Social Intelligence: The New Science of Human Relationships

by Daniel Goleman

  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 by anthropologist Irven DeVore and his star student, Robert Trivers, who were just starting to develop their theory of evolutionary psychology—today, widely influential. At the time these schools of thought were vehemently opposed by a group led by paleontologist Stephen Jay Gould and geneticist Richard 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 sober reading of the article was that a single test of the same behavior was no longer enough; the study raised the methodological bar for the field. Now, as Crabbe commented, “When someone knocks out a gene for anxiety, you see them using three tests to show the effect, where before they could get away with just one.”

  4. The methyl molecule consists of just four atoms—a carbon and three hydrogen; precisely how they attach 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 group relaxes 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 Bulletin 126 (2000), pp. 806–28.

  6. Michael J. Meaney, “Nature, Nurture, and the Disunity of Knowledge,” Annals of the New York Academy of Sciences 935 (2001), pp. 50–61.

  7. On the plasticity of genetic mechanisms that regulate behavior, see Elizabeth Hammock and Larry Young, “Microsatellite Instability Generates Diversity in Brain and Sociobehavioral Traits,” Science 308 (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 General Psychiatry 52 (1995), pp. 916–24.

  9. Michael Meaney, “Maternal Care, Gene Expression, and the Transmission of Individual Differences 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 Middle Childhood,” 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.: Harvard University Press, 2000).

  12. Every child’s unique experience of the same family is called a “nonshared environment” in behavior 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 a third of the genes that influence antisocial behavior in the early teen years no longer do so by midadolescence; they are by then replaced by new social and genetic factors that were not operating earlier.

  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 own sociability. Either way, how parents treat the baby seems to intensify the genes involved, amplifying how 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 entails glutamate activating a receptor on one neuron while calcium channels open on another, which triggers the synthesis of proteins in the cell body that “glue together” their receptors. That connection results in a larger response from cell to cell. At the cellular level, learning means that the input from one cell now has a larger output. Joseph LeDoux, presentation at the meeting of the Consortium for Research on Emotional Intelligence in Organizations, Cambridge, Mass., December 12, 2004.

  17. On experience and the development of neural systems, see B. J. Casey, “Imaging the Developing Brain: 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 HPA function, and results in emotional hyperreactivity. See C. L. Coe et al., “Prenatal Stress Diminishes Neurogenesis 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., “The Anterior Cingulate Cortex: The Evolution of an Interface Between Emotion and Cognition,” Annals of the 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 malleable throughout the life span, and which circuits may be particularly plastic early in life but then become relatively 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 Response to 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.

  Chapter 11. A Secure Base

  1. On the suicidal patient, see John Bowlby, A Secure Base: Parent-Child Attachment and Healthy Human Development (New York: Basic Books, 1988).

  2. On secure children, see Mary Ainsworth et al., “Infant-Mother Attachment and Social Development: Socialization as a Product of Reciprocal Responsiveness to Signals,” in M.P.M. Richards, ed., The Integration of a Child into a Social World (London: Cambridge University Press, 1974).

  3. On protoconversation and thinking, see Trevarthen, “The Self Born in Intersubjectivity: The Psychology of Infant Communicating,” in Ulric Neisser, ed., The Perceived Self: Ecological and Interpersonal Sources of Self-knowledge (New York: Cambridge University Press, 1993), pp. 121–73.

  4. On brain circuits for attachment, see Jaak Panksepp, Affective Neuroscience: The Foundations of Human and Animal Emotions (New York: Oxford University Press, 1998).

  5. Attachment circuits include “the cingulate cortex, septal area, bed nucleus of the stria terminalis, and preoptic and medial areas of the hypothalamus, along with their respective mesencephalic projection areas,” according to Panksepp, Affective Neuroscience, p. 249. Lesions in the bed nucleus of the stria terminalis, which has a profusion of oxytocin receptors, severely impair mothering.

  6. On secure babies and their mothers, see Russell Isabella and Jay Belsky, “Interactional Synchrony and the Origins of Infant-Mother Attachments: A Replication Study,” Child Development 62 (1991), pp. 373–94.

  7. See, for example, M. J. Bakermans-Kranenburg et al., “The Importance of Shared Environment in Infant-Father Attachment: A Behavioral Genetic Study of the Attachment Q-Sort,” Journal of Family Psychology 18 (2004), pp. 545–49; C. L. Bokhorst et al., “The Importance of Shared Environment in Mother-Infant Attachment Security: A Behavioral Genetic Study,” Child Development 74 (2003), pp. 1769–82.

  8. On attachment style, see Erik Hesse, “The Adult Attachment Interview: Historical and Current Perspectives,” in Jude Cassidy and Phillip Shaver, eds., Handbook of Attachment: Theory, Research and Clinical Applications (New York: Guilford Press, 1999).

  9. Synchrony between babies and their mothers was judged by their simultaneous movements, the similar tempos of their actions, and the coordination of their interactions. Frank Bernieri et al., “Synchrony, Pseudosynchrony, and Dissynchrony: Measuring t
he Entrainment Prosody in Mother-Infant Interactions,” Journal of Personality and Social Psychology 2 (1988), pp. 243–53.

  10. The lullaby in Italian: “Batti, batti, le manine, / Che tra poco vie-ne papà. / Ti porta le cara-mel-line / Fabiana le man-ge-rà.”

  11. On the depressed mother and baby, see Colwyn Trevarthen, “Development of Intersubjective Motor Control in Infants,” in M. G. Wade and H.T.A. Whiting, Motor Development in Children (Dordrecht, the Netherlands: Martinus Nijhoff, 1986), pp. 209–61.

  12. On the depressed loop, see Edward Z. Tronick, “Emotions and Emotional Communication in Infants,” American Psychologist 44 (1989), pp. 112–19.

  13. Meaney argues that it makes more sense to identify not just the relevant genes but also the parenting styles (and any other such factors) that might alter levels of the expression of the genes for depression. In other words, what experiences might help inoculate that child against depression? Answers to that question could then guide essential interventions that might lower the risk the child will later become depressed herself. See Michael Meaney, “Maternal Care, Gene Expression.”

  14. On depressed mothers and infant cortisol, see Tiffany Field et al., “Maternal Depression Effects on Infants and Early Interventions,” Preventive Medicine 27 (1998), pp. 200–03.

  15. On preventing transmission of mood deficits, see A. Cumberland-Li et al., “The Relation of Parental Emotionality and Related Dispositional Traits to Parental Expression of Emotion and Children’s Social Functioning,” Motivation and Emotion 27, no. 1 (2003), pp. 27–56.

  16. On children of depressed mothers, see Tronick, “Emotions and Emotional Communication.”

  17. On neglected children’s emotion recognition, see Seth Pollak et al., “Recognizing Emotion in Faces: Developmental Effects of Child Abuse and Neglect,” Developmental Psychology 36 (2000), pp. 679–88.

  18. A poignant extreme can be seen in the thousands of infants placed in Romanian orphanages during the severe economic troubles in the 1980s. These infants spent up to twenty hours a day in their cribs, with no one to attend their needs. As eight-year-olds, a sample of those adopted by American families still showed troubling symptoms: they were ultrastoic, neither crying nor expressing pain; they were uninterested in playing; and they hoarded food. Many of their problems improved as they fit into their new families. Even so, brain scans showed that key areas of their social brains were underactive, including the orbitofrontal cortex. See Harry Chugani et al., “Local Brain Functional Activity Following Early Deprivation: A Study of Postinstitutionalized Romanian Orphans,” NeuroImage 14 (2001), pp. 1290–1301.

  19. On abused children and angry faces, see Seth Pollak et al., “P3b Reflects Maltreated Children’s Reactions to Facial Displays of Emotion,” Psychophysiology 38 (2001), pp. 267–74.

  20. On scanning for anger, see Seth Pollak and Stephanie Tolley-Schell, “Selective Attention to Facial Emotion in Physically Abused Children,” Journal of Abnormal Psychology 112 (2003), pp. 323–38.

  21. On parents’ shaping of the orbitofrontal cortex, see Allan Schore, Affect Regulation and the Origin of the Self: The Neurobiology of Emotional Development (Hillsdale, N.J.: Erlbaum, 1994).

  22. On repairing childhood trauma, see Daniel J. Siegel, The Developing Mind: How Relationships and the Brain Interact to Shape Who We Are (New York: Guilford Press, 1999).

  Chapter 12. The Set Point for Happiness

  1. E. Z. Tronick and J. F. Cohn, “Infant-Mother Face-to-Face Interaction: Age and Gender Differences in Coordination and the Occurrence of Miscoordination,” Child Development 60 (1989), pp. 85–92.

  2. On hostile couples and preschoolers, see Lynn Fainsilber Katz and Erica Woodin, “Hostility, Hostile Detachment, and Conflict Engagement in Marriages: Effect on Child and Family Functioning,” Child Development 73 (2002), pp. 636–52.

  3. On parents’ and teachers’ ratings of children, see John Gottman and Lynn Fainsilber Katz, “Parental Meta-emotion Philosophy and the Emotional Life of Families: The Theoretical Models and Preliminary Data,” Journal of Family Psychology 10 (1996), pp. 243–68.

  4. On positive affective core, see Robert Emde, “The Pre-presentational Self and Its Affective Core,” Psychoanalytic Study of the Child 38 (1983), pp. 165–92.

  5. On the three scenarios, see Daniel J. Siegel, The Developing Mind: How Relationships and the Brain Interact to Shape Who We Are (New York: Guilford Press, 1999).

  6. On the orbitofrontal cortex, see Allan Schore, Affect Regulation and the Origin of the Self: The Neurobiology of Emotional Development (Hillsdale, N.J.: Erlbaum, 1994).

  7. This attunement starts in the first year of life, when the sympathetic nervous system comes on line, branching beyond the brain out into the body to control physiological arousal such as heart rate. The sympathetic branch operates as an energizer for the body, generating upbeat emotions like excitement and interest, pleasure and joy—the exuberant happiness of infancy. When parents match this energy with their own—by, say, looping with a baby’s joy—they teach their infant that joyousness and other positive states can be shared and that they can feel safe expressing them. In healthy families most communications between infant and parent during the first year of life are loops aligning positive feelings. In the second year of life the parasympathetic nervous system develops; this branch operates as a brake, modulating or inhibiting impulses—it calms us down and relaxes us. Note the felicitous timing: the parasympathetic branch matures just as babies become more mobile and independent—capable of climbing that table with a lamp. See ibid.

  8. On parenting styles, see Siegel, Developing Mind.

  9. Far more rare are parents who, in a rage, throw a lamp down. They respond to the child as an It, not a You. In such moments they have no empathy but are driven only by their worst impulses. Whenever such parents react to naughtiness with an utter failure to control their own emotional impulse, they fill their children with terror, who learn to fear for their own safety. Neurologically, Siegel proposes, the child endures a simultaneous, contradictory surge in the nervous system, as though accelerating and braking at the same time. The parent—often himself a victim of a troubled childhood—unwittingly offers a disorienting model and becomes an ongoing source of fear for the child rather than offering a secure base. The child suffers a “double insult,” being engulfed by terror at the parent, and losing the one relationship that might have helped him emotionally survive by offering safety. As adults, such children often find their closest relationships stormy and chaotic; their history with partners typically is replete with intense emotions and confusing, disastrous endings.

  10. Emily Fox Gordon, “In the Garden of Childish Delights,” Time, January 17, 2005, p. A22.

  11. Mary Ainsworth et al., Patterns of Attachment (Hillsdale, N.J.: Erlbaum, 1978).

  12. On brain circuitry for play, see Jaak Panksepp, Affective Neuroscience: The Foundations of Human and Animal Emotions (New York: Oxford University Press, 1998).

  13. Ibid.

  14. On play and epigenetics, see Nakia Gordon et al., “Socially Induced Brain ‘Fertilization’: Play Promotes Brain-Derived Neurotrophic Factor Transcription in the Amygdala and Dorsolateral Frontal Cortex in Juvenile Rats,” Neuroscience Letters 341 (2003), p. 17.

  15. Panksepp, Affective Neuroscience.

  16. On tickling, see Jaak Panksepp et al., “Empathy and the Action-Perception Resonances of Basic Socio-emotional Systems of the Brain,” Behavioral and Brain Sciences 25 (2002), pp. 43–44.

  17. On ADHD and play, see Panksepp, Affective Neuroscience. The idea of a vigorous recess instead of medications, he notes, has never been rigorously tested and remains a speculation. However, since prolonged use of the medications commonly prescribed for ADHD may produce lasting changes in a child’s catecholamine system, such nondrug interventions may be more desirable should they prove effective.

  18. On charisma, see Panksepp, Affective Neuroscience.

  19. On emotional set point, see R. J. Davidson an
d W. Irwin, “The Functional Neuroanatomy of Emotion and Affective Style,” Trends in Cognitive Neuroscience 3 (1999), pp. 11–21.

  20. As Davidson is the first to point out, such data are highly suggestive of a link between how we are parented and our lifelong happiness, but they by no means prove it. It may just be, for instance, that contented adults remember their good times from childhood more readily than the bad ones and so rate their parents as more caring than they actually were. It will take a longitudinal study of many children over decades to establish with greater scientific certainty the relationship between the kind of care we get as children and our brain’s capacity for joy in adulthood.