差异产生了那些可见差异。
The distinction is important — the distance is enormous between being able to say that a trait “is genetic” and being able to say which gene variants are contributing to the emergence of that trait (much less being able to say how they are contributing).
这种区别很重要 ——能够说一个特征“是遗传的”，和能够说出哪些基因变异正在促成该性状的涌现，这之间有着巨大的鸿沟（更别提说出它们是如何促成的）。
The basic idea for the classical method has been around since the pioneering statistician and father of modern eugenics, Francis Galton, published “The History of Twins” in 1875 — long before anyone knew anything about DNA. In its simplest contemporary form, geneticists compare identical and fraternal twins on a trait of interest, whether heart disease, schizophrenia, or performance on IQ tests.
自统计学先驱和现代优生学之父Francis Galton以来，经典方法的基本思想就已经出现，Galton于1875年发表了《双胞胎的历史》，那时人们还不知道DNA。在当时最简单的形式中，遗传学家比较同卵和异卵双胞胎的目标性状，无论是心脏疾病，精神分裂症，或智商测试的表现。
The first premise of such investigations is that identical twins are nearly 100% genetically similar and fraternal twins share on average only 50% of their genetic material. The second premise is that identical twins and fraternal twins are raised in equally similar environments.
这种调查的第一个前提是同卵双胞胎遗传上近乎100％的相似，而异卵双胞胎则平均只有50％的遗传物质相似。第二个前提是，同卵双胞胎和异卵双胞胎在同样相似的环境被养大。
If one accepts those premises and observes that genetically identical twins are more similar with respect to some trait than fraternal twins, then one has reason to make the simple but profound inference that genetic factors help explain why the identical twins are more similar to each other than are the fraternal twins.
如果一个人接受这些前提并观察到同卵双胞胎的某些特质比异卵双胞胎更相似，那么他便有理由做出简单而深刻的推论，即遗传因素能够帮助解释为什么同卵双胞胎之间比异卵双胞胎更相似。
Over time, by deploying ever more sophisticated variations on that basic logic, behavioral geneticists have demonstrated that identical twins (whether raised together or apart) are not only more similar with respect to traits like height and weight and heart rate, but are also more similar with respect to traits like depression, schizophrenia, aggression, and intelligence.
随着时间的推移，在该基本逻辑的基础上增加更复杂的变量，行为遗传学家已证明同卵双胞胎（无论是一起或分开抚养）不仅在诸如身高、体重和心率等性状上更为相似，而且在诸如抑郁症，精神分裂症，攻击性行为和智力等性状上也更相似。
As Schaffner’s Behavioral Geneticist patiently explains to the Judge, such classical studies produce what are called “heritability estimates.” These are the numbers that are invoked when it is said that depression “is 40% genetic” or that intelligence “is 60% genetic.”
正如Schaffner的行为遗传学家耐心地给法官大人解释的，这样的经典研究产生了所谓的“遗传率估计”。当讨论到抑郁症“40 ％是遗传性的”，或智慧“60 ％是遗传性的”时，有数字可以列。
They are estimates of how much of the variation with respect to a given trait in a given population can be attributed to variation in genetic factors and how much can be attributed to variation in environmental factors. However, in a different environment the observed variation can be different, and thus so can the heritability estimates.
这些估计反映了：对于一个给定群体特定性状的差异，有多少可以归因于遗传因素的差异，多少可以归因于环境因素的差异。毕竟，在不同的环境中可观察到的差异可以是不同的，因此，这样就可以估计遗传率。
To say that heritability estimates can be different in different environments is not to say that heritability estimates tell us nothing! (Indeed, how our genes can affect the environments we choose is an area of behavioral genetic research.)
如果说，遗传率在不同的环境下可以是不同的，这并不意味着遗传率什么都没告诉我们！ （事实上，我们的基因如何影响我们为自己选择身处其中的环境，是行为遗传学研究的一个领域。）
An old but ever-relevant example of how much heritability estimates can tell us comes from the 1960s, when behavioral geneticists used classical studies to discredit the then-popular idea that schizophrenia and autism were due solely to bad environments — in particular, to “refrigerator mothers.”
关于遗传率，有个老旧但十分相关的例子，来自1960年代。当时行为遗传学家采用经典的研究方法，以贬斥当时十分流行的观点：精神分裂症和自闭症纯粹由恶劣环境引发—— 尤其是“冰箱妈妈”。【译者注：让孩子感到缺乏母爱的妈妈。】
The good news is that these studies helped relieve already-devastated mothers of the burden and social stigma associated with believing that their mothering had caused the disease in their child.
好消息是，这些研究有助于缓解已经受创颇深的母亲们的负担和社会污名，这些负担和污名来自这样一种见解：这些妈妈的抚育方式导致了她们孩子的疾病。
The bad news is that the knowledge gleaned from those classical studies does not help diagnose or treat — much less prevent — a disorder like schizophrenia. To go from noticing that genetic differences were making a difference to knowing which genetic differences were making a difference, geneticists had to move from the classical twin methods to the modern “molecular” methods.
坏消息是，从经典研究中获取的知识并不能帮助诊断或治疗——更不用说预防——如精神分裂症之类的疾病。从注意到遗传差异，到知道哪个遗传差异导致某种不同，遗传学家必须从经典的双胞胎方法跨越到现代的“分子”方法。
The Genome: A “Molecular Crystal Ball”?
基因组：一个“分子层面的水晶球”？
This move only became possible in the second half of the 20th century, when researchers began to understand the molecular structure of genes and how to map and sequence human genomes. Indeed, the purpose of the Human Genome Project (HGP), which officially launched in 1990, was to map the genome and to specify the sequence of the base pairs, the As, Gs, Cs, and Ts, that are the building blocks of genes.
此举直到20世纪下半叶才成为可能，当时研究人员开始了解基因的分子结构，以及如何对人类基因组进行绘制和测序图谱。事实上，于1990年正式启动的人类基因组计划（HGP）的目的，便是绘制基因组，并指定基因的积木——碱基对AS、GS 、CS和TS的序列。
The fervent hope was that knowledge of those sequences would lead rather quickly and directly to understanding and treating human disease. In reflecting back on that time, the geneticists Linda and Edward McCabe speak ruefully of the dream that an individual’s genome would be like a “molecular crystal ball.”
人们热切希望有关这些序列的知识将相当快且相当直接的导致对人类疾病的理解和治疗。忆起那个时候，遗传学家Linda 和 Edward McCabe懊丧的谈起当时的梦想：一个人的基因组将会像一个“分子层面的水晶球”。
This idea of identifying “genes for” diseases made intuitive sense. After all, one year before the official launch of the HGP, in 1989, Francis Collins — who would go on to direct the National Human Genome Research Institute and who now directs the entire NIH — did co-discover “the gene for” cystic fibrosis, which constituted a prime supporting case in point for the idea dubbed OGOD: One-Gene-One-Disease.
直觉上，确定“致病基因”的想法是有道理的。毕竟，正式启动人类基因组计划前一年，即1989年，Francis Collins ——美国国家人类基因组研究所后来的领袖，也是现在整个美国国家卫生研究院（NIH）的领袖——和他人共同发现了囊性纤维化的“致病基因” ，这构成了OGOD理念，即一个基因对应一种疾病（One-Gene-One-Disease）的主要支撑例证。
If a rare medical disorder like cystic fibrosis could be caused by one gene, then maybe common medical diseases like heart disease could, too. And if common medical diseases could be caused by single genes, then maybe the same was true for psychiatric disorders and behavioral traits.
若是像囊性纤维化这样一种罕见的医学疾病可以由一个基因引起，那么也许常见病，如心脏病，也可能如此。如果普通疾病可能由单个基因引起的，那么也许精神疾病和行为特征同样如此。
Sure enough, in the 1990s, articles in the scientific and lay presses announced discoveries of “genes for” everything from bipolar disorder to aggression. But as Schaffner’s Behavioral Geneticist tells the Judge, those findings (which sparked the Judge’s initial interest) could not be replicated. “Genes for” diseases like cystic fibrosis and Huntington’s and sTay Sach were exceptions to the rule.
诚然，在1990年代，科普界的文章宣布发现各种各样的“致病基因”，从躁郁症到攻击性人格，无所不包。但正如Schaffner的行为遗传学家告诉法官的，这些（引发了法官最初兴趣的）发现无法被复制。诸如如囊性纤维化、亨廷顿舞蹈症和Tay-Sachs 病的“致病基因”是这一规律的例外。
“Failures to replicate” reminded geneticists of the yawning gap between discovering that a trait “is genetic” and figuring out which genes help explain it.
这些研究“无法被复制”提醒遗传学家们，在发现一种特质“是遗传的” ，和搞清哪些基因有助于解释该特质之间的存在着巨大鸿沟。
Genetic Reductionism: A Panacea or a Boondoggle?
遗传学还原论：万灵药还是打水漂？
One of the fascinating features of Schaffner’s book is his commitment to telling the story of how he came to reform — not renounce — his own vision of reductionism. When he began his career in the 1970s, he resonated with the hardcore genetic reductionists, who dreamt that understanding the operation of genes would be a panacea: a cure for our ignorance with respect to how disease and behavior come into being.
Schaffner这本书的一个令人赞叹的特点是，他坚持讲述他如何变革——而不是抛弃——自己对还原论的看法。当他的职业生涯在1970年代开始时，他和铁杆遗传还原论者很合得来，这些还原论者有一个梦想，即理解基因的操作将会是一个万灵药：在疾病和行为是如何产生的这个问题上，能治愈我们的无知。
But already at that time people who called themselves developmentalists (such as the much-discussed evolutionary biologist Richard Lewontin) were challenging that dream, suggesting that, especially in the context of behavior, genetic reductionism was a boondoggle.
但在那时自称是发育展主义者的人士（如备受争议的进化生物学家Richard Lewontin）则挑战了这一梦想，他提出，基因还原论打了水漂，尤其是在行为问题上。
To understand how Schaffner arrived at a middle path, it helps to understand the developmentalists’ challenge. According to Schaffner, that challenge boils down to five core concepts, two of them helpful and three overstated.
了解Schaffner如何到达一条中间道路，有助于理解发育主义者的挑战。据Schaffner看，这一挑战可以归结为五大核心理念，当中有两个有用，有三个被夸大其辞了。
The first helpful one concerns “contextualism” — the idea that genes do not have inherent meaning, but only acquire meaning “in context with other genes, and in the environment that is cellular, extracellular, and extraorganismic” (p. 95).
第一个有用的理念和“背景主义”相关——即基因不具有固有的意义，但仅“在其他基因的背景中，并且在细胞内环境，细胞外环境，和生物体外的环境中”获得了意义（第95页）。
The other helpful (or at least wholly unobjectionable) core concept is “nonpreformationism” — the developmentalists’ rejection of the very old idea that genes contain within them little copies of the traits with which they are associated.
另一个有用的（或至少是完全无法反驳的）核心理念是“非预成论”——即发育主义者拒绝了基因中含有与其相关的性状的微小副本这一古旧想法。
As for the overstated ones, they include the core concept of “parity” — the idea that genes have no more explanatory power than many other features of the organism and environment. Schaffner dismisses this as an exaggeration, at least insofar as it ignores the extent of our current understanding of the molecular structure and function of DNA.
而那些夸大的理念，包括“等价性”——即基因和生物体以及环境的许多其他特征相比，并没有更多的解释力。至少目前，Schaffner把这作为一种夸张来驳斥，因为它忽略了我们当下对DNA分子结构和功能的了解程度。
“Unpredictability,” their fourth core concept, is also exaggerated: genes can contribute to some predictions. As for the developmentalists’ fifth concept, “indivisibility,” Schaffner reminds us of the extent to which reductionism can make incremental progress in “dividing” behavior into analyzable components.
他们的第四个核心理念 “不可预测性”，也是夸张的：基因可以帮助做出一些预测。而对于发育主义的第五个理念， “不可分割性”，Schaffner提醒我们在把行为分割成可分析组件方面，还原论能够取得何种程度的渐进性进展。
To better illustrate his revised vision for reductionism, he introduces the humble roundworm, a wonderful organism for research purposes precisely because we have such highly detailed knowledge of its genes, neurons, neuronal connections and circuits, and of the typical behaviors it engages in during its short life.
为了更好地说明他的修正版还原论，他介绍了不起眼的蛔虫。对做研究来说，这个生物真是棒极了。我们对它的基因，神经元，神经连接和回路，及其短暂一生中的典型行为都有非常详细的知识。
In his characteristically even-handed way, Schaffner actually begins his account of worm behavior with one of those exceptional cases that can mesmerize journalists, pop psychologists, bioethicists, and others — a case where mutations in a single gene do indeed appear to be the necessary condition for a behavior: specifically, in this case, for determining whether a roundworm eats alone or in groups. In other words: one gene appears to determine the worm’s dining preference!
以其特有的不偏不倚的方式，Schaffner实际上用一个极好的例子开始阐释蛔虫的行为，这例子可以让记者，通俗心理学家，伦理学家和其他人着迷。那就是某个基因的变异看起来确实可以是一种行为改变的必要条件：具体来说，决定了一条蛔虫单独进食还是和群体一起进食。换句话说：看来是一个基因决定着该蠕虫的进食喜好！
But then the remainder of his discussion of the roundworm illuminates what’s wrong with the One-Gene-One-Behavior idea — and more generally, with the One-Gene-One-Disease (OGOD) idea.
但书中关于蠕虫的讨论的余下篇幅阐明了“一个基因一种行为”， 更宽泛的来说是“一个基因一种疾病”（One-Gene-One-Disease ，缩写为OGOD）这一理念的谬误之处，。
To show why the “gene for style of eating” example is an exception to the big rule of thumb that behaviors cannot be reduced to genes, much less to single genes, Schaffner introduces eight smaller “rules.”
为了解释为何“决定进食偏好的基因”只是“行为不能被还原为基因，更不能被还原为单个基因”这条更一般性的经验法则的一个例外，Schaffner 介绍了八条较小的“法则”。
These emphasize the interactions, occurring on multiple levels of analysis (from genes to neurons and nutrients), which change over time, and which shape and are shaped by the cellular, extracellular, and extraorganismic environments.
这些法则强调了发生在多个分析层次上的交互作用，从基因到神经元和营养物，而且这些交互作用一直在变化，并且塑造着细胞内，细胞外和生物体外的环境，反过来又受到这些环境的影响。
For example, “social deprivation,” he patiently explains, can adversely affect even the development of worms. Those raised in isolation were slower to respond to taps on the plates that constitute their environments (the “tap withdrawal reflex”), were physically smaller, and had delayed development — and the delay was correlated with the altered expression of a gene coding for a protein involved in the tap response.
他耐心地解释道，例如“社交剥夺”，甚至对蠕虫的发育也会造成负面影响。那些在孤独中被培育的蠕虫对轻拍培养皿的反应更慢，而培养皿构成了它们的生存环境（轻拍回撤反射实验），而且它们身形更小，发育更迟缓。而这迟缓与一个基因表达上的改变相关，这一基因编码了一种与轻拍反射相关的蛋白质。
Schaffner quotes the researcher’s conclusion: “Experience … can alter both gene expression and the structure of the nervous system” (p. 92). Even in the roundworm, there is no “gene for” the tap response; instead, the tap response is the result of a complex network, including, at a minimum, genes, neurons, and environments. If we hope to explain behavior, then, according to Schaffner, we need a “network perspective.”
Schaffner 引用研究者的结论：“经验……能够改变基因表达和神经系统结构”（第92页）。即使在蠕虫里，也没有负责轻拍反应的基因；反之，轻拍反应是一个复杂网络的结果，这一网络至少包括基因、神经元、和环境。如果我们希望解释行为，那么根据Schaffner 的观点，我们需要一个“网络视角”。
If this “network” type of genetic explanation holds for most behaviors, including even more complex organisms than worms and fruit flies, such as mice and humans, it raises barriers both to any simplistic type of genetic explanation, and the prospects of easily achievable medical and psychiatric pharmacological interventions into behaviors (ital. added, p. 95).
如果这个“网络”型遗传学解释能对大多数行为成立，包括比蠕虫和果蝇复杂得多的生物体，比如老鼠和人，它就使以下二者变得更困难：一，任何还原论版本的遗传学解释；二，发明出针对行为的，容易实现的医药或精神病学的药物干涉的希望。
In other words, to appreciate the leap from genes to worm behaviors should put us on notice that there will be even more “barriers” in going from genes to human behaviors, disorders, and diseases. The once-intuitively plausible idea of the genome as a molecular crystal ball has come to seem quaint.
换言之，理解从基因到蠕虫行为的思维跳跃，应该让我们注意到，从基因推及人的行为、失调和疾病，存在更多的困难。把基因组当分子层面的水晶球，这一曾是直觉上可行的的理念已经变得古旧。
It is essential to recognize, however, the difference between the notion that behaviors can be reduced to the operation of genes and the idea that behaviors can be reduced. The former notion, according to Schaffner, is wildly inaccurate, but the latter is not. The fact that we can’t achieve what he calls “sweeping reductions” of the sort first fantasized about at the start of the Human Genome Project does not mean that the enterprise of reductionism is a bust.
然而，有必要认识到，行为可以被还原为基因运作的结果，与行为可以被还原，这两种想法是不同的。在Schaffner看来，前者是非常不精确的，但是后者不是。在人类基因组开始时，人类开始沉迷于Schaffner的所谓“全面还原”的愿景，我们不能达成“全面还原”的愿景这一事实并不意味着还原论的雄心只是个泡影。
It means, among other things, that we need to accept the fact that, in complex systems, we should expect what he calls “patchy” or “partial” or “creeping” reductions. Genes can help to illuminate one “patch” of the huge field or network that would in theory constitute something like a complete explanation of a behavior.
而且这意味着，我们得接受一个事实：在复杂系统中，我们应该期待他所谓的打补丁的，或部分的，或是“小步推进”的还原。基因能帮助弄清这个网络或巨大场域的一个补丁，这在理论上构成了对一种行为的完整解释的一部分。
Finding a Path Forward to Understanding Human Behavior
发现通向理解人类行为的路径
Schaffner nimbly moves from worms to human beings. What geneticists have not been able to discover regarding human personalities should reassure, even gladden, skeptics.
Schaffner 灵活地从蠕虫跳到人类。关于人格，遗传学家一直没能发现的部分，应该会安慰和甚至鼓舞怀疑论者。
At the turn of the century, some psychologists and geneticists hypothesized that there were three domains of personality temperament — novelty seeking, harm avoidance, and reward dependence; each linked to a distinct neurotransmitter — dopamine, serotonin, and epinephrine; and thus linked to “genes for” the production and regulation of one of those neurotransmitters.
在世纪之交，一些心理学家和遗传学家假设人类气质有三个方面——猎奇性，避害性，和趋奖性；每种都和不同的神经递质相关——多巴胺，血清素，和肾上腺素；因此也和产生及管理这些神经递质的基因相关。
The idea was that specific gene variants associated with the regulation of dopamine, for example, had significant effects on novelty seeking. Again, those initial results failed to replicate. Among the reasons for those failures was the mistaken assumption that single “candidate” genes would, independent of their interaction with other genes and environmental variables, have large effects on traits as complex as personality.
这种理念认为，与管理多巴胺有关的基因的特定变异，会对猎奇性有显著影响。再一次，这些最初的结果未能被重复。单个基因会独立于其他基因和环境变量而对诸如人格这样的复杂性状产生巨大影响，这一错误的假设，算是失败的原因之一。
Combine that mistaken assumption with the all-too-human appetite of scientists, university PR departments, and journal editors for big, exciting findings, and voila: a variety of subtle statistical errors crept in.
这个错误的假设，加上科学家们的野心（这也是人之常情），大学公关部门和追求巨大且令人振奋发现的期刊编辑，于是：一系列微妙的统计学谬误渗透了进来。
Even the study of the interaction of genetic and environmental variables in the early 2000s was plagued with replication problems, perhaps due to their depending on the idea of “candidate” genes with large effects. Since then, extraordinary advances in technologies designed to compare genome sequences, combined with powerful new statistical methods, make it increasingly possible to detect genetic variants associated with tiny effects.
即使在21世纪初，对遗传和环境变量相互作用的研究也被结果不能重复这一问题所困扰，也许是因为研究者依赖“候选”基因有强大影响这一理念。此后，旨在比较基因组序列的非凡的技术进步，结合功能强大的新统计方法，使得发现与微小影响相关的遗传变异变得越来越可能。
The new, emerging picture boils down to this: common complex traits are the result of hundreds or thousands of gene variants of small effect size, which often interact with other gene variants as well as a gigantic range of environmental variables. It remains to be seen how much of practical value will result from this.
正在浮现中的新图景可以归结为：常见的复杂性状是几百或几千种效果较小的基因变异所产生的效果，并且它们通常与其他基因变异以及为数众多的环境变量相互作用。这个途径能带来多少实际价值仍有待观察。
Moreover, as Schaffner observes, it may be that huge categories like “novelty seeking” and “harm avoidance” are just too vague or indistinct to establish pathways from genes to behaviors like these. Again, to know that personality “is genetic” is massively different from knowing which genes are at work, much less how they are contributing to a given trait.
此外，Schaffner 指出，这可能是因为诸如“猎奇性”和“避害性”的宽泛类别太过含糊不清，以至于无法建立从基因到此类行为的途径。再次，要知道个性“是遗传的”和知道哪个基因在起作用是非常不同的，更不用说它们是如何导致一个特定性状的。
While Schaffner’s account of personality genetics may dishearten aficionados of genetic explanations, his account of schizophrenia should gladden them. Schizophrenia, too, is a large and heterogeneous category, but researchers have made headway in characterizing that heterogeneity — in specifying the symptoms and subtypes of schizophrenia. It’s in the context of schizophrenia that Schaffner elaborates on his conception of successfully reductionist scientific explanations.
虽然Schaffner关于个性遗传学的阐释会让遗传学解释狂人气馁，他关于精神分裂症的论述应该鼓舞他们。精神分裂症，也同样是一个宽泛且异质的类别，但研究人员在描述其异质性——即详细描述其症状和亚型——上已取得了进展。在精神分裂症问题上，Schaffner成功阐述了他的还原论者科学解释的概念。
Such explanations, whether of schizophrenia or any other disorder or behavior, will have to be “interlevel”; in other words, they will need to draw on what is known at the level of ions, molecules, cells, cell-cell circuits, and organs — and will have to tell a story about how, over time, the factors at those different levels interact with each other and their environments.
这样的解释，无论是针对精神分裂症或任何其他病症或行为，将必须是“层次间的”；换言之，他们将需要利用在离子、分子、细胞、细胞间回路和器官等各层面的知识构建一个故事——且必须解释在不同层次上的各个因素如何一直互动并和环境相互作用。
In the case of schizophrenia, this includes genes implicated in the production and regulation of specialized nerve cells, specialized parts of those nerve cells, connections among those nerve cells, and, ultimately, brain wave patterns thought to be associated with the activation of those neuronal circuits and associated with at least some features of schizophrenia.
在精神分裂症的例子中，那将包括所有涉及下列事情的基因：特化神经细胞的生成和调控、这些神经细胞的特化部位、这些神经细胞之间的连接，以及最后，被认为是和这些神经回路相关联的脑波模式，这些脑波模式也被认为至少和神经分裂症的一些特征相关联。
Need one say that the model he describes is not anywhere close to complete? (Nor is the elaboration of this model, which has recently received high-profile attention.) Rather, it offers a “creeping” reduction — incremental progress in using the tools of genetics and neuroscience to understand one patch of the massively complex phenomenon we call schizophrenia.
可以说他描述的模型离完成还差十万八千里吗？（阐述这个模型让他最近引人瞩目。）然而，这提供了一个“小步推进”的还原论解释——即在利用遗传学和神经科学方面的渐进性进展，可用来理解我们称之为精神分裂的极为复杂现象的一个方面。
Clearly, this model shouldn’t inspire euphoric expectations of imminent cures. Again, to his credit, Schaffner is adamant in stating that, “DNA sequence per se increasingly seems impoverished as a biological explainer” (p. 197). And, again, this is not to say that DNA sequence is unimportant — it’s just not important in the simple ways we once imagined, which notably still linger in the imagination.
很显然，这种模式不该激发关于治愈方案立即诞生的欣快预期。令人佩服地，Schaffner 再次坚决指出， “ 单单用DNA序列本身去解释生物学现象，似乎越来越困窘” （第197页） 。并且再次，这不是说 DNA序列是不重要的——只是不像我们曾经想象得那样，以简单的方式而显出其重要性，很明显，这些简单方式仍徘徊在想象中。
A Grownup Conception of Freedom
一个成熟的“自由”概念
So, is human behavior genetically determined? Different from what a sweeping genetic reductionist would hope, we have seen that the answer is plainly no. But nor is human behavior not determined. On the contrary, Schaffner thinks that human behavior is determined — and that it admits of reductionist explanations. Does this mean freedom is an illusion?
所以，人类行为是遗传决定的吗？不同于全面遗传学简化论者所指望的，我们已经看到答案明显是否定的。但这也不是说人类行为不是决定的。相反，Schaffner 认为人类行为是决定的——这使得还原论者的解释成为可能。这意味着自由是幻觉吗？
No, it doesn’t, even if it does mean that we have to give up conceptions of freedom of the sort that best-selling authors like Sam Harris like to set up in order to knock down. Yes, we have to give up the idea of freedom as an extra-natural capacity or force that is somehow insulated from the impact of the natural and social forces at work in the world.
不，这没有，即使这意味着我们必须放弃畅销书作家如 Sam Harris 为了作品成功而设定的那种自由概念。是的，我们必须放弃这一理念：自由某种程度上是一种能绝缘于世上自然和社会力量影响的超自然能力。
But accepting that our behaviors are determined by natural and social forces that, at least in principle, admit of explanation does not mean that we have to give up the conception of freedom that mature adults should want, or that, as Daniel Dennett puts it, “is worth having.”
但是接受我们的行为是被自然和社会决定的，或者至少在原则上承认该解释，并不意味着我们必须放弃有关心智成熟的成人应该渴望的那种——或者如 Daniel Dennett所说的，“值得拥有的”——自由的概念。
To get at what such a conception of freedom is, Schaffner introduces philosopher Harry Frankfurt’s influential distinction between first- and second-order desires. Consider, for example, an alcoholic with insight into her alcoholism. She might have a second-order desire not to drink, while also having a first-order desire to drink.
为了说清楚如此的自由概念究竟是什么，Schaffner 介绍了哲学家Harry Frankfurt所说的第一阶渴望和第二阶渴望之间的显著区别。试想，一个酗酒者很清楚的认识到她的成瘾问题。她也许有种不喝酒的二阶渴望，但同时又有想喝酒的一阶渴望。
The person who cannot bring her first-and second-order desires into alignment lacks what warrants being called free will. If, on the other hand, she can get those first- and second-order desires into alignment, and if she can, as it were, desire what she wants to desire, we can say that she is free.
这个不能把一阶和二阶渴望协调好的人缺乏确保自由意志的能力。反之，如果她能协调好一阶和二阶渴望，并且如果某种程度上她能渴望她想渴望的，我们可以说她是自由的。
The behavioral geneticist and philosopher of psychiatry, Kenneth Kendler explains how human beings can, “through their decision-making capacity, intervene in causal pathways from genes to behavior.” Kendler’s first example is alcohol dependence. We know from classical behavioral genetics studies that alcoholism “is genetic” in the real but limited sense that the genes that children inherit from parents can put them at increased risk of becoming alcoholics.
行为遗传学家和精神病哲学家 Kenneth Kendler 解释了人类如何能“通过他们的决策能力，在从基因到行为的因果性路径上进行干涉。”Kendler的第一个例子是酒精依赖。从经典的行为遗传学研究我们知道，酗酒在真实但有限的意义上是“遗传性的”，即孩子从父母那里继承的基因能增加他们成为酗酒者的风险。
We also know, however, that children of alcoholics are also at increased “risk” of becoming teetotalers — practicing complete abstinence from alcohol; Donald Trump’s response to his father’s and brother’s alcoholism is a case in point. Kendler and Schaffner both want us to notice how a grownup conception of freedom retains a place both for genes and for choice.
但我们也知道，酗酒者的孩子成为滴酒不沾者——也就是实际上完全戒绝酒精——的可能性也增加了；川普对于其父兄酗酒的回应就是一个与此有关的例子。Kendler 和Schaffner都想让我们注意到一个成人的自由概念，如何能给基因和选择都留有余地。
In other words, human decisions can be an essential factor in the multilevel causal network that gives rise to our behaviors. If we notice that genes, neurons, hormones, neighborhoods, cultures, histories — and human desires and choices — can be among the determinants of human behavior, determinism should be less anxiety-producing.
另一方面，人类决策能够成为导致我们的行为的多层次因果网络中的一个关键因素。如果我们注意到，基因，神经元，荷尔蒙，邻里，文化，历史——还有人的渴望和选择——都能算作人类行为的影响因素，决定论就应该不那么让人焦虑。
In offering his view of the sort of freedom of choice that any grownup should want, he reminds us that scientific researchers choose which level of the causal network they will study. There is nothing wrong with having a preference for a given level of analysis, but there is something wrong with forgetting that a preferred level won’t be the only one needed to make headway in the sorts of reductions that can contribute to practically useful explanations.
在阐释他关于（任何成年人都应向往的那种）选择自由的观点时，他提醒我们不要忽略科学研究者选择何种层次的因果网络来研究。对某层次的分析有偏好完全没有错，但如果想要在那种能够产生有实际用处的解释的还原工作上取得进展，忘记你所偏爱的层次不是所需的唯一条件，则是不对的。
An Anxiolytic and a Mood Stabilizer
一种抗焦虑剂和情绪稳定剂
This brings us full circle to the growing anxiety swirling around the idea of “designer babies,” and more specifically to the idea that it will be possible to use “gene editing technologies” like CRISPR-Cas9 to engineer traits like intelligence. As we begin to appreciate that such traits involve hundreds or thousands of genes interacting with each other and with the cellular, extracellular, and extraorganismic environments, then the less seriously we can take the notion that it will be possible to enhance such traits by making changes at the level of the gene.
这把我们带回到文章开头提到的那萦绕在“设计婴儿”这一概念周围的日益增长的焦虑，或者更确切地说，带回到对利用“基因编辑技术”（如CRISPR-Cas9）来对诸如智力之类的性状进行工程设计的焦虑。当我们开始注意到这些性状涉及数百个基因的互动，以及和细胞内、细胞间和生物体外环境的交互作用，那么我们就更不会认为在基因层面做改动来增强这些性状是可能的了。
Moreover, as mentioned earlier, understanding this complexity can help stabilize the mania precipitated by the Human Genome Project. Ever since its launch in 1990, we have heard ecstatic claims about the imminent arrival of medical diagnoses, treatments, and preventive interventions tailored to individual genomes.
而且，如早先提到的，理解这种复杂性可以帮助平息人类基因组计划带来的急躁冒进。早在该项目于90年代发起之际，我们已经听到欣喜若狂的宣告，即针对个人基因定制的疾病诊疗预防手段即将问世。
While it is absolutely crucial to appreciate the real and important strides in diagnosis and treatment linked to advances in understanding the genome, it is equally important to appreciate that, with few exceptions, knowledge at the level of the genome alone will likely not be able to produce as much clinically relevant information as was once promised.
当然，重视由对基因组的深入理解而带来的诊疗方面的真实且重要的进步是绝对关键的，但同样重要的是要明白，除了少数几个例外，仅靠基因组层面的知识产生相关的临床信息，很可能不如之前曾经承诺的那么多。
As we taxpayers begin to pour hundreds of millions of dollars into the Human Genome Project’s offspring, The Precision Medicine Initiative, we should hold its leaders to their word when they say that they are getting the mania under control. Given how ardently some of the leaders of that initiative — not least Francis Collins — have been committed to a geneocentric approach, and given how mesmerizing and cheap gene-sequencing has become, it may take significant effort on their part to live up to their new promise of pursuing a more multilevel and, dare one say, balanced approach. Reading Schaffner’s book could strengthen their resolve to live up to that promise.
既然我们纳税人已开始把数亿美元投入人类基因组计划的续集，精准药物计划，当计划的领袖们说他们正在控制关于基因疗法的急躁冒进，我们应当让他们遵守承诺。考虑到一些项目领袖们是如此热忱，不光Francis Collins一人决心采用基因导向的方法，而且目前基因测序已变得如此便宜又吸引人，让这些领袖信守他们采用更加多层次的，当然也就是更平衡的方法的承诺也许需要更大的努力。读Schaffner的书可以加强他们实现这个承诺的决心。
Erik Parens is a senior research scholar at The Hastings Center, a bioethics research institute in Garrison, New York, and is the author of Shaping Our Selves: On Technology, Flourishing, and a Habit of Thinking.
Erik Parens 是Hastings中心（一个坐落于纽约州Garrison的生物伦理研究机构）的一位高级学者，他著有《塑造自我：关于技术，繁荣，和思维的习惯》。
翻译：Tankman
校对：Drunkplane （@Drunkplane-zny）
编辑：辉格@whigzhou