Chapter 15. The Biology of Compassion
1. The quote is slightly paraphrased from John Bowlby, A Secure Base (New York: Basic Books, 1988), p. 62.
2. On romantic partners, see Brooke Feeny, “A Secure Base: Responsive Support of Goal Strivings and Exploration in Adult Intimate Relationships,” Journal of Personality and Social Psychology 87, no. 5 (2004), pp. 631–48.
3. On the other hand, someone who lacks confidence in his ability to deal with the world may actually find reassurance in a partner who takes control, welcoming the intrusiveness as comforting, relieved to have the chance to be dependent.
4. On attachment anxiety and caregiving, see Mario Mikulincer et al., “Attachment, Caregiving and Altruism: Boosting Attachment Security Increases Compassion and Helping,” Journal of Personality and Social Psychology 89 (2005), pp. 817–39.
5. On selfish altruism, see R. B. Cialdini et al., “Empathy-based Helping: Is It Selflessly or Selfishly Motivated?” Journal of Personality and Social Psychology 52 (1987), pp. 749–58.
6. The secure types offered to help the woman even when her difficulties seemed more extreme: they were told that she was not only destitute but also severely depressed. Presumably she would still be down even if they helped her out, but they were nonetheless willing to lend a hand. This seems to refute theories that hold that people help others in order to feel the pleasure of making someone happy—interpreted by these theoreticians as a “selfish” motive for compassion.
7. Jack Nitschke et al., “Orbitofrontal Cortex Tracks Positive Mood in Mothers Viewing Pictures of Their Newborn Infants,” NeuroImage 21 (2004), pp. 583–92.
8. Oxytocin is produced in nuclei of the hypothalamus, from where it flows to the pituitary and then is released into the bloodstream. In other pathways from the hypothalamus, oxytocin acts on many other areas, such as the amygdala, the raphe nuclei, and the locus coeruleus (among others), as well as the spinal fluid.
9. On voles and oxytocin, see C. Sue Carter, “Neuroendocrine Perspectives on Social Attachment and Love,” Psychoneuroimmunology 23, no. 8 (1998), pp. 779–818.
10. On the complex connections between oxytocin and testosterone, see Helen Fisher, Why We Love (New York: Henry Holt, 2004).
11. On social allergies, see Michael R. Cunningham et al., “Social Allergies in Romantic Relationships: Behavioral Repetition, Emotional Sensitization, and Dissatisfaction in Dating Couples,” Personal Relationships 12 (2005), pp. 273–95. The passage about the wet towels and toilet paper roll is quoted from the 2000 Rob Reiner film, The Story of Us.
12. On basic neural systems, see Jaak Panksepp, Affective Neuroscience: The Foundations of Human and Animal Emotions (New York: Oxford University Press, 1998).
13. On meeting emotional needs, see John Gottman, The Relationship Cure (New York: Three Rivers Press, 2002).
14. See John Gottman, What Predicts Divorce: The Relationship Between Marital Processes and Marital Outcomes (Hillsdale, N.J.: Erlbaum, 1993).
15. On facial similarity in couples, see R. B. Zajonc et al., “Convergence in the Physical Appearance of Spouses,” Motivation and Emotion 11 (1987), pp. 335–46.
16. S. M. Drigotas et al., “Close Partner as Sculptor of the Ideal Self,” Journal of Personality and Social Psychology 77 (1999), pp. 293–323.
17. Erik Filsinger and Stephen Thoma, “Behavioral Antecedents of Relationship Stability and Adjustment: A Five-Year Longitudinal Study,” Journal of Marriage and the Family 50 (1988), pp. 785–95.
18. See, for example, Gottman, What Predicts Divorce.
19. On older couples and pleasures, see Robert W. Levenson et al., “The Influence of Age and Gender on Affect, Physiology, and Their Interrelations: A Study of Long-term Marriages,” Journal of Personality and Social Psychology 67, no. 1 (1994), pp. 56–68.
20. On the five-to-one ratio, see Gottman, Relationship Cure.
PART V
Chapter 16. Stress Is Social
1. For the tale of the Tolstoy marriage, see William L. Shirer, Love and Hatred: The Stormy Marriage of Leo and Sonya Tolstoy (New York: Simon & Schuster, 1994).
2. On survival after congestive heart failure, see H. M. Krumholz et al., “The Prognostic Importance of Emotional Support for Elderly Patients Hospitalized with Heart Failure,” Circulation 97 (1988), pp. 958–64.
3. Men who reported feeling loved most strongly had the very lowest levels of coronary artery disease. While having a loving mate offers protection, being trapped in a toxic relationship may be harmful to health. See T. E. Seeman and S. L. Syme, “Social Networks and Coronary Heart Disease: A Comparative Analysis of Network Structural and Support Characteristics,” Psychosomatic Medicine 49 (1987), pp. 341–54.
4. On poor relationships as a health risk, see Janice Kiecolt-Glaser et al., “Marital Stress: Immunologic, Neuroendocrine, and Autonomic Correlates,” Annals of the New York Academy of Sciences 840 (1999), pp. 656–63.
5. On relationships and disease, see Teresa Seeman, “How Do Others Get Under Our Skin: Social Relationships and Health,” in Carol Ryff and Burton Singer, eds., Emotion, Social Relationships, and Health (New York: Oxford University Press, 2001).
6. Activation of the HPA axis starts when the hypothalamus releases corticotropin hormone (CRH), which in turn triggers the pituitary to release adrenocorticotropin hormone (ACTH), which then stimulates the adrenal cortex to release cortisol, which floods into the bloodstream and has widespread effects throughout the body. See Robert Sapolsky et al., “How Do Glucocorticoids Influence Stress Responses?” Endocrine Reviews 21 (2000), pp. 55–89. The Sapolsky laboratory was among the first to document that sustained stress can damage the hippocampus, a region of the brain central to learning and memory. Their work has pinpointed glucocorticoids, a class of steroid hormones secreted from the adrenal gland during stress, as critical to such neurotoxicity. Moreover, they were the first to demonstrate that glucocorticoids will impair the capacity of hippocampal neurons to survive a variety of neurological diseases, including stroke and seizure. A major focus of the laboratory is to examine the cellular and molecular events underlying hippocampal neuron death, and to identify the components of such death worsened by glucocorticoids.
7. The key areas are in the prelimbic cingulate.
8. Via the social brain, our interactions can matter biologically for our resilience in the face of threats to our health. But at this point researchers can only sketch the bare beginning of a map for the specific brain mechanisms involved. More specifically, social information is processed first by the sensory systems of the neocortex; and it is then fed via the temporal lobe to the amygdala and hippocampus, which then send signals to the HPA axis and the noradrenergic and serotonergic systems. See Seeman, “How Do Others.”
9. For better or worse, the steady accumulation of such emotions over years and years is what matters—not just a few intense but passing episodes—as was found when thousands of men and women were tracked for ten years in a study of stress and heart disease. If their stress soared only in the first year, or only in the tenth year, the likelihood that they would end up with cardiovascular problems was much lower because the stress was temporary, not chronic. But people who had high stress levels in both the first year and the last—suggesting that stress was more likely a constant feature of their emotional diet—were most at risk for getting heart disease. See James House et al., “Social Relationships and Health,” Science 241 (1989), pp. 540–45.
10. On the case of Elysa Yanowitz, see Steven Greenhouse, “Refusal to Fire Unattractive Saleswoman Led to Dismissal, Suit Contends,” New York Times, April 11, 2003, p. A14.
11. The causes of hypertension are, of course, complex. Medicine assumes that an underlying genetic predisposition is always at play, though life’s stresses (as well as diet and exercise) also determine how rapidly or strongly that predisposition transforms into an actual malady. Naming a specific person as the “cause” of hypertension seems dubious.
12. Nadia Wager, George Feld
man, and Trevor Hussey, “Impact of Supervisor Interactional Style on Employees’ Blood Pressure,” Consciousness and Experiential Psychology 6 (2001).
13. While the jury is still out on the case of Elysa Yanowitz’s hypertension, medical data suggest that her disapproving bosses played at least some role in her rising blood pressure. Chronic jumps in blood pressure can raise the set point to which blood pressure returns after recovering from the rise, thus gradually leading to hypertension. In theory, epigenetics means that someone with a genetic vulnerability for hypertension could be rushed into the disease by distressing, ongoing circumstances like these. On the other hand, simple fluid hydraulics may accomplish the same thing. See, for example, B. D. Perry et al., “Persisting Psychophysiological Effects of Traumatic Stress: The Memory of States,” Violence Update 1, no. 8 (1991), pp. 1–11. However, for a skeptical review see Samuel A. Mann, “Job Stress and Blood Pressure: A Critical Appraisal of Reported Studies,” Current Hypertension Reviews 2 (2006), pp. 127–38.
14. S. P. Wamala et al., “Job Stress and the Occupational Gradient in Coronary Heart Disease Risk in Women,” Social Science and Medicine 51 (2000), pp. 481–98; M. G. Marmot and M. J. Shipley, “Do Socio-economic Differences in Mortality Persist after Retirement? 25-Year Follow-up of Civil Servants in the First Whitehall Study,” British Medical Journal 313 (1996), pp. 1177–80.
15. On fairness and bosses, see M. Kivimaki et al., “Justice at Work and Reduced Risk of Coronary Heart Disease Among Employees: The Whitehall II Study,” Archives of Internal Medicine 165 (2005), pp. 2245–51.
16. Some have argued the higher rate of disease among those in lower rungs stems from their having less education, or lower salaries, or less control over how they do their job. Such factors certainly could play a role. But in extensive analyses, toxic interaction between bosses and employees has emerged as the critical variable. See: R. G. Wilkinson, Unhealthy Societies: The Afflictions of Inequality (London: Routledge, 1996).
17. Y. Gabriel, “An Introduction to the Social Psychology of Insults in Organizations,” Human Relations 51 (1998), pp. 1329–54.
18. On status and blood pressure, see James Lynch, The Broken Heart (New York: Basic Books, 1979).
19. On heightened risk of cardiovascular disease, see, for example, S. P. Thomas, “Women’s Anger: Relationship of Suppression to Blood Pressure,” Nursing Research 46 (1997), pp. 324–30; T. M. Dembroski et al., “Components of Type A, Hostility, and Anger-in: Relationship to Angiographic Findings,” Psychosomatic Medicine 47 (1985), pp. 219–33.
20. On blood pressure during interactions, see Julianne Holt-Lunstad et al., “Social Relationships and Ambulatory Blood Pressure: Structural and Qualitative Predictors of Cardiovascular Function During Everyday Social Interactions,” Health Psychology 22, no. 4 (2003), pp. 388–97.
21. On false accusation and heart disease, see Jos A. Bosch et al., “Acute Stress Evokes Selective Motibliation of T Cells that Differ in Chemokine Receptor Expression: A Potential Pathway Linking Reactivity to Cardiovascular Disease,” Brain, Behavior and Immunity 17 (2003), pp. 251–59.
22. This provoked the T cells to attack the endothelium, where deadly plaque formation begins. This recruitment of T cells, which inflame tissue as they fight off invading bacteria, fits the emerging understanding of the crucial role for such inflammation in atherosclerotic plaque buildup.
23. Cohen assessed the emotional quality of their social interactions in one of his groups of volunteers in the days before coming into the lab. Unpleasant interactions, especially prolonged conflicts (as with heightened levels of cortisol), predicted that a person would be more likely to come down with a severe cold. See Sheldon Cohen, “Social Relationships and Susceptibility to the Common Cold,” in Ryff and Singer, Emotion, Social Relationships, pp. 221–44.
24. Sheldon Cohen et al., “Sociability and Susceptibility to the Common Cold,” Psychological Science 14 (2003), pp. 389–95. The study measured social encounters in the weeks before exposure to the rhinovirus, rather than in the days during and after the exposure (since volunteers were in quarantine by then), and so it does not answer the question of whether pleasant or unpleasant encounters just before and on the day of exposure affect immune defenses. That study remains to be done.
25. Sociability—seeking out others in a friendly, genial way—was linked to better moods, better sleep efficiency, and lower levels of cortisol, which in turn predicted less risk of a cold. But, Dr. Cohen notes, searching for a more robust connection might show with greater precision how sociability might “get inside the body”—a question that remains a mystery in need of a more rigorous solution. See Sheldon Cohen, “Psychosocial Models of Social Support in the Etiology of Physical Disease,” Health Psychology 7 (1988), pp. 269–97. Relationships with a spouse, grandchildren, neighbors, friends, fellow volunteers, or fellow religious congregants all predict that a person will be less susceptible to colds when exposed to rhinoviruses. See Sheldon Cohen, “Social Relationships and Health,” American Psychologist (November 2004), pp. 676–84.
26. On meta-analysis, see Sally Dickerson and Margaret Kemeny, “Acute Stressors and Cortisol Responses: A Theoretical Integration and Synthesis of Laboratory Research,” Psychological Bulletin 130 (2004), pp. 355–91.
27. Some of the studies also assayed levels of ACTH, another stress hormone activated by the HPA axis. The effects were much the same, although ACTH acts more quickly, peaking at around ten to twenty minutes after exposure to a stressor, while cortisol peaks later, around thirty to forty minutes after first exposure. There are two widely used scientific measures of cortisol: how much the body secretes and how long those levels take to fall back to normal. People differ greatly in their recovery times; some bounce back quite quickly from a stressful moment, while others seem to remain stuck in the bad mood.
28. For some reason, we may not realize how greatly social stress actually affects our biology. Subjectively people rated the noise just as distressing as the subtraction task, despite the far greater cortisol hike from the subtraction.
29. Social stress tends to activate the following neural areas (all key in the social brain): right prefrontal cortex, amygdala, anterior cingulate, hippocampus, insula.
30. When they felt they were being evaluated during the math problems, their cortisol rise was, again, higher than when they were doing the math alone in a room. See Tara Gruenewald et al., “Acute Threat to the Social Self: Shame, Social Self-esteem, and Cortisol Activity,” Psychosomatic Medicine 66 (2004), pp. 915–24.
31. When a critical observer made humiliating remarks, people continued to brood—and so maintain stress arousal—long afterward. But they did not obsess nearly so much if their ordeal was impersonal, like being shocked when a computer program detected they were too slow to push a button whenever they heard a tone. See Laura Glynn et al., “The Role of Rumination in Recovery from Reactivity: Cardiovascular Consequences of Emotional States,” Psychosomatic Medicine 64 (2002), pp. 714–26.
32. On decline, see Teresa Seeman et al., “The Price of Adaptation: Allostatic Load and Its Health Consequences,” Archives of Internal Medicine 157 (1997), pp. 2259–68; Teresa Seeman et al., “Exploring a New Concept of Cumulative Biologic Risk: Allostatic Load and Its Health Consequences,” Proceedings of the National Academy of Sciences 98 (2001), pp. 4770–75.
33. On the cumulative emotional tone of relationships and health, see Ryff and Singer, Emotion, Social Relationships. The negative health impact of relationships was worse for men than for women, particularly because they tended to have higher readings for indicators of heart disease, while women adversely affected showed highly elevated readings of stress hormones.
34. The left dorsal-superior zone of the prefrontal cortex, to be precise.
35. On relationships and immune function, see Rosenkrantz et al., “Affective Style and In Vivo Immune Response: Neurobehavioral Mechanisms,” Proceedings of the National Academy of Sciences 100 (2003), pp. 11, 148–52.
36
. In his research on how mother lab rats treat their pups, Michael Meaney discovered that differences in parental care affect genes in the hippocampus that control HPA output via glucocorticoid, a precursor of cortisol. Glucocorticoids are steroids that regulate changes in blood glucose levels, heart rate, and neuron functioning. Genetic research on the complex ways that glucocorticoids themselves are regulated shows they are heavily influenced by social encounters, particularly stressful ones. The pups in Meaney’s research whose moms licked and groomed them the most ended up with genes that expressed little of the stress hormone, while those pups who were neglected expressed a great deal. In well-nurtured pups the genes for regulating stress hormones were twice as active as those in neglected pups. The key zone of the left frontal area in the Wisconsin high schoolers appears identical to that found in Meaney’s rodents as being altered by the amount of nurturance during puphood. Meaney’s research has identified precise mechanisms that tie nurturance to the body’s response to stress. Under stress, the brain response begins with cells in the hypothalamus that secrete corticoid-releasing factor (CRF), which signals the brain to mobilize. CRF activates cells in the pituitary, which release ACTH into the blood, triggering the adrenals to secrete glucocorticoids. These hormones travel up to the brain, where they trigger cells in the hippocampus that monitor CRF levels; these cells in turn signal cells in the hypothalamus to lessen levels of CRF. This regulatory system for adjusting levels of CRF operates constantly. As Meaney notes, how those genes are modified during childhood has lifelong consequences: once their level of expression has been set, it persists in that pattern through life. Good parenting, Meaney finds, produces genes that make the hippocampus better at monitoring stress hormones, so that optimal levels are emitted when under stress—making a person more resilient. We humans share the identical stress hormone circuits with all mammals, including Meaney’s lab rats. See 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.
Social Intelligence: The New Science of Human Relationships Page 47
