持续压力的危害
畅销书《奔腾年代》(Seabiscuit )的作者劳拉·希伦布兰德长期以来一直受到慢性疲劳综合征的困扰,她经常会感到身体虚弱、筋疲力尽,因此需要别人长期照顾。在她写《奔腾年代》的时候,照顾她的是体贴的丈夫博登。他当时正在忙于攻读研究生,但是仍然尽量抽出时间来照顾妻子,服侍她吃饭喝水,在她需要走动的时候帮助她,还为她读书读报。
但是希伦布兰德回忆说,有一天晚上自己在卧室的时候,“听到一个低沉的声音”。她从楼梯上看下去,发现博登“正在大厅里踱步,而且还在抽泣”。她本来想叫他,但是又觉得他可能想一个人静一静,所以就算了。
第二天早晨博登又像往常一样来帮助她,“情绪和以前一样愉快、稳定”。[37]
博登尽量隐藏自己的痛苦,以免影响脆弱的妻子。但是任何一个像博登这样要日夜照顾所爱之人的人都要承受巨大的压力,而且这种压力还会不可避免地侵害他们的身心健康,即使是最富有爱心的人也不例外。
这方面最有力的证据来自俄亥俄大学的一个跨领域研究小组,由心理学家贾尼丝·基科尔特·格拉泽和她的丈夫——免疫学家罗纳德·格拉泽所领导。[38]通过一系列研究,他们发现,持续的压力会改变抵抗感染和帮助治愈创伤的免疫细胞的基因状况。
他们的研究小组对10名60多岁的女性进行了研究,她们都在照顾患有老年痴呆症的丈夫。[39]她们承受着巨大的压力,一天24小时照顾病人,感觉非常孤单而且无暇自顾。对承受类似压力的女性进行的早期调查发现,流感病毒灭活疫苗对她们已经不起作用了,她们的免疫系统已经无法产生这种疫苗通常可以引发的抗体了。[40]现在科学家们对免疫功能进行了更加严谨的实验,他们发现,照顾患有老年痴呆症丈夫的女性身体的许多指标都有问题。
首当其冲的就是遗传信息。实验表明,这些女性体内可以调节一系列关键免疫机制的一种基因的表达比其他同龄女性要低50%。GHmRNA这种受损基因可以提高淋巴细胞的产量,并且增强杀伤细胞和巨噬细胞的活跃度,从而消灭入侵的细胞。[41]这也可以解释另外一个早期发现:处于压力下的女性细小刺伤伤口愈合的时间要比对比组中没有压力的女性多出9天。
而且,巨大的压力还会侵袭这些照料者的DNA,加速细胞的老化。其他科学家在研究长期照顾患有慢性病孩子的母亲的DNA后发现,孩子患病时间越久,母亲的细胞老化程度就越严重。
照顾患有慢性病孩子的母亲比同龄女性的平均生理状态要老10岁。当然这种情况也有例外,比如那些遭受了打击但是能从其他人那里得到情感抚慰的女人,即使她们需要照顾身患疾病的亲人,她们的细胞仍然能够保持年轻状态。
集体社交商也可以抵消长期照顾别人产生的负面影响。下面是新罕布什尔州三维治市的一个场景。这是一个阳光灿烂的秋日,菲利普·西蒙斯坐在轮椅上,被一群朋友和邻居簇拥着。西蒙斯是位大学英语教师,有两个年幼的孩子,他在35岁的时候被诊断出患有鲁盖瑞氏症(肌萎缩性侧索硬化症),医生当时断定他只剩下2—5年的寿命。现在他已经比医生预言的多活了几年了,但是他的瘫痪慢慢由下身扩散到了双臂,因此他生活已经不能自理了。这个时候,他送给朋友一本名为《分享照料》的书,这本书里描述了如何为重症病人建立一个团队来共同照顾他。
于是,35位邻居决定共同帮助西蒙斯和他的家人。他们的日程大部分都是通过电话和电子邮件来安排的,他们在西蒙斯家里充当厨师、司机、保姆、佣人的角色,在那个秋日他们还当起了园艺工人。他们一直这样无私地奉献着,直到西蒙斯45岁去世。这个大家庭的出现极大改善了西蒙斯和他的妻子凯瑟琳·菲尔德的状况。最起码,正是因为他们的帮助,身为艺术家的菲尔德才能继续工作。而且他们还为菲尔德减轻了经济压力,使整个家庭,用菲尔德的原话来说,“感觉到被整个社区的人们所关爱”。[42]
这些邻居称自己为FOPAK(“菲利普和凯瑟琳的朋友”的英文简写),他们都认为自己才是从中受益匪浅的人。
- For the tale of the Tolstoy marriage, see William L. Shirer, Love and Hatred: The Stormy Marriageof Leo and Sonya Tolstoy (New York: Simon and Schuster, 1994).
- On survival after congestive heart failure, see H. M. Krumholz et al., “The Prognostic Importanceof Emotional Support for Elderly Patients Hospitalized with Heart Failure,” Circulation 97 (1988), pp.958–64.
- 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 tohealth. See T. E. Seeman and S. L. Syme, “Social Networks and Coronary Heart Disease: AComparative Analysis of Network Structural and Support Characteristics,” Psychosomatic Medicine 49(1987), pp. 341–54.
- 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 ofSciences 840 (1999), pp. 656–63.
- On relationships and disease, see Teresa Seeman, “How Do Others Get Under Our Skin: SocialRelationships and Health,” in Carol Ryff and Burton Singer, eds., Emotion, Social Relationships, andHealth (New York: Oxford University Press, 2001).
- 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 thenstimulates the adrenal cortex to release cortisol, which floods into the bloodstream and has widespreadeffects throughout the body. See Robert Sapolsky et al., “How Do Glucocorticoids Influence StressResponses?” Endocrine Reviews 21 (2000), pp. 55–89. The Sapolsky laboratory was among the first todocument that sustained stress can damage the hippocampus, a region of the brain central to learningand memory. Their work has pinpointed glucocorticoids, a class of steroid hormones secreted from theadrenal gland during stress, as critical to such neurotoxicity. Moreover, they were the first todemonstrate that glucocorticoids will impair the capacity of hippocampal neurons to survive a varietyof neurological diseases, including stroke and seizure. A major focus of the laboratory is to examine thecellular and molecular events underlying hippocampal neuron death, and to identify the components ofsuch death worsened by glucocorticoids.
- The key areas are in the prelimbic cingulate.
- Via the social brain, our interactions can matter biologically for our resilience in the face of threatsto our health. But at this point researchers can only sketch the bare beginning of a map for the specificbrain mechanisms involved. More specifically, social information is processed first by the sensorysystems 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.”
- 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 weretracked for ten years in a study of stress and heart disease. If their stress soared only in the first year, oronly in the tenth year, the likelihood that they would end up with cardiovascular problems was muchlower because the stress was temporary, not chronic. But people who had high stress levels in both thefirst 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 andHealth,” Science 241 (1989), pp. 540–45.
- On the case of Elysa Yanowitz, see Steven Greenhouse, “Refusal to Fire Unattractive SaleswomanLed to Dismissal, Suit Contends,” New York Times, April 11, 2003, p. A14.
- The causes of hypertension are, of course, complex. Medicine assumes that an underlying geneticpredisposition is always at play, though life’s stresses (as well as diet and exercise) also determine howrapidly or strongly that predisposition transforms into an actual malady. Naming a specific person asthe “cause” of hypertension seems dubious.
- Nadia Wager, George Feldman, and Trevor Hussey, “Impact of Supervisor Interactional Style onEmployees’ Blood Pressure,” Consciousness and Experiential Psychology 6 (2001).
- While the jury is still out on the case of Elysa Yanowitz’s hypertension, medical data suggest thather disapproving bosses played at least some role in her rising blood pressure. Chronic jumps in bloodpressure can raise the set point to which blood pressure returns after recovering from the rise, thusgradually leading to hypertension. In theory, epigenetics means that someone with a geneticvulnerability for hypertension could be rushed into the disease by distressing, ongoing circumstanceslike 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, “JobStress and Blood Pressure: A Critical Appraisal of Reported Studies,” Current Hypertension Reviews,2, (2006) pp. 127–38.
- S. P. Wamala et al., “Job Stress and the Occupational Gradient in Coronary Heart Disease Risk inWomen,” Social Science and Medicine 51 (2000), pp. 481–98; M. G. Marmot and M. J. Shipley, “DoSocio-economic Differences in Mortality Persist after Retirement? 25 Year Follow-up of Civil Servantsin the First Whitehall Study,” British Medical Journal 313 (1996), pp. 1177–80.
- On fairness and bosses, see M. Kivimaki et al., “Justice at Work and Reduced Risk of CoronaryHeart Disease Among Employees: The Whitehall II Study,” Archives of Internal Medicine 165 (2005),pp. 2245–51.
- Some have argued the higher rate of disease among those in lower rungs stems from their havingless education, or lower salaries, or less control over how they do their job. Such factors certainly couldplay a role. But in extensive analyses, toxic interaction between bosses and employees has emerged asthe critical variable. See: R. G. Wilkinson, Unhealthy Societies: The Afflictions of Inequality (London:Routledge, 1996).
- Y. Gabriel, “An Introduction to the Social Psychology of Insults in Organizations,” HumanRelations 51 (1998), pp. 1329–54.
- On status and blood pressure, see James Lynch, The Broken Heart (New York: Basic Books,1979).
- 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 AngiographicFindings,” Psychosomatic Medicine 47 (1985), pp. 219–33.
- On blood pressure during interactions, see Julianne Holt-Lunstad et al., “Social Relationships andAmbulatory Blood Pressure: Structural and Qualitative Predictors of Cardiovascular Function DuringEveryday Social Interactions,” Health Psychology 22, no. 4 (2003), pp. 388–97.
- On false accusation and heart disease, see Jos A. Bosch et al., “Acute Stress Evokes SelectiveMotibliation of T Cells that Differ in Chemokine Receptor Expression: A Potential Pathway LinkingReactivity to Cardiovascular Disease,” Brain, Behavior and Immunity 17 (2003), pp. 251–59.
- This provoked the T cells to attack the endothelium, where deadly plaque formation begins. Thisrecruitment of T cells, which inflame tissue as they fight off invading bacteria, fits the emergingunderstanding of the crucial role for such inflammation in atherosclerotic plaque buildup.
- Cohen assessed the emotional quality of their social interactions in one of his groups of volunteersin the days before coming into the lab. Unpleasant interactions, especially prolonged conflicts (as withheightened levels of cortisol), predicted that a person would be more likely to come down with a severecold. See Sheldon Cohen, “Social Relationships and Susceptibility to the Common Cold,” in Ryff andSinger, Emotion, Social Relationships, pp. 221–44.
- Sheldon Cohen et al., “Sociability and Susceptibility to the Common Cold,” PsychologicalScience 14 (2003), pp. 389–95. The study measured social encounters in the weeks before exposure tothe rhinovirus, rather than in the days during and after the exposure (since volunteers were inquarantine by then), and so it does not answer the question of whether pleasant or unpleasantencounters just before and on the day of exposure affect immune defenses. That study remains to bedone.
- Sociability—seeking out others in a friendly, genial way—was linked to better moods, better sleepefficiency, and lower levels of cortisol, which in turn predicted less risk of a cold. But, Dr. Cohennotes, 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. SeeSheldon Cohen, “Psychosocial Models of Social Support in the Etiology of Physical Disease,” HealthPsychology 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 tocolds when exposed to rhinoviruses. See Sheldon Cohen, “Social Relationships and Health,” AmericanPsychologist (November 2004), pp. 676–84.
- On meta-analysis, see Sally Dickerson and Margaret Kemeny, “Acute Stressors and CortisolResponses: A Theoretical Integration and Synthesis of Laboratory Research,” Psychological Bulletin130 (2004), pp. 355–91.
- Some of the studies also assayed levels of ACTH, another stress hormone activated by the HPAaxis. The effects were much the same, although ACTH acts more quickly, peaking at around ten totwenty minutes after exposure to a stressor, while cortisol peaks later, around thirty to forty minutesafter first exposure. There are two widely used scientific measures of cortisol: how much the bodysecretes and how long those levels take to fall back to normal. People differ greatly in their recoverytimes; some bounce back quite quickly from a stressful moment, while others seem to remain stuck inthe bad mood.
- 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 greatercortisol hike from the subtraction.
- Social stress tends to activate the following neural areas (all key in the social brain): rightprefrontal cortex, amygdala, anterior cingulate, hippocampus, insula.
- 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 Threatto the Social Self: Shame, Social Selfesteem, and Cortisol Activity,” Psychosomatic Medicine 66(2004), pp. 915–24.
- When a critical observer made humiliating remarks, people continued to brood— and so maintainstress 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 wheneverthey 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.
- On decline, see Teresa Seeman et al., “The Price of Adaptation: Allostatic Load and Its HealthConsequences,” 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 HealthConsequences,” Proceedings of the National Academy of Sciences 98 (2001), pp. 4770–75.
- 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 womenadversely affected showed highly elevated readings of stress hormones.
- The left dorsal-superior zone of the prefrontal cortex, to be precise.
- On relationships and immune function, see Rosenkrantz et al., “Affective Style and In VivoImmune Response: Neurobehavioral Mechanisms,” Proceedings of the National Academy of Sciences,100 (2003), pp. 11, 148–52.
- In his research on how mother lab rats treat their pups, Michael Meaney discovered thatdifferences 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, heartrate, and neuron functioning. Genetic research on the complex ways that glucocorticoids themselves areregulated shows they are heavily influenced by social encounters, particularly stressful ones. The pupsin Meaney’s research whose moms licked and groomed them the most ended up with genes thatexpressed little of the stress hormone, while those pups who were neglected expressed a great deal. Inwellnurtured pups the genes for regulating stress hormones were twice as active as those in neglectedpups. The key zone of the left frontal area in the Wisconsin high-schoolers appears identical to thatfound in Meaney’s rodents as being altered by the amount of nurturance during puphood. Meaney’sresearch has identified precise mechanisms that tie nurturance to the body’s response to stress. Understress, 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 ACTHinto 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 inthe hypothalamus to lessen levels of CRF. This regulatory system for adjusting levels of CRF operatesconstantly. As Meaney notes, how those genes are modified during childhood has lifelongconsequences: once their level of expression has been set, it persists in that pattern through life. Goodparenting, Meaney finds, produces genes that make the hippocampus better at monitoring stresshormones, so that optimal levels are emitted when under stress—making a person more resilient. Wehumans share the identical stress hormone circuits with all mammals, including Meaney’s lab rats. SeeMichael Meaney, “Maternal Care, Gene Expression, and the Transmission of Individual Differences inStress Reactivity Across Generations,” Annual Review of Neuroscience 24 (2001), pp. 1161–92.
- On Borden, see Laura Hillenbrand, “A Sudden Illness—How My Life Changed,” The NewYorker, July 7, 2003.
- The group centers on Janice Kiecolt-Glaser, a psychologist, and her husband, Ronald Glaser, animmunologist, and has also included William B. Malarkey, a physician at te Ohio State College ofMedicine and John T. Cacioppo, a founder of social neuroscience, now at the University of Chicago.See, for example, John T. Cacioppo et al., “Autonomic, Endocrine, and Immune Response toPsychological Stree: The Reactivity Hypothesis,” Annals of the New York Academy of Sciences 840(1998), pp. 664–73.
- On women caregivers, see William B. Malarkey et al., “Chronic Stress Down- Regulates GrowthHormone Gene Expression in Peripheral Blood Mononuclear Cells of Older Adults,” Endocrine 5(1996) 1, pp. 33–9.
- On an earlier study of Alzheimer’s Disease caregivers, see Janice Kiecolt-Glaser et al., “Slowingof Wound Healing by Psychological Stress,” Lancet 346 (1995), pp. 1,194–6
- On cell aging, see Elissa Epel et al., “Accelerated Telomere Shortening in Response to LifeStress,” Proceedings of the National Academy of Science 101 (2004) 49, pp. 17,312–5.
- Suki Casanave, “Embracing this Imperfect Life,” Hope (March/April 2002), pp. 32–35.
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