情商2：影响你一生的社交商（第3版）

我还记得杰罗姆·卡根在20世纪80年代曾经讲过他在波士顿以及中国进行的研究，那时他通过观察婴儿对于新鲜事物的反应来推断他们长大后是否会拥有害羞、胆怯的性格。卡根教授现在虽然已退休，但是仍在继续他的研究，他仍在跟踪调查当年的“卡根婴儿”。^[22]每隔几年我都会去他在威廉·詹姆斯大楼顶层的办公室拜访他，他的办公室也是整个哈佛大学的制高点。

在我最近一次去拜访的时候，他告诉了我通过对当年的“卡根婴儿”进行大脑成像得出的最新发现。卡根一直喜欢采用最新的科研方法，这次也不例外，他已经开始使用功能性核磁共振成像系统了。他告诉我，当年的“卡根婴儿”现在都已经20多岁了，对他们进行研究后发现，那些当年被认为内向的孩子的杏仁核现在遇到新鲜刺激时仍然会过度兴奋。^[23]

胆小羞怯在神经学上的表现之一就是在杏仁核检测到异常，特别是危险信号时，丘脑的活动会异常活跃。当我们察觉到任何异常情况，比如看到一张鹿身人面照片时，丘脑都会被激活。并非只有明确的危险信号才能引发丘脑的活动，任何陌生或者不同寻常的信号都可以做到这一点。

丘脑反应不那么剧烈的孩子往往性格开朗，喜欢交际。而丘脑反应剧烈的孩子一般都拒绝新鲜事物。孩子的这种性格会日益加强，因为父母往往会保护这些胆小的孩子，不让他们与陌生人接触，但是这反而更加妨碍了他们学会与别人打交道。

在早期的研究中卡根发现，如果父母鼓励或者强制羞怯的孩子与同伴玩耍的话，他们的胆小基因是可以被克服的，这种情况很普遍。在进行了几十年的跟踪观察之后，卡根发现出生后被认定为内向的孩子成年后只有1/3会有胆小羞怯的表现。

现在他意识到，这些孩子杏仁核和丘脑的反应仍然剧烈，因此发生变化的并不是神经系统的兴奋性，而是大脑对冲动的抑制。孩子如果能够长期压制羞怯、退缩的冲动，慢慢地他就可以正常地与人交往了，不会再出现羞怯的行为。

神经学家用“神经支架”这个术语来描述大脑的某个神经通道一旦形成后，它的连接就会随着不断的使用而得到加强，就像在建筑工地搭建脚手架一样。它也可以解释为什么某种行为模式一旦形成就需要很大力气才能改变。当然，如果有机会的话，通过有意识的努力，我们也可以形成并且加强新的神经通道。

卡根告诉我，内向的孩子“70%长大后都很健康。一个人的气质可能会影响命运，但是并不能决定他的命运。那些孩子现在已经不再胆怯或者过度兴奋了”。

比如一个在婴儿时期被认定为性格内向的男孩，在十几岁的时候就学会感受并且克服了自己的恐惧，他说现在已经没有人认为他害羞了。但是这需要别人的帮助和自己的努力，比如一些小的成功可以帮助人们克服恐惧心理，这似乎是一个利用大路神经系统来驯服小路神经系统的过程。

他自己记得的一次成功是克服了对打针的恐惧。在童年时期他非常惧怕打针，以至拒绝去看牙医，直到有一次他遇到了一位赢得自己信任的牙医，这种恐惧就消失了。看到姐姐跳进游泳池也给了他接触水的勇气，于是他学会了游泳。最初他不得不求助于父母来排解自己的噩梦，但后来他慢慢地学会了依靠自己平静下来。

“我能够克服自己的恐惧，”这位曾经羞怯的孩子在学校布置的作文中写道，“是因为我现在了解了自己容易焦虑的气质，我已经能够克服一般的恐惧了。”^[24]

因此，许多内向孩子的性格是可以在别人的帮助下自然地发生积极变化的。来自家庭的正确引导，或者孩子本人对自己沉默寡言个性的有意克服，都可以帮助他们。利用自然发生的“威胁”来不断挑战他们的内向性格，也会产生同样的效果。

卡根说自己的孙女6岁的时候非常害羞，一次孙女跟他说：“你要假装我不认识你，我必须通过练习来克服害羞的习惯。”

卡根补充说：“父母们还没有意识到，尽管基因可以影响孩子的某些特征，但是它并不能决定孩子的性格。”

虽然培养方式并不能改变所有的基因，也不能修正所有的神经缺陷，但是孩子们的日常经历的确可以重塑神经通道，而且神经科学现在已经可以详细地描述这些神经通道被重塑的过程了。

1. Even more heat was being generated in the 1970s by another theorist on the Harvard faculty,biologist Edwin O. Wilson, who had begun to articulate his theory of sociobiology, and byanthropologist Irven DeVore and his star student, Robert Trivers, who were just starting to developtheir theory of evolutionary psychology— today, widely influential. At the time these schools ofthought were vehemently opposed by a group led by paleontologist Stephen Jay Gould and geneticistRichard Lewontin, also Harvard faculty members.
2. John Crabbe et al., “Genetics of Mouse Behavior: Interactions with Laboratory Environment,”Science 284 (1999), pp. 1670–72.
3. Some behavior geneticists objected to what they saw as an “emperor has no clothes” finding,largely because that was the angle played up in an accompanying commentary. But the more soberreading of the article was that a single test of the same behavior was no longer enough; the study raisedthe methodological bar for the field. Now, as Crabbe commented, “When someone knocks out a genefor anxiety, you see them using three tests to show the effect, where before they could get away withjust one.”
4. The methyl molecule consists of just four atoms—a carbon and three hydrogen; precisely how theyattach to one gene determines what happens. In one formation, the methyl group inactivates the gene,coiling its DNA tighter so the gene cannot be expressed. In another configuration, the methyl grouprelaxes the DNA coils, enabling the gene to manufacture its particular RNA (and so its protein).
5. On genes and environment, see Robert Plomin and John Crabbe, “DNA,” Psychological Bulletin126 (2000), pp. 806–28.
6. Michael J. Meaney, “Nature, Nurture, and the Disunity of Knowledge,” Annals of the New YorkAcademy of Sciences 935 (2001), pp. 50–61.
7. On the plasticity of genetic mechanisms that regulate behavior, see Elizabeth Hammock and LarryYoung, “Microsatellite Instability Generates Diversity in Brain and Sociobehavioral Traits,” Science308 (2005), pp. 1630–34.
8. On bad families of origin and kids adopted by good or bad homes, see R. J. Cadoret et al., “Genetic-Environmental Interaction in the Genesis of Aggressivity and Conduct Disorders,” Archives of GeneralPsychiatry 52 (1995), pp. 916–24.
9. Michael Meaney, “Maternal Care, Gene Expression, and the Transmission of IndividualDifferences in Stress Reactivity Across Generations,” Annual Review of Neuroscience 24 (2001), pp.1161–92.
10. On behavior genetics, see S. McGuire and J. Dunn, “Nonshared Environment in MiddleChildhood,” in J. C. DeFries et al., eds., Nature and Nurture During Middle Childhood (Oxford, U.K.:Blackwell, 1994).
11. On genetic closeness, see David Reiss et al., The Relationship Code (Cambridge, Mass.: HarvardUniversity Press, 2000).
12. Every child’s unique experience of the same family is called a “nonshared environment” inbehavior genetics. See Judy Dunn and Robert Plomin, Unshared Lives: Why Siblings Are So Different(New York: Basic Books, 2000).
13. It gets more complicated by a genetic timetable. For example, the study discovered that about athird of the genes that influence antisocial behavior in the early teen years no longer do so bymidadolescence; they are by then replaced by new social and genetic factors that were not operatingearlier.
14. On the other hand, an outgoing baby who flirts and loves to cuddle gets more cuddling in return.As the child grows, she will continue to elicit warmth and engagement from others, reinforcing her ownsociability. Either way, how parents treat the baby seems to intensify the genes involved, amplifyinghow the child acts one way or the other.
15. On neurogenesis: Fred Gage, Salk Institute, personal communication.
16. Fire together, wire together: For example, at the cellular level, the process of learning entailsglutamate activating a receptor on one neuron while calcium channels open on another, which triggersthe synthesis of proteins in the cell body that “glue together” their receptors. That connection results ina larger response from cell to cell. At the cellular level, learning means that the input from one cell nowhas a larger output. See Joseph LeDoux, presentation at the meeting of the Consortium for Research onEmotional Intelligence in Organizations, Cambridge, Mass., December 12, 2004.
17. On experience and the development of neural systems, see B. J. Casey, “Imaging the DevelopingBrain: What Have We Learned About Cognitive Development?”Trends in Cognitive Science 9 (2005),pp. 104–10.
18. Such stress impairs neurogenesis, reduces hippocampal volume, produces alterations in HPAfunction, and results in emotional hyperreactivity. See C. L. Coe et al., “Prenatal Stress DiminishesNeurogenesis in the Dentate Gyrus of Juvenile Rhesus Monkeys,” Biological Psychiatry 54 (2003), pp.1025–34.
19. On neural defaults, see Gerald Edelman, Neural Darwinism (New York: Basic Books, 1987).
20. On spindle cells and stress while migrating to their proper place, see John Allman et al., “TheAnterior Cingulate Cortex: The Evolution of an Interface Between Emotion and Cognition,” Annals ofthe New York Academy of Science 935 (2001), pp. 107–17.
21. Davidson adds that we still need to identify more precisely what circuits may be more malleablethroughout the life span, and which circuits may be particularly plastic early in life but then becomerelatively fixed in adulthood.
22. Jerome Kagan and Nancy Snidman, The Long Shadow of Temperament (Cambridge, Mass.:Harvard University Press, 2004).
23. Carl Schwartz et al., “Inhibited and Uninhibited Infants ‘Grown Up’: Adult Amygdalar Responseto Novel Versus Newly Familiar Faces,” Science 399 (2003), pp. 1952–53.
24. On the once-fearful boy, see Kagan and Snidman, Long Shadow, pp. 28–29.