【2022-02-20】 @yiqin_fu Kathryn Paige Harden 的书《The Genetic Lottery》总结了过去几十年关于基因和人类各种特征相关性的研究。不管是比较同异卵双胞胎、兄弟姐妹、所有人，最后算出来的这个遗传系数都比我想象中高很多（基因差异能解释形状差异的百分之几）。作者的其他几个结论是：1）系数解读要小心，因为也有社会因素。这个系数也会随着社会变化而变化；2）因果机制我们不知道；3）承认基因差别之后我们可以设计机制帮助大家（例如给近视的人戴眼镜）。 不过更大的问题仍然存在——绝大多数先天差异无法通过“戴个眼镜”这样的方案完全去掉；不同时代、不同社会奖励的技能在道德上是完全随机的。 我还特别想请教做道德哲学的朋友，有人在根据实证的这些研究重新思考 Rawls/Nozick/Friedman 的理论吗？任何一派都需要面对“遗传系数这么高”这件事？ 其他我印象深刻的结论是：4）遗传系数在一个人二十多岁的时候最高，因为基因和努力相互作用；5）很多非认知能力甚至比认知能力的系数还要高，例如受到挫折后坚持的意愿、对新鲜事物的好奇心（当然，这些概念都是实验室做游戏测量的，你可以说实验室的游戏和现实生活不一样）。 @whigzhou: 如果你没被PC滤网局限住信息视野的话，这些事情早该知道了，这本书并没什么新东西，只不过因为配上了左派政策主张，才通过了PC滤网，另外，道德哲学家也不需要通过修正罗尔斯才找到立足点，他们是在二战后的修正中丧生了立足点，斯宾塞及其维多利亚同道和进化事实共存的很好 @whigzhou: 与个体成就密切相关的那些特性，大多有着50-70%的遗传率，这一事实圈内早就人所共知了，圈外很多人不知道，对此很惊讶，甚至表现的难以置信，说明PC滤网确实很强大， 不过我发现更有意思的是，不少人听到50-70%这个数字后，庆幸自己至少还有机会改变剩下的那30-50%，其实这也是个大大的误解，而且这个误解更难消除，因为其背后的原理解释/理解起来更困难， 简单说，剩下的那30-50%，其实大部分来自三种随机因素： 1）测量误差：比如同一个被测对象，不同的测试者去测，测得的数字不同，其中定有误差，这种误差在心理学测量中比其他（比如生理）领域更严重， 2）指标设计偏差，也就是一个度量指标的设计，使得它无法完全准确的反映出它本来想要测量的那个东西，任何指标都存在这种问题，心理学指标当然更严重， 3）运气成分：所谓运气就是你无法干预控制的东西，换句话说，你啥也做不了， 这样你就理解了，为何 Robert Plomin 他们发现，所有他们考察过的个体成长中的共享环境条件（比如是否共享家庭，是否共享父母，是否共享学校，是否共享某种教育模式，是否共享某种财富水平……），都对解释个性差异的毫无贡献，就是说，是否纳入这些因素，丝毫不能改变个性差异中的未解释部分的比例， 通俗的说就是，试图通过改变这些因素来改进孩子的个性/智力发育，是徒劳的，（当然，这绝不是说做这些事情毫无意义，它们可能有其他效果，比如让孩子过的更开心，更有见识，更有教养，更有品味……这些都可以很有意义，但改变不了他们的个性和智力）， 当然，也别太绝望，并不是说个性/智力发育问题上你什么也不能做，那些测量的一个缺陷就是他们的采样对象基本上都是美国的普通正常家庭，所以自动排除了一些极端条件，而某些极端条件确实是会造成显著影响的， 比如某种水平以上的铅污染和营养不良显然会影响智力发育，幼儿期的严重虐待或许也会影响某些个性成分，营养不良和缺钙当然会影响身高…… 所以，父母们在孩子的生理/个性/智力发育上至少有一件事情可以做：帮他们避免那些恶性极端条件， @揶哼:如果平均值以下的环境有影响，那么远高于平均值的环境（比如前0.1%的家庭）是否也有提升呢？ @whigzhou: 1）恶性极端条件可远远不只是*均值以下*，2）正向极端条件没啥用，就好比你成吨成吨的喝奶补钙，也养不出姚明来 @windflower188026:那么智商中值回归咋解释 @whigzhou: 均值回归是运气因素的一种特定表现，可以这么理解：对均值的偏离不仅是某些贡献因子的独立作用，也是其特定组合的效果，而幸运组合可能会在有性繁殖过程中被打破，而人类是有性繁殖生物 @whigzhou: 今天闲着，不妨再展开一下均值回归这个问题， 假设智力有五个贡献因子，A-E，贡献率（r）分别为：A=3, B=1.2, C=5, D=0.5, E=1，意思是，其他条件相同时，拥有其中某个将提高智力 r 个基点（这里姑且不用管基点到底是啥意思）， 再假设这些因子都是可加的（additive），意思是每多一个就更好一点，但它们又不是线性可加的（linear additive），意思是，比如，单有A高3个基点，单有B高1.2个基点，但同时有(A+B)并不是高(3+1.2=4.2)个基点，而是比4.2更高或更低，如果更高，就说明A和B具有组合红利， 大大偏离均值的个体，往往具有特别幸运的组合（也就是其拥有的各贡献因子的总贡献中包含了更多组合红利），偏离越远，其组合的幸运度越高，因而在有性繁殖中因特定组合被打破而丧失的组合红利也越多，因而向均值回归的幅度也越大， 在现有方法中，对遗传率的计算是基于遗传关系和个体表现型之间的统计相关性，而不是基于对各贡献因子之微观机制的直接理解的，这就意味着，在统计上，组合红利无法从运气成分中被分离出来， 比如某甲的父亲拥有上述五个因子中的（A，C，E），母亲拥有（A，B，D），重组之后，甲拥有（A，C，D），而（A，C，E）恰好是个特别幸运的组合，可是在繁殖过程中被打破了，于是，即便智力由基因型完全决定，甲的智力值也无法由其父母的智力值充分解释（因为要充分解释需要了解各贡献因子的微观作用机制），而无法解释的那部分看起来好像就只是运气而已， @whigzhou: 补充一句：如果各贡献因子都是线性可加的，那么单一子女的智力也无法由父母智力充分解释，但假如这对夫妻生的足够多，那么子女的平均智力可以由他们两人的智力充分解释，但如果贡献因子不是线性可加的，那么哪怕生再多，子女平均智力也无法由父母智力充分解释

Giving Genes Their Due, But Not More 正视基因的功劳，但不要过誉 作者：Erik Parens @ 2015-5-21 译者：Tankman 校对：Drunkplane （@Drunkplane-zny） 来源：quillette，http://quillette.com/2016/05/21/giving-genes-their-due-but-not-more/ 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”。（http://content.ucpress.edu/pages/10867/10867.ch01.pdf） 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 notbeen 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》。 （编辑：辉格@whigzhou） *注：本译文未经原作者授权，本站对原文不持有也不主张任何权利，如果你恰好对原文拥有权益并希望我们移除相关内容，请私信联系，我们会立即作出响应。

——海德沙龙·翻译组，致力于将英文世界的好文章搬进中文世界——

（晕，晚饭时又想了想才发现犯了个低级错误，此因素与意愿生育数的奇偶无关，只与生下最后一对双胞胎之前的已生育数的奇偶有关，数字问题很容易犯错啊）

周末上松鼠会论坛，看到一个很有趣的问题，cecil问：

能不能生双胞胎貌似跟基因有关系。
如果是的话，由于科技发展，新生儿的存活率上升，他们长大后，又带着生双胞胎的基因，因而双胞胎在人类中占的比例会越来越高？
长此以往，人类会不会变成跟北极熊差不多，大多一胎两个？
又或者，因为再怎么生双胞胎的几率达不到1，而使得新生儿总人口中，双胞胎成一定的比例呢？这个比例又会是多少呢？

我觉得这个题目难度很适宜，不需要太多背景知识，但体现了基于进化论的思考角度，特别适合用作进化生物学的课后练习题。我的回答是（第四点是刚加上的）：

嗯，是会增加，但我认为增加不会太多

首先，这一分析成立的基础是：人口增长的瓶颈不再是生存压力而是生育意愿。
我认为这一假定目前只在较富裕国家可以成立，但在长期，从全球范围看，未必能成立。

设意愿生育数为X，实际生育数期望值为Y=f(X)，双胞胎概率为r，假设r=0.2，那么：
1）若X=1，Y=0.8+0.2*2=1.2;
2）若X=2，Y=0.8*(1+f(1))+0.2*2=2.16;
3）若X=3，Y=0.8*(1+f(2))+0.2*(2+f(1))=3.168;
依此类推，若X=i,i>3，Y=0.8*(1+f(i-1))+0.2*(2+f(i-2));
超生数在0.16和0.168之间来回摆动，并逐渐趋近于1/6，而超生率则随X增大而下降。
4）若X事先不确定，即：事先没有计划孩子数、而是随着生育经历随时决定是否继续生的夫妻，则结果取决于最后一胎是否为双胞胎，且此前离意愿数差多少，
Y=0.8*X+0.2*(0.5*X+0.5*(X+1))=X+0.1。

不过这里暂且接受这一假定，那么：
1）对于原本就想生育偶数个子女的夫妻，该因素没有影响，因为双胞胎并未使其子女数超出其生育意愿；
2）对于原本就想生育2个以上、但计划数为奇数的夫妻，该因素有影响，比如：原本打算生三个，开始生了两个，没料到又来了对双胞胎，超出计划数了。
3）对于原本只想生育1个的夫妻，该因素影响最大，双胞胎的到来总是会突破其计划数，但同时要考虑：这些生育意愿如此之低的夫妻，其中种群中的数量原本就处于萎缩趋势，因而其所携带的双胞胎基因并不会因这一因素的影响而得到很大传播。
4）对于生育意愿比较模糊，事先没有计划孩子数、而是随着生育经历随时决定是否继续生的夫妻，该因素的影响类似于（2），但程度较弱，比如：原本他们可能在生下第三个之后决定“再也不生了”，但第三胎恰好是双胞胎，因而他们的孩子数就比原本会有的数字多出了一个。

（注：上述分析未考虑强制性计划生育、政府生育鼓励或抑制政策、选择性堕胎等条件）

谁有兴趣，可以把上述四种情况用一个模型模拟一下，结论会更精确。

 

从基因的设计到性状的形成，是一个连续的发育过程，基因没有手，不能自己去搭建出最终的产品，它只能借助各种蛋白质、激素和其他化学物质来完成建造过程，每一步都涉及极其复杂的化学过程，后天环境因素随时可能在任何步骤上施加干扰，并且基因所设计的发育过程本身包含了许多收集环境参数的环节，这就像安装操作系统，完全一样的安装包，因为安装过程需要收集大量环境参数，最终的安装结果千差万别，发育过程更复杂，不仅要收集参数，还有大量干扰。

性别算是基因决定最纯粹的例子了，但实际上，如果你精确地安排一个激素注射序列，完全可能把一个XX型胎儿培养成标准的男孩。

laoyao把我关于文化宽容与同性恋关系的观点做了个重新表述：

从ESS的角度，你上次的文章也可以反过来说：

人类的反同性恋文化的出现，应该远在同性恋基因的出现之后。按照DNA贴的link的文章的说法，果蝇已经有这个基因，那应该是在人类出现的时候就已经携带了这个基因。因此，在人类的反同性恋文化出现时，同性恋基因在人群中应该已经达到了ESS的平衡。

但反同性恋文化的出现，改变了外在环境，使携带同性恋基因的人比以前更可能与异性生育后代，也就打破了平衡，使同性恋基因在人群中的比例反常地走高（但表现出来的同性恋性状不见得会更高）。

这其实是个双输的结果。对反同性恋的人来说，他们所痛恨的种子反而更广地传开。对携带同性恋基因的人来说，他们承受着先天与后天矛盾的痛苦，但这个痛苦本来也许只有1%（随便瞎举的数字）承受，现在却可能有3%的人承受。

所以，不是说现在社会对同性恋的宽容会导致同性恋的灭绝或减少，而只是让同性恋回到以前正常的状态。而我也想如同辉格上篇文章那样跳跃一下，得个启示说：宽容之后的比例，才是正常的本来该有的比例，任何外力恐怕都只能导致双输。

如果谁有心，可以调查一下各个不同文化下同性恋的比例。比如有的文化对同性恋完全不闻不问，有的甚至鼓励（部分古希腊），有的不反对、但强调男性生育（古代中国），有的强烈反对、处以极刑（中世纪，现代的某些伊斯兰国家），有的不犯法，但社会仍然有禁忌（现代中国、美国的某些地区）。有些文化风气的历史还太短，可能不能作为进化意义上的论据，还有些很难采集到数据，而且对古代社会，只能知道人们的表现，不能肯定是先天还是后天。不过假如能够比较准确地测出或推出同性恋基因的比例，并和毫无同性恋文化的原始部落想比较，那结果会很有价值。

这正是我想表达的意思。最后提出的调查，尽管很困难，但如果真花功夫去做，我相信中等程度的相关性大概能够找到。行为学和心理学的许多实验和统计方法，其想象力和设计之精妙，常常令人叹为观止。

一个细节有点异议，关于果蝇的研究，对讨论人类同性恋问题，只有启发意义，而没有证据价值；这两个物种的亲缘关系太远，依我看，它们的性别系统是两个物种在进化树上分化之后，各自发展出来的，它们的共同祖先很可能是无性的；实际上，跟眼睛一样，性别系统在进化史上被重新发明了多次，各自的基因基础和荷尔蒙机制都不是同源的。

摘自Matt Ridley的Genome: the autobiography of a species in 23 chapters，第8章CHROMOSOMES X AND Y Conflict：

……Forgive the digression into intelligence. Let's get back to sex. Probably one of the most sensational, controversial and hotly dis puted genetic discoveries was the announcement by Dean Hamer in 1993 that he had found a gene on the X chromosome that had a powerful influence on sexual orientation, or, as the media quickly called it, 'a gay gene'.11

Hamer's study was one of several published about the same time all pointing towards the conclusion that homo sexuality was 'biological' — as opposed to being the consequence of cultural pressure or conscious choice. Some of this work was done by gay men themselves, such as the neuroscientist Simon LeVay of the Salk Institute, keen to establish in the public mind what they were convinced about in their own minds: that homosexuals were 'born that way'. They believed, with some justice, that prejudice would be less against a lifestyle that was not a deliberate 'choice' but an innate propensity. A genetic cause would also make homo sexuality seem less threatening to parents by making it clear that gay role models could not turn youths gay unless they had the propensity already. Indeed conservative intolerance of homosexual ity has recently taken to attacking the evidence for its genetic nature. "We should be careful about accepting the claim that some are "born to be gay", not just because it is untrue, but because it provides leverage to homosexual rights organisations', wrote the Conservative Lady Young in the Daily Telegraph on 29 July 1998.

But however much some of the researchers may have desired a particular outcome, the studies are objective and sound. There is no room for doubt that homosexuality is highly heritable. In one study, for example, among fifty-four gay men who were fraternal twins, there were twelve whose twin was also gay; and among fifty-six gay men who were identical twins, there were twenty-nine whose twin was also gay. Since twins share the same environment, whether they are fraternal or identical, such a result implies that a gene or genes accounts for about half of the tendency for a man to be gay. A dozen other studies came to a similar conclusion.12

Intrigued, Dean Hamer decided to seek the genes that were involved. He and his colleagues interviewed no families with gay male members and noticed something unusual. Homosexuality seemed to run in the female line. If a man was gay, the most likely other member of the previous generation to be gay was not his father but his mother's brother.

That immediately suggested to Hamer that the gene might be on the X chromosome, the only set of nuclear genes a man inherits exclusively from his mother. By comparing a set of genetic markers between gay men and straight men in the families in his sample, he quickly found a candidate region in Xq28, the tip of the long arm of the chromosome. Gay men shared the same version of this marker seventy-five per cent of the time; straight men shared a different version of the marker seventy-five per cent of the time. Statistically, that ruled out coincidence with ninety-nine per cent confidence. Subsequent results reinforced the effect, and ruled out any connection between the same region and lesbian orientation.

To canny evolutionary biologists, such as Robert Trivers, the suggestion that such a gene might lie on the X chromosome immedi ately rang a bell. The problem with a gene for sexual orientation is that the version that causes homosexuality would quite quickly become extinct. Yet it is plainly present in the modern population at a significant level. Perhaps four per cent of men are definitively gay (and a smaller percentage bisexual). Since gay men, are, on average, less likely to have children than straight men, the gene would be doomed to have long since dwindled in frequency to vanishing point unless it carried some compensating advantage.
Trivers argued that, because an X chromosome spends twice as much time in women as it does in men, a sexually antagonistic gene that benefited female fertility could survive even if it had twice as large a deleterious effect on male fertility. Suppose, for example, that the gene Hamer had found determined age of puberty in women, or even something like breast size (remember, this is just a thought experiment). Each of those characteristics might affect female fertil ity. Back in the Middle Ages, large breasts might mean more milk, or might attract a richer husband whose children were less likely to die in infancy. Even if the same version of the same gene reduced male fertility by making sons attracted to other men, such a gene could survive because of the advantage it gave daughters.

Until Hamer's gene itself is found and decoded, the link between homosexuality and sexual antagonism is no more than a wild guess. Indeed, it remains a possibility that the connection between Xq28 and sexuality is misleading. Michael Bailey's recent research on homosexual pedigrees has failed to find a maternal bias to be a general feature. Other scientists, too, have failed to find Hamer's link with Xq28. At present it looks as if it may have been confined to those families Hamer studied. Hamer himself cautions that until the gene is in the bag, it is a mistake to assume otherwise.14

Besides, there is now a complicating factor: a completely different explanation of homosexuality. It is becoming increasingly clear that sexual orientation correlates with birth order. A man with one or more elder brothers is more likely to be gay than a man with no siblings, only younger siblings, or with one or more elder sisters. The birth order effect is so strong that each additional elder brother increases the probability of homosexuality by roughly one-third (this can still mean a low probability: an increase from three to four per cent is an increase of thirty-three per cent). The effect has now been reported in Britain, the Netherlands, Canada and the United States, and in many different samples of people.15

For most people, the first thought would be a quasi-Freudian one: that something in the dynamics of growing up in a family with elder brothers might predispose you towards homosexuality. But, as so often, the Freudian reaction is almost certainly the wrong one. (The old Freudian idea that homosexuality was caused by a pro tective mother and a distant father almost certainly confused cause and effect: the boy's developing effeminate interests repel the father and the mother becomes overprotective in compensation.) The answer probably lies, once more, in the realm of sexual antagonism.

An important clue lies in the fact that there is no such birth-order effect for lesbians, who are randomly distributed within their families. In addition, the number of elder sisters is also irrelevant in predicting male homosexuality. There is something specific to occupying a womb that has already held other males which increases the probability of homosexuality. The best explanation concerns a set of three active genes on the Y chromosome called the H-Y minor histocompatibility antigens. A similar gene encodes a protein called anti-Mullerian hormone, a substance vital to the masculinis ation of the body: it causes the regression of the Mullerian ducts in the male embryo — these being the precursors of the womb and Fallopian tubes. What the three H-Y genes do is not certain. They are not essential for the masculinisation of the genitals, which is achieved by testosterone and anti-Mullerian hormone alone. The significance of this is now beginning to emerge.

The reason these gene products are called antigens is because they are known to provoke a reaction from the immune system of the mother. As a result, the immune reaction is likely to be stronger in successive male pregnancies (female babies do not produce H-Y antigens, so do not raise the immune reaction). Ray Blanchard, one of those who studies the birth-order effect, argues that the H-Y antigens' job is to switch on other genes in certain tissues, in particu lar in the brain - and indeed there is good evidence that this is true in mice. If so, the effect of a strong immune reaction against these proteins from the mother would be partly to prevent the masculini sation of the brain, but not that of the genitals. That in turn might cause them to be attracted to other males, or at least not attracted to females. In an experiment in which baby mice were immunised against H-Y antigens, they grew up to be largely incapable of success ful mating, compared with controls, though frustratingly the experimenter did not report the reasons why. Likewise, male fruit flies can be irreversibly induced to show only female sexual behaviour by the switching on at a crucial point in development of a gene called 'transformer'.16

People are not mice or flies, and there is plenty of evidence that the sexual differentiation of the human brain continues after birth. Homosexual men are clearly not, except in very rare cases, 'mental' women trapped inside 'physical' men. Their brains must have been at least partly masculinised by hormones. It remains possible, how ever, that they missed some hormone during some early and crucial sensitive period and that this permanently affects some functions, including sexual orientation.

……

 

 

 

 

说明：说某一性状或行为具有基因基础，并不暗示该性状或行为完全由基因决定。

摘自维基百科“同性恋”条目：
http://zh.wikipedia.org/w/index.php?title=同性恋&variant=zh-cn#.E5.90.8C.E6.80.A7.E6.88.80.E8.80.85.E4.BA.BA.E5.8F.A3.E6.AF.94.E4.BE.8B

苏珊•布莱克摩尔（Susan Blackmore）则认为性倾向及其行为是有基因决定的，一种观点认为大部分有同性恋基因的人因为社会压力而过着“异性恋”的生活，与异性结婚并繁衍后代，按照这种观点，在进入资讯时代以后，认为同性恋下流低劣的人数会减少，因为人们会解决到更多的同性恋议题并逐渐接受这种现象和群体，进而，那些携带同性恋基因的人也就不会按照异性恋的生活方式来安排自己的生活，生育的现象在同性恋群体中将会减少。
西蒙•列维（Simon LeVay）关于同性恋男尸下丘脑的研究和Marc Breedloves关于生者的出生顺序以及手指长度比例研究，都显示出出生前荷尔蒙对性取向决定问题上所产生的影响，前者指出男性同性恋者的女性化趋势，后者则指出同性恋者，不论男性还是女性，都有男性化的趋势。

摘自维基百科“性取向”条目：
http://zh.wikipedia.org/w/index.php?title=性取向&variant=zh-cn

对非异性恋的研究和试验为另外一个观点开辟了道路：性取向是在孩童时期或更早的时候被固定的。对同性恋双胞胎的研究表明，如果其中一个人是同性恋，那么另一个人有40-60%的机会成为同性恋者；异卵双生的比率为15-30%。对于不是双胞胎的同性兄弟姐妹来说，这个比率是5-10%（参看：http://www.worldpolicy.org/americas/sexorient/twins.html 和 http://researchmag.asu.edu/stories/supporting.html ）。
对很多人来说，这些数据有力的表明了性取向的一个生物因素。对其他的人，包括引用的研究的三名作者中的两名（贝利和波勒德，Bailey&Pollard）则担心来自于同性恋鼓吹者杂志的读者可能会歪曲这个结果。

摘自wikepedia的Biology and sexual orientation条目：
http://en.wikipedia.org/wiki/Biology_and_sexual_orientation#Chromosome_linkage_studies

Chromosome linkage studies

Earlier chromosome studies of homosexuality in males have not been replicated, or have had doubt cast on these early suggestions. For example, in 1993, Dean Hamer and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families.[15] Hamer et al. found that the gay men had more gay male uncles and cousins on the maternal side of the family than on the paternal side. Gay brothers who showed this maternal pedigree were then tested for X chromosome linkage, using twenty-two markers on the X chromosome to test for similar alleles. In another finding, thirty-three of the forty sibling pairs tested were found to have similar alleles in the distal region of Xq28, which was significantly higher than the expected rates of 50% for fraternal brothers. This was popularly (but inaccurately) dubbed as the 'gay gene' in the media, causing significant controversy.

However, a later analysis by Hu et al. revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28.[16] Sanders et al. (1998) replicated the study, finding 66% Xq28 marker sharing in 54 pairs of gay brothers.[17] On the other hand, two other studies (Bailey et al., 1999; McKnight and Malcolm, 2000) failed to find a preponderance of gay relatives in the maternal line of homosexual men.[17] Also, a study by Rice et al. in 1999 failed to replicate the Xq28 linkage results.[18]

Additionally, Mustanski et al. (2005) performed a full-genome scan (instead of just an X chromosome scan) on individuals and families previously reported on in Hamer et al. (1993) and Hu et al. (1995), as well as additional new subjects.[19] With the larger sample set and complete genome scan, the study found much weaker link for Xq28 than reported by Hamer et al. However, they did find other markers with significant likelihood scores at 8p12, 7q36 and 10q26, the latter two having approximately equivalent maternal and paternal contributions.

这是上述条目的有关参考文献：

^ Rutter, M. (2006). Genes and Behavior. Oxford, UK: Blackwell Publishing.
^ Hamer DH, Hu S, Magnuson VL, Hu N, Pattatucci AM (July 1993). "A linkage between DNA markers on the X chromosome and male sexual orientation". Science (journal) 261 (5119): 321–7. doi:10.1126/science.8332896. PMID 8332896.
^ Hu S, Pattatucci AM, Patterson C, et al (November 1995). "Linkage between sexual orientation and chromosome Xq28 in males but not in females". Nat. Genet. 11 (3): 248–56. doi:10.1038/ng1195-248. PMID 7581447.
^ a b Wilson, G.D., & Rahman, Q. (2005). Born Gay: The Biology of Sex Orientation. London: Peter Owen Publishers.
^ Vilain E (2000). "Genetics of sexual development". Annu Rev Sex Res 11: 1–25. PMID 11351829.

非常感谢子蛇和laoyao对我《宽容是同性恋的坟墓？》一文的评论，laoyao说：

这个思路我以前在Aaron Lynch的Thought Contagion里看到过。那个家伙是较早研究memetics的，但过度看重meme的垂直传播，这在internet时代其实已经比较次要了。但正因如此，他的书里讨论了大量meme和gene相互作用的案例，其中一个就是同性恋。这确实很有趣，我当时看了颇惊叹了一阵。

至于别人基于误读的抨击，大可不必理会。对同性恋的宽容，照我看是据于人权，跟同性恋是先天、后天，会繁荣还是会灭绝，都没关系。义理如此，其他论据不过是用来说服反对者的捷径，但整个宽容本身是建立在人和人之间的相互尊重这一最基本的原则上的。

况且宽容显然不会导致同性恋灭绝，只会导致减少，但减少之后又会慢慢地再反弹，最后应该是动态平衡的(gene and meme)evolutionary steady比例。辉格所说的消失，应该就是这个意思，不是说再没同性恋了，而是说没谁再对此大惊小怪了。就象美国人对肤色的看法的慢慢变化一样。

当然这么一个例子对于文章最后的结论还是显得有些薄弱，因为同性恋是个不利于繁衍的基因影响下的行为的特例。不过我还是同意辉格的结论，即“如果它仅仅是与你的价值观相悖，而没有伤害旁人，”那最后发展的结果必然是meme的evolutionary steady状态。这跟由基因变异推动生物进化的道理有点类似，但也不尽相同，不过那个话题就太大了。

最后想说的是，辉格认为“同性婚姻的合法化之争，更多的是一种名分之争”，我觉得不确切。婚姻不仅仅是双方的契约，也是社会和法律所认同的契约，因此，并不是两个人都同意就可以得到一切权利和保护，还需要从社会那里得到法律的承认和保护。比如异性夫妻领养小孩天经地义，但同性union在美国的很多州仍然不能领养小孩。甚至连通过了反歧视同性恋法的州都还没到一半。详情可见：http://en.wikipedia.org/wiki/Same-sex_marriage_in_the_United_States

所以同性恋婚姻合法化，更多还是争取利益，不是意识形态。而这也使我对同性恋婚姻的前景感到乐观，因为争口气的激情容易消退，争利益的动机却会一直坚持下去。

我没读过Aaron Lynch，但我对meme的兴趣一直很浓，有空找来读一下。垂直或者窄通道的转播，虽然条件过于严苛，因而针对的范围过于狭窄，但人类历史的很长一段，传播的通道都是十分狭窄的，而那段时间，对人性和符号体系的塑造、对一些基本特征的建构，应该有着决定性的地位，其影响在可见的未来仍将是压倒性的；因而，正如进化生物学家以更新世稀树草原的狩猎采集生活，作为分析人性之基因基础的基本环境背景，当我们思考观念系统的深层结构和基本特征时，也应赋予早期背景同等重要性。 第二点，“这么一个例子对于文章最后的结论还是显得有些薄弱”，是的，所以我原本打算以此为引子进而说明北美殖民社区从早期的宗教极端主义盛行，到后来宗教宽容的发展过程，这个题材才更切合结尾处的那句话，可是受饭文写作的选题和篇幅限制，只好放弃了。 第三点，关于领养权的问题我的确了解不多，考虑到你提示的这些情况，加上我原本就搁置了的税收和福利优惠，我关于“名分之争”的说法需要修正，或许这只是问题的一半。

非常感谢子蛇和laoyao对我《宽容是同性恋的坟墓？》一文的评论，子蛇说：

1、文中说了，同性恋是双性恋的一种极端情况，双性恋还会结婚生子，生下极端情形的。
2、同性恋倾向恐怕不仅仅是先天因素，似乎后天养成的也不少。
3、基因会变异，异性恋父母也会生出同性恋孩子。

首先我得承认，同性恋大概不会消失，我的观点的逻辑结果应该只是大比例减少，因此，这篇文章的题目确实有点哗众取宠，需要反省；其次，需要强调一下（虽然上下文已经暗示了），我文章后半部分专门针对男同性恋，而且是稳定的同性恋者，不包括那种受特定环境条件（比如监狱和军队）诱导下的偶发同性性行为。

子蛇的第一点我同意，但即便如此，基因向下传播的通道仍然被收窄了，所以在新的均衡点上，数量会大为减少，对吧？

第二，按我所采信的理论，决定性取向的诸多因素中，基因基础是首要的，其次是兄弟排行，至于成长环境是否存在非随机的影响，我存疑。

第三，异性恋父母会出同性恋孩子，这没错，但通常不是因为基因突变（这种情况的概率极小），而是因为受精卵减数分裂时的染色体重组，因为影响性取向的基因基础并非单一基因，而是分布在多个染色体上的一组基因，它们的特定组合才会导致同性恋，同性恋孩子的父母可能分别拥有该组合的一部分；所以，同性恋的同卵双胞胎兄弟也是同性恋的概率接近50%，而异卵双胞胎的相关性则低得多，只有不到20%。

（按二：此文发表后，遭到不少同性恋权利支持者的激烈抨击，他们从文中读出了这样的意思：我主张灭绝同性恋。阿弥陀佛~~）

（按一：最后一段言犹未尽，本想乘机说说美国各教派从偏激走向宽容的历史，可惜篇幅满了，再找机会吧）

宽容是同性恋的坟墓？
辉格
2009年2月12日

去年11月，就在美国自由派赢得总统和国会选举的同时，却在别处遭遇了一次出乎他们意料的失败。加利福尼亚选民在选举日除了对总统候选人投票，还要为一系列州内选举和表决投票，其中包括了禁止同性婚姻的八号提案。提案以52%的支持率通过，这一失败让自由派在半年前赢得的那场胜利化为乌有，当时，加州最高法院以4：3裁决同性婚姻合法。八号提案的通过随即全美80多个城市引发了一场大规模抗议，许多个人、团体、甚至地方政府向加州高院提起诉讼，法院已决定受理这些诉讼，并安排在下月初开庭。自由派的愤怒源自他们对失败的震惊，此前他们在舆论上已完全占据主导，支持提案的捐助者甚至不敢公开捐助记录，"沉默的多数"用选票说话了。

近年来，在同性恋社团和自由派的推动下，争取同性恋者权利的运动，在具有深厚保守传统的美国，正取得越来越多的进展。实际上，同性恋行为本身在美国早已得到保护，也就是说，从消极权利的角度看，同性恋者已拥有全部公民权利，他们现在主张的同性婚姻，实际上是在改变对婚姻的定义，从而创制一种与传统婚姻同等地位的新的民事关系，而正是这一条，遭到了保守派的强烈抵制。在基督教传统中，婚姻不仅是一种民事关系，还有深厚的宗教内涵，历史上，婚姻法作为教会法的一部分，独立于普通法，婚姻事务也一直由教会管辖。所以不难理解，保守派为何在此问题上如此顽固，这已经成为他们最后的防线。

现在，这条防线正在被突破。加州去年五月的裁决让它成为继马萨诸塞之后第二个承认同性婚姻的州，就在八号提案通过后几天，康涅狄格最高法院承认同性婚姻的裁决正式生效，而同性婚姻合法化法案正在佛蒙特、罗德岛、缅因和新罕布什尔等多个州议会讨论。

撇开宗教内涵，从民法角度看，婚姻实际上就是一种涵盖了财产共享、继承和子女抚养等责任的民事契约；理论上，通过双方协商签约，婚姻关系像其他民事关系一样可以得到合同法的保护，而不需要专门的婚姻法，通过商定各种责任关系，每对夫妻都可以建立独特的婚姻关系；但实践上，婚姻契约涵盖的内容过于广泛，时间跨度又很大，如果每对夫妻都从头商议全部条款细节，交易费用大到无法接受；婚姻法恰好解决了这个问题，它提供了一种包含了大量默示条款的标准契约，其内容来自社会对于婚姻所含责任的普遍看法，同时，借助婚前协议，夫妻可以对契约内容进行个性化和微调。

从民法角度看，只要契约自由原则得到贯彻，同性婚姻是否被承认，其实对于争议双方都无关紧要（暂不考虑与婚姻有关的税收和福利优惠），想结婚的同性恋者，不妨订立这样的契约：我们同意承担异性夫妻在婚姻法下被规定的全部责任，直到任一方死亡或双方同意解除契约。同性恋社团也可以参照开源组织为开源软件所设计的GPL授权协议，为同性夫妻设计一套标准婚姻契约，按经验，美国法官是会承认这种契约的，这将是法律自发演进的经典模式。

如此看来，同性婚姻的合法化之争，更多的是一种名分之争，自由派希望通过不断突破一些社会心理禁区，来求得宽容同性恋的文化氛围，而这也正是保守派不愿看到的，在这方面，自由派显然获得了更多成果。然而有趣的是，双方都没有看到一种前景：恰恰是对同性恋的文化宽容，或许会在未来导致同性恋的急剧减少甚至灭绝。

对于进化生物学家，同性恋一直是个难题，这种看起来对个体繁衍有害无益的性状，不仅有基因基础，而且在各种族的基因库中拥有稳定的比例，好像跟天生不爱吃饭爱吃沙子一样奇怪。近年来有一种相对可信的理论认为，同性恋其实是双性恋的一种极端状态，而双性恋是有遗传优势的，这是因为双性恋者通常更早开始性行为，而且平均拥有数倍于单性恋者的性伴侣。正是双性恋的这种遗传优势，附带使同性恋作为其副产品也长期存在着。

在我看来，同性恋的存在还有一个重要的条件，那就是文化传统和伦理体系对娶妻生子的看重，在各种文化中，这都被视为人生头等大事。因而，在传统社会，同性恋者虽然对异性没兴趣，但为了履行伦理和家族义务，同样会娶妻生子；即使在当代，许多社会的同性恋者为了掩盖其性取向，也会娶妻生子。因此，在这种严苛的伦理约束下，同性恋者留下的后代通常并不比异性恋者少，这样同性恋基因便无法被排除出基因库。

显然，文化宽容将瓦解同性恋的这一存在基础，在同性行为被普遍接受、同性婚姻得到伦理正当性之后，同性恋不再需要履行娶妻生子义务，也不必用异性婚姻来掩盖性取向，于是，他们也就不再会留下后代了。这一结果，或许只要几代人时间就会在统计上表现出来。

从这一前景中，我们实际上可以得到一个更广泛的启示，那就是，对于一种罕见、奇特甚至令你反感的行为方式，如果它仅仅是与你的价值观相悖，而没有伤害旁人，那就最好宽容它；长期的宽容会让原本极端的行为融入主流，或许最终还会消失。

 

土摩托在<基因VS进化论>一文中呼吁松鼠会向大众介绍进化论和基因科学，对此我十分赞赏，但文章里面有两段话我感觉可能会对读者形成误导，说一下我的看法。第一段是：

……进化论非常简单，只用几句话就可以说完。……进化论出现之后，生命科学的基石就算打好了。生物学的所有新发现都是在不断地证明进化论的正确性，尤其是基因的发现和DNA结构的发现，都可以说是被进化论预言过的。

这段给人的感觉是，达尔文以后的进化生物学是在达尔文纲领指导下的一个连续发展过程，我不这么认为。进化生物学在达尔文之后至少经历了两次革命性变化（所谓革命性，用拉卡托斯的说法，就是用改变了硬核内容的新纲领取代了旧纲领）。

第一次是孟德尔革命，孟德尔（Gregor Johann Mendel）把基因概念和孟德尔定律加入了硬核，在孟德尔被重新发现后，并经过20世纪初几十年的发展，杜布赞斯基（Theodosius Dobzhansky）等人最终在四十年代将进化生物学的新纲领表述为现代进化综合论（modern evolutionary synthesis）：

1. All evolutionary phenomena can be explained in a way consistent with known genetic mechanisms and the observational evidence of naturalists.
2. Evolution is gradual: small genetic changes, recombination ordered by natural selection. Discontinuities amongst species (or other taxa) are explained as originating gradually through geographical separation and extinction (not saltation).
3. Selection is overwhelmingly the main mechanism of change; even slight advantages are important when continued. The object of selection is the phenotype in its surrounding environment. The role of genetic drift is equivocal; though strongly supported initially by Dobzhansky, it was downgraded later as results from ecological genetics were obtained.
4. The primacy of population thinking: the genetic diversity carried in natural populations is a key factor in evolution. The strength of natural selection in the wild was greater than expected; the effect of ecological factors such as niche occupation and the significance of barriers to gene flow are all important.
5. In palaeontology, the ability to explain historical observations by extrapolation from micro to macro-evolution is proposed. Historical contingency means explanations at different levels may exist. Gradualism does not mean constant rate of change.

第二次革命似乎未被学界命名，我称之为汉密尔顿-史密斯革命，威廉·唐纳德·汉密尔顿（William Donald Hamilton）为进化理论引入了汉密尔顿法则（Hamilton's rule），该法则通俗的说就是，选择的单位是基因而非个体，即，计算遗传收益的单位是基因传播率，而非个体繁殖率；约翰·梅纳德·史密斯（John Maynard Smith）也独立获得了这一思想（虽然最初并未显明表达），并且用博弈论重建了进化理论的数学基础，其核心便是“进化策略均衡”（evolutionarily stable strategy, ESS），其地位相当于瓦尔拉斯均衡在经济学中的地位（而汉-史革命的地位类似于边际革命在经济学发展史中的地位）。理查德·道金斯（Richard Dawkins）在《自私的基因》一书里用通俗语言介绍了汉密尔顿-史密斯革命的成果，此后学术界内外引用汉-史纲领时，经常直接借助道金斯的术语（selfish gene）转引，科普普到这份上，算是极致了。

追随汉密尔顿-史密斯纲领的学者被称为新达尔文主义者（neo-Darwinists），他们以此纲领为基础把革命广泛扩展到动物行为学、人类行为学、社会生物学、认知心理学等多个学科，这场革命带来的冲击波远未平息，它注定要影响这些学科未来几十年的发展方向。

第二段是：

正是那些没有理解进化论的真谛，而又心怀鬼胎的人（比如希特勒），才会错误地把进化论用在社会学领域，提出了很多荒谬的论点，它们其实和进化论毫无关系。

“错误地把进化论用在社会学领域”这句话有两种语义：1）把进化论用在社会学领域，这种做法是错的；2）可以把进化论用在社会学领域，但他用得不对。

进化论当然可以并且已经广泛用在社会学领域，我预期，进化论未来几十年的进展将大部分从这方面取得。至于希特勒，他既不懂进化论，也不懂社会学，他也从未对这两个学科表现出兴趣，他无非是个失意的三流画家、沮丧的一战退伍兵和十足的流氓恶棍。

雌性在受孕期可能与多个雄性交配，因而精子会在体内为争夺进入卵子的机会而展开激烈竞争，这读过《精子战争》一书的都知道。许多时候，雌性会故意造成这种竞争局面，以便筛选出在精子战争中表现最佳的精子，这也很容易想到。最近，对果蝇的研究发现，雌性引发精子战争还有另外的作用：通过强化精子竞争来抑制不合作基因的扩散，这些“坏基因”试图通过扭曲配子性别比（我猜大概是通过干扰[[Meiosis|减数分裂]]过程来实现）来提高自己进入子代的机会，但因为这种扭曲常对精子的功能有伤害，它们在精子战争中的表现往往较差。下面摘自ScienceNOW的有关报道：

Females take multiple partners, a behavior called polyandry, in many species, including mice. Some researchers have suggested that polyandry evolved to help females boost the likelihood that their offspring will carry certain positive traits such as virility. They can collect sperm through multiple matings, and only the most competitive of this "sperm cocktail" will fertilize their eggs...

To test whether females might evolve polyandry in response to the gene, the researchers ran an evolutionary experiment. They compared mating behavior between four fruit fly lines in which the selfish gene was present in about 30% of the males, and eight fruit fly lines lacking the gene entirely. Females in all the fruit fly lines showed nearly identical mating rates at the outset of the experiment. But after 10 generations, females from the selfish gene population remated, on average, almost a full day sooner than females from the populations without the selfish gene, the researchers report today in Science (p. 1241)...

这是Science上的论文摘要：

It is unknown why females mate with multiple males when mating is frequently costly and a single copulation often provides enough sperm to fertilize all a female's eggs. One possibility is that remating increases the fitness of offspring, because fertilization success is biased toward the sperm of high-fitness males. We show that female Drosophila pseudoobscura evolved increased remating rates when exposed to the risk of mating with males carrying a deleterious sex ratio–distorting gene that also reduces sperm competitive ability. Because selfish genetic elements that reduce sperm competitive ability are generally associated with low genetic fitness, they may represent a common driver of the evolution of polyandry.

注：这里的selfish gene不是道金斯意义上的自私基因（他认为所有基因都是自私的），而是特指基因组里那些不合作的基因，它们通过损害其它基因的遗传利益来增加自己进入子代的机会。

（按：为了把旧文章装扮的看上去不那么旧，只好为它们写一点按语。不久之前，提及性别和种族差异还是政治错误的，要是敢说这些差异还有遗传基础，那就是罪大恶极了，现在情况有所松动，那也无非是因为分子生物学进展神速，事实明摆在那里，再也无法否认了，但政治正确的力量依然强大，萨默斯就为此丢了哈佛校长的乌纱，为了应付科学进展，政治正确的公式有了调整：今天你可以说性别种族差异，甚至可以说它们的遗传基础，但只能说好，不能说差，虽然好差总是比较出来的，但政治正确检查员可不这么认为，A>B等价于B<A，这一逆反律在政治正确学中是不成立的，所以，请记住，政治正确学第一定律：A>B不等价于B<A。） 为什么是牙买加？ 辉格 2008年8月19日 在本届奥运会的短跑项目中，牙买加运动员以其优异成绩震惊了世界，博尔特以破纪录成绩获得男子百米金牌，女子百米更是被牙买加选手包揽前三名，正在进行的二百米预赛中，又有大批牙买加选手小组出线，他们有望夺得更多短跑奖牌。这一人口仅260万的加勒比岛国的惊人表现引起了世人极大的好奇，究竟是什么因素让他们在短跑项目上如此出色？依我看，任何单一因素都难以作出解释，这一成就，是遗传、收入水平、地理位置和体育商业化等多个因素的恰当组合所结出的硕果。 非洲黑人在田径和球类项目中的运动天赋是众所周知的，他们的骨骼肌肉和心肺系统都非常适合于奔跑。然而，同样是擅于奔跑的黑人，生活在西非丛林地区的黑人擅长短跑、跳远、篮球等需要强爆发力的项目，而生活在东非稀树草原的黑人则更擅长长跑和自行车等耐力项目。这显然是环境选择的结果，丛林中的捕猎和战斗需要灵活、快速和爆发力，而开阔的草原上则更需要耐力。最新的遗传学研究揭示了这一差别的微观机制：合成α辅肌动蛋白的ACTN3基因的某种变异体在西非裔黑人的基因库中频率很高，而这些变体所合成的肌动蛋白恰恰提高了肌肉快速运动能力。 遗传优势让西非产生了大批优秀足球运动员，但田径方面却没有类似牙买加这种表现，这大概是经济发展水平的差异所致。与足球相比，田径项目需要更专业的场地、训练和选拔体系，因而对经济水平和教育体系的要求更高，这解释了为何巴西在非常贫困的时候便已拥有繁荣的足球业，而田径大国则很少是穷国。牙买加人均GDP约4000美元，处于中等偏下水平，这一经济水平意味着，国民已摆脱贫困，儿童能获得足够营养，多数儿童能接受基础教育，因而也有机会参加有组织的训练、比赛和选拔活动。于是我们看到，牙买加从小学生到大学生都参加田径运动，每年大约有260个田径队、8万多人参加近20种各级比赛，而金斯敦理工大学更成为运动员的摇篮。 同时，牙买加又不是太富，没有富裕到让青年们看不上体育这碗青春饭的程度，欧洲足球业越来越依赖于移民和外籍球员，就是因为富裕生活让本土孩子们不再愿意忍受体育的艰辛、高淘汰率和短职业寿命，同为加勒比岛国的巴哈马，也因为太富裕（人均GDP近2万美元），虽然人种构成与牙买加相同，体育业却乏善可陈。 仅凭遗传因素和中等富裕两个条件，像牙买加这样的小国是不可能支撑起一个繁荣的体育业的，幸运的是，加勒比背靠美国这个体育大市场。美国各大学每年都会来牙买加挑选录取一批体育尖子，正如NBA选秀激励了全球大批中学生对篮球的热爱，进入美国大学进而在美国体育界飞黄腾达的机会同样激励了大批牙买加学生热衷于各项体育运动。而繁荣的培训和选拔市场也催生了牙买加本土的体育商业组织，MVP俱乐部便是其中的成功典范，该私人俱乐部1999年成立以来，经过多年卧薪尝胆，其精心挑选和培养的运动员终于开花结果，近年来在各种大赛中取得众多奖项，其中以两度创造百米纪录的阿萨法·鲍威尔为最杰出代表。相比之下，官方机构牙买加奥委会反而显得碌碌无为，坐享其成而已。 相信，牙买加运动员在本届奥运会上的优异表现将更加激励他们的年轻人投身体育运动，也将吸引更多资金和人力投入该国的体育产业，体育或许将成为这一加勒比小国的一大产业，他们的成功经历值得世人关注和学习。