User:Jchiang18/sandbox

Source: Wikipedia, the free encyclopedia.

Social stress is stress that stems from one’s relationships with others and social environment. The broad term stress refers to the psychological state that an organism is in when it confronts an external stimulus (stressor) that it judges to be threatening or can’t be coped with given the organism’s ability and resources. When confronted with a stressor, people assess whether they have the ability to manage and cope with the stress. If they judge the demands of the stressor to be greater than their ability to manage or cope with it, they feel stress. This then leads to emotional, behavioral, and physiological changes that can put one under greater risk for developing mental and physical illness.

Since social stress is stress arising from interpersonal experiences and the social context, specific examples include caring for a child or spouse with a chronic illness, low position of status in society and other groups, giving a speech, interviewing with potential employers, meeting new people at a party, death of a loved one, divorce, and discrimination. These social stressors convey that social stress can arise from one’s microenvironment (e.g., family ties) and macroenvironment (e.g., hierarchical societal structure). In addition, these social stressors do not actually have to occur in order to experience social stress. The mere threat of divorce, death, or evaluation of potential employers and friends can also cause social stress.

As social beings, humans benefit from establishing close relationships (i.e., nurturance, reproductive success, and social connection) [1] and therefore humans have a fundamental need and desire to maintain positive social ties and social inclusion [2]. Any threat that disrupts social ties or social inclusion results in social stress. Given that humans are driven to establish and maintain positive relational ties, it may not be surprising that social stress is the most frequent type of stressor that people experience in their daily lives [3]. Moreover, social stress affects people more intensely than physical or other type of stressors [3]. Social stress compared to other types of stress, then, may be a more potent risk factor for developing disease.

Measurement

Self-reports

Social stress is typically studied by asking people about their social experiences and relationships or by inducing social stress in the laboratory. A variety of questionnaires are used to assess self-reports of stressful social experiences, including the Test of Negative Social Exchange (TENSE) [4], Martial Adjustment Test [5], Risky Families Questionnaire [6]. Richer, more detailed information can be gathered by asking open-ended questions about one’s recent social stress experiences. For instance, the UCLA Life Stress Interview includes questions about romantic partners, closest friendships, other friendships, and family relationships.

Induction

In rodent models, social disruption and social defeat are two common social stress paradigms. In the social disruption paradigm, the naturally established social hierarchy within a group of caged male mice is disrupted daily by the introduction of an aggressive intruder. This disruption is a social stressor. Similarly, the social defeat paradigm introduces an intruder male rodent into the home cage of a resident male rodent. The two rodents fight, leading one of them to experience defeat, which is considered social stress.

In human research, the Trier Social Stress Task (TSST) and conflict discussion are common inductions of social stress. The TSST involves giving an impromptu speech and performing mental arithmetic as quickly and accurately as possible in the presence of an evaluative committee trained to provide nonverbal negative feedback [7]. The threat of negative evaluation is the social stressor. In a laboratory conflict discussion between two people, a topic of disagreement is determined and the participants are asked to discuss the topic for a predetermined amount of time. Discussion of the topic will presumably lead to tension.

The variety of ways to assess social stress reflects the fact that social defeat, family environment, quality of relationships, social evaluation, and conflict are all specific social stressors. The decision to use a particular questionnaire or manipulation really depends on the type of social stress one is interested in.

Mental Health

In line with the notion that humans have a fundamental need for social inclusion and maintenance of social relationships, research has consistently demonstrated that social stress increases risk for developing a number of negative mental health outcomes. One prospective study asked 15,530 Finnish employees whether they had “considerable difficulties with [their] coworkers/superiors/inferiors” during the last 6 months, 5 years, earlier, or never.” Information on suicidal deaths, hospitalizations due to psychosis, alcoholism, suicidal behavior, alcohol intoxication, and depressive symptoms, and medication for chronic psychiatric disorders, was gathered from the national registries of mortality and morbidity. Those who had experienced conflict in the workplace with coworkers and/or supervisors in the last five years were more likely to be diagnosed with a psychiatric condition [8].

Depression

Social stress may be especially predictive of depression, as risk for this mental disorder significantly increases after social stress [9] and interpersonal loss, such as bereavement and separations or threats of separation often precipitates depression [10-11]. Moreover, depressed individuals rejected by others had become depressed about three times more quickly than those who experienced non-socially rejecting stress [12]. Among non-clinically depressed populations, individuals whose relationships with friends and family make too many demands, criticize, and create tension and conflict endorse more depressive symptoms [13-14]. Relationships that make many demands such as caregiving has reliably shown to predict depressive symptoms [15]. Conflict between spouses also leads to more psychological distress and depressive symptoms especially for wives [16]. Specifically, unhappy married couples were 10-25 times more at risk for developing major depression [17-18]. Relatedly, social stress arising from discrimination is related to greater depressive symptoms. In one study, African-Americans and non-Hispanic Whites reported on their perceptions of major lifetime events and daily experiences of discrimination, lifetime exposure to social stress, and depressive symptoms in the last month. Regardless of race, those who perceived more discrimination had higher depressive symptoms [19].

Sensitive period

When social stress occurs in life influences the risk for developing negative health outcomes. In particular, social stress occurring early in life appears to make one more vulnerable to negative mental health conditions that develop or persist in adulthood. One 16-18 year longitudinal study that assessed a broad range of maladaptive parental behavior found that children with parents exhibiting greater degree of maladaptive parenting were more likely to have a psychiatric disorder in late adolescence and early adulthood. Maladaptive child-rearing behaviors included loud arguments between parents, verbal abuse, difficulty controlling anger toward the child, parental support/availability, and harsh punishment. Psychiatric disorders included anxiety, depressive, disruptive, personality, and substance use disorder. Childhood temperament and parental psychiatric disorders did not explain this association [20]. Other studies have documented the robust relationships between children’s social stress within the family environment and depression, aggression, antisocial behavior, anxiety, suicide, and hostile, oppositional, and delinquent behavior [21].

Relapse and recurrence

Social stress can also exacerbate current psychopathological conditions and compromise recovery. For instance, patients recovering from depression or biopolar disorder are two times more likely to relapse if there is familial tension. People with eating disorders are also more likely to relapse if their family members make more critical comments, are more hostile, or are over-involved [22]. Similarly, outpatients with schizophrenia or schizoaffective disorder showed greater psychotic symptoms if the most influential person in their life was critical [23] and were more likely to relapse if their familial relationships were marked by tension [22]. In regard to substance abuse, cocaine-dependent individuals report greater cravings for cocaine following exposure to a social stressor [24].

Physical Health

Research has also repeatedly found a robust relationship between various social stressors and aspects of physical health.

Mortality

Social status, a macro social stressor, is a robust predictor of physical health. In a study of over seventeen hundred British civil servants, socioeconomic status (SES) was related to mortality in a gradient fashion [25]. It is not just that those who are poor or only have a high school diploma that have worse health than the rich or the highly educated. Rather, with each step up the socioeconomic ladder, better health is predicted. Other studies have replicated this relationship between SES and mortality in a range of diseases including infectious, digestive, and respiratory diseases [26-27]. Similarly, social stressors in the microenvironment is also linked to increased mortality. Loneliness or social isolation is linked to increased mortality. This seminal longitudinal study of nearly seven thousand people found that people who had fewer social and community ties had greater risk of dying from all causes [28].

Morbidity

The relation to increased mortality is at least partially due to the fact that social stress appears to make people sicker. People who have fewer social contacts are at greater risk for negative physical health outcomes, including cardiovascular disease, and for worse recovery after disease onset [29]. The lower one’s social status, the more likely s/he is to have a cardiovascular, gastrointestinal, musculoskeletal, neoplastic, psychiatric, pulmonary, renal, or other chronic disease. These associations are not explained by other factors such as race, health behaviors, age, sex, and even access to health care [30]. Critical and demanding interactions are predictive of angina [31]. In one particularly noteworthy laboratory study, researchers interviewed participants to determine whether they had been experiencing social conflicts with spouses, close family members and friends lasting at least a month. They then exposed the participants to the common cold virus and found that the likelihood for developing a cold was more than two times for participants with conflict-ridden relationships than for those without such enduring conflicts [32].

Sensitive period

Exposure to social stress in childhood can also have long-term effects, increasing risk for developing diseases later in life. Children who are maltreated (emotionally, physically, sexually abused or neglected) report more disease outcomes, such as stroke, myocardial infarction, diabetes, and hypertension [35] or greater severity those outcomes [36]. The Childhood Experiences Study that included over seventeen hundred adults found that people were 20% more likely to experience CHD for each kind of chronic social stressor experienced, and this was not due to typical risk factors for CHD such as demographics, smoking, exercise, adiposity, diabetes, and hypertension [37].

Recovery

Social stress has also been tied to worse health outcomes among patients who already have a disease. Patients with end-stage renal disease faced a 46 percent increased risk for mortality the when there was more relationship negativity with their spouse even when controlling for severity of disease and treatment [33]. Similarly, women who had experienced an acute coronary event were three times more likely to experience another coronary event if they experienced moderate to severe marital strain. This finding remained even after controlling for demographics, health behaviors, and disease status [34].

Physiological Pathways

Social stress leads to a number of physiological changes that mediate its relationship to physical health. In the short term, the physiological changes outlined below are adaptive, as they enable the stressed organism to cope better. However, dysregulation of these systems or repeated activation of them over the long-term can be detrimental to health [38].

Sympathetic adrenomedullary system (SAM)

In response to stress, the sympathetic adrenomedullary system becomes activated to help the organism cope with the stressor. Sympathetic arousal stimulates the medulla of the adrenal glands to secrete epinephrine and norepinephrine into the blood stream, which facilitates the efficient use of metabolic resources for fight or flight. Blood pressure, heart rate, and sweating increase, veins constrict to allow the heart to beat with more force, arteries leading to muscles dilate, and blood flow to parts of the body not essential for the fight or flight response decreases. If stress persists in the long run, then blood pressure remains elevated, leading to hypertension and atherosclerosis, both precursors to cardiovascular disease.

A number of animal and human studies have confirmed that social stress increases risk for negative health outcomes by increasing SAM activity. Rodent models of the effects of social stress show that social stress causes hypertension and atherosclerosis [39]. Studies of non-human primates also show that social stress clogs arteries [40]. Although humans cannot be randomized to receive social stress due to ethical concerns, studies have nevertheless shown that negative social interactions characterized by conflict lead to increases in blood pressure and heart rate [41-42]. Social stress stemming from perceived daily discrimination is also associated with elevated levels of blood pressure during the day and a lack of blood pressure dipping at night [43-44].

Hypothalamic-pituitary adrenocortical axis (HPA)

The HPA axis also gets activated in response to stress. The hypothalamus releases corticotrophin-releasing hormone (CRH), stimulating the pituitary to release adrenocorticotropic hormone (ACTH). ACTH then stimulates the adrenal cortex to secrete glucocorticoids, including cortisol. The levels of cortisol in the bloodstream then signal to the hypothalamus to stop secreting CRH so as to stop the cascade of events leading to increased production of cortisol.

Social stress can lead to adverse health outcomes by chronically and/or repeatedly activating the HPA axis or disrupting the HPA system. For instance, rhesus monkey infants who were neglected by their mothers showed prolonged cortisol responses following a challenging event [45]. In humans, abused women exhibit a prolonged elevation in cortisol following a standardized psychosocial laboratory stressor compared to those without an abuse history [46]. Maltreated children not only show higher morning cortisol values than non maltreated children [47], but their HPA systems also fail to recover after a stressful social interaction with their caregiver [48]. Over time, low-SES children show progressively greater output of cortisol [49-50]. Taken together, these studies demonstrate that various social stressors can lead to a dysfunctional HPA response to stress, thereby increasing risk for developing or exacerbating diseases such as diabetes, cancer, cardiovascular disease, and hypertension [51].

Inflammation

Inflammation is a natural, early response of the immune system and is essential to fighting infections and repairing injured tissue. Communication molecules known as proinflammatory cytokines coordinate and promote inflammatory processes, thus playing a major role in this healing process. Although acute inflammation is adaptive, chronic inflammatory activity can contribute to adverse health outcomes. Specifically, proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) are linked to hypertension [52], atherosclerosis [53], coronary heart disease [54-55], depression [56], diabetes [57] and some cancers [58-59].

Research has elucidated a relationship between different social stressors and markers of inflammation. Chronic social stressors such as caring for a spouse with dementia leads to greater circulating levels of cytokine IL-6 [60] whereas acute social stress tasks in the laboratory have been shown to elicit increases in pro inflammatory cytokines [61]. Similarly, when faced with another type of social stress, namely social evaluative threat, participants showed increases in IL-6 and a soluble receptor for TNF-α [62-64]. Increases in inflammation may persist over time, as studies have shown that chronic relationship stress characterized by conflict, mistrust, and instability, have been tied to greater lipopolysaccharide-stimulated IL-6 production 6 months later [65] and a cold and conflict-ridden early family environment has been tied to elevated levels of CRP in adulthood [66].

There is extensive evidence that the above physiological systems affect one another’s functioning. For instance, cortisol tends to have a suppressive effect on inflammatory processes. However, repeated exposure to social stress and cortisol may lead to resistance to the anti-inflammatory effects of glucocorticoids [67-68]. Proinflammatory cytokines can also activate the HPA system and thus chronic inflammation may also lead to a chronically activated HPA system. Sympathetic activity can also upregulate inflammatory activity [69-70]. Given the relationships among these physiological systems, social stress may also affect health via indirectly affecting a particular physiological system that in turn affects a different physiological system.

References

  1. Slavich, G.M., O’Donovan, A., Epel, E.S., & Kemeny, M.E. (2010). Black sheep get the blues: A psychobiological model of social rejection and depression. Neuroscience and Biobehavioral Reviews, 35, 39-45.
  2. Baumeister, R.F., & Leary, M.R. (1995). The need to belong: Desire for interpersonal attachments as a fundamental human motivation. Psychological Bulletin, 117, 497-529.
  3. Almeida, D.M. (2005). Resilience and vulnerability to daily stressors assessed via diary methods. Current Directions in Psychological Science, 14, 64-68.
  4. Ruehlman, L.S., & Karoly, P. (1991). With a little flak from my friends: Development and preliminary validation of the test of negative social exchange (TENSE). Psychological Assessment, 3, 97-104.
  5. Locke, H.J. & Wallace, K.M. (1959). Short marital-adjustment and prediction tests: Their reliability and validity. Marriage and Family Living, 21, 251-255.
  6. Taylor, S.E., Lerner, J.S., Sage, R.M., Lehman, B. J., & Seeman, T. E. (2004). Early environment, emotions, responses to stress, and health. Journal of Personality, 72, 1365-1393.
  7. Kirschbaum, C., Pirke, K.M., Hellhammer, D.H. (1993). The ‘Trier Social Stress Test’—a tool for investigating psychobiological stress responses in laboratory setting. Neuropsychobiolog, 28, 76-81.
  8. Romanov, K., Appelberg, K., Honkasalo, M.L., & Koskenvuo, M. (1996). Recent interpersonal conflict at work and psychiatric morbidity: A prospective study of 15,530 employees aged 24-64. Journal of Psychosomatic Research, 40(2), 169-176.
  9. Monroe, S.M., Slavich, G.M., & Georgiades, K., 2009. The social environment and life stress in depression. In: Gotlib, L.H., Hammen, C.L. (Eds.), Handbook of Depression. Second ed. Guilford Press, New York, pp. 340-360.
  10. Paykel, E.S. (2003). Life events and affective disorders. Acta Psychiatrica Scandinavica, 108, 61– 66.
  11. Mazure, C.M. (1998). Life stressors as risk factors in depression. Clinical Psychology: Science and Practice, 5, 291-313.
  12. Slavich, G.M., Thornton, T., Torres, L.D., Monroe, S.M., & Gotlib, I.H., 2009. Targeted rejection predicts hastened onset of major depression. Journal of Social and Clinical Psychology. 28, 223–243.
  13. Schuster, T.L., Kessler, R.C., & Aseltine, R.H. (1990). Supportive interactions, negative interactions, and depressed mood. American Journal of Community Psychology, 18, 423-438.
  14. Finch, J.F., Okun, M.A., Pool, G.J., & Ruehlman, L.S. (1999). A comparison of the influence of conflictual and supportive social interactions on psychological distress. Journal of Personality, 67(4), 581-621.
  15. Pinquart, M., & Sorensen, S. (2003). Associations of stressors and uplifts of caregiving with caregiver burden and depressive mood: A meta-analysis. Journal of Gerontology: Psychological and Social Sciences, 58b(2), 112-128.
  16. Horwitz, A.V., McLaughlin, J., & White, H.R. (1997). How the negative and positive aspects of partner relationships affect the mental health of young married people. Journal of Health and Social Behavior, 39, 124-136.
  17. Weissman, M.M. (1987). Advances in psychiatric epidemiology: Rates and risks for major depression. American Journal of Public Health, 77, 445–451.
  18. O’Leary, K.D., Christian, J.L., & Mendell, N.R. (1994). A closer look at the link between marital discord and depressive symptomatology. Journal of Social and Clinical Psychology, 13, 33–41.
  19. Taylor, J. & Turner, R.J. (2002). Perceived discrimination, social strss, and depression in the transition to adulthood: Racial contrasts. Social Psychology Quarterly 65, (3), 213-225.
  20. Johnson, J. G., Cohen, P., Kasen, S., Smailes, E., & Brook, J. S. (2001). Association of maladaptive parental behavior with psychiatric disorder among parents and their offspring. Archives of General Psychiatry, 58, 453– 460.
  21. Repetti, R.L., Taylor, S.E., & Seeman, T.E. (2002). Risky families: Family social environments and the mental and physical health of offspring. Psychological Bulletin, 128, 330-366.
  22. Butzlaff, R.L. & Hooley, J.M. (1998). Expressed emotion and psychiatric relapse: A meta- analyses. Archives of General Psychiatry, 55, 547-552.
  23. Docherty, N.M., St-Hilaire, A., Aakre, J.M., Seghers, J.P., McCleery, A., & Divilbiss, M. (2011). Anxiety interacts with expressed emotion criticism in the prediction of psychotic symptom exacerbation. Schizophrenia Bulletin, 37(3), 611-618.
  24. Back, S.E., Hartwell, K., DeSantis, S.M., Saladin, M., McRae-Clark, A.L., Price, K.L., Moran-Santa Maria, M.M., Baker, N.L., Spratt, E., Kreek, M.J., & Brady, K.T. (2010). Reactivity to laboratory stress provocation predicts relapse to cocaine. Drug and Alcohol Dependence, 106(1), 21-27.
  25. Marmot, M.G., Rose, G., Shipley, M., & Hamilton, P.J. (1978). Employment grade and coronary heart disease in British civil servants. Journal of Epidemiology and Community Health, 32(4), 244-249.
  26. Adler, N.E., Boyce, T., Chesney, M.A., Cohen, S., Folkman, S., Kahn, R.L., & Syme, S.L. (1994). Socioeconomic status and health: The challenge of the gradient.
  27. Kaplan, G.A. & Kell, J.E. (1993). Socioeconomic factors and cardiovascular disease: a review of the literature. Circulation, 88, 1973-1998.
  28. Berkman, L.F. & Syme, S.L. (1979) Social networks, host resistance, and mortality: A nine-year follow-up study of Alameda County residents. American Journal of Epidemiology, 109, 186-204.
  29. Seeman, T.E. (2000). Health promoting effects of friends and family on health outcomes in older adults. American Journal of Health Promotion, 14(6), 362-370.
  30. Pincus, T., Callahan, L.F., & Burkhauser, R.V. (1987). Most chronic diseases are reported more frequently by individuals with fewer than 12 years of formal education in the age 18-64 U.S. population. Journal of Chronic Disease, 40, 865-874.
  31. Seeman, T. (2010). Health promoting effects of friends and family on health outcomes in older adults. American Journal of Health Promotion, 14(6), 362-370.
  32. Cohen, S., Frank, E., Doyle, W.J., Skoe, D.P., Rabin, B.S., & Gwaltney, J.M., Jr. (1998). Types of stressors that increase susceptibility to the common cold in healthy adults. Health Psychology, 17, 214-223.
  33. Kimmel, P.L., Peterson, R.A., Weihs, K.L, Shidler, N., Simmens, S.J., Alleyne, S., Cruz, I., Yanovski, J.A., Veis, J.H., & Phillips, T.M. (2000). Dyadic relationship conflict, gender, and mortality in urban hemodialysis patients. Journal of the American Society of Nephrology, 11, 1518–1525.
  34. Orth-Gomer, K., Wamala, S.P., Horsten, M., Schenck-Gustafsson, K., Schneiderman, N., & Mittleman, M.A. (2000). Marital stress worsens prognosis in women with coronary heart disease. Journal of the American Medical Association, 284, 3008–3014.
  35. Rich-Edwards, J.W., Spiegelman, D., Lividoti Hibert, E.N., Jun, H., Todd, T.J., Kawachi, I., & Wright, R.J. (2010). Abuse in childhood and adolescence as a predictor of type 2 diabetes in adult women. American Journal of Preventive Medicine, 39(6), 529-536.
  36. Wegman, H.L. & Stetler, C. (2009). A meta-analytic review of the effects of childhood abuse on medical outcomes in adulthood. Psychosomatic Medicine, 71, 805-812.
  37. Dong, M., Giles, W.H., Felittie, V.J., Dube, S.R., Williams, J.E., Chapman, D.P., & Anda, R.F. (2004). Insight into causal pathways for ischemic heart disease: Adverse childhood experiences study. Circulation, 110, 1761-1766.
  38. McEwen, B. S. & Stellar, E. (1993). Stress and the Individual: Mechanisms leading to disease. Archives of Internal Medicine, 153, 2093-2101.
  39. Sgoifo, A., Koolhaas, J., De Boer, S., Musso, E., Stilli, D., Buwalda, B., & Meerlo, P. (1999). Social stress, autonomic neural activation, and cardiac activity in rats. Neuroscience and Biobehavioral Reviews, 23, 915-923.
  40. Manuck, S., Marsland, A., Kaplan, J., & Williams, J. (1995). The pathogenicity of behavior and its neuroendocrine mediation: An example from coronary artery disease. Psychosomatic Medicine, 57, 275-283.
  41. Gerin, W., Pierper, C., Levy, R., & Pickering, T. (1992). Social support in social interaction: A moderator of cardiovascular reactivity. Psychosomatic Medicine, 54, 324-336.
  42. Nealey-Moore, J.B., Smith, T.W., Uchino, B.N., Hawkins, M.W., & Olson-Cerny, C. (2007). Cardiovascular reactivity during positive and negative marital interactions. Journal of Behavioral Medicine, 30, 505-519.
  43. Tomfohr, L., Cooper, D.C., Mills, P.J., Nelesen, R.A., & Dimsdale, J.E. (2010). Everyday discrimination and nocturnal blood pressure dipping in black and white Americans. Psychosomatic Medicine, 72(3), 266-272.
  44. Richman, L.S., Pek, J., Pascoe, E., & Bauer, D.J. (2010), The effects of perceived discrimination on ambulatory blood pressure and affective responses to interpersonal stress modeled over 24 hours. Health Psychology 29(4), 403-411.
  45. Dettling, Al, Pryce, C.R., Martin, R.D., & Dobeli, M. (1998). Physiological responses to parental separation and a strange situation are related to parental care received in juvenile Goldi’s monkeys (Callimico goeldii). Developmental Psychobiology, 33(1), 21-31.
  46. Heim, C., Newport, D.J., Heit, S., Graham, .P., Wilcox, M., Bonsall, R., Miller, A.H., & Nemeroff, C.B. (2000). Increased pituitary-adrenal and autonomic responses to stress in adult women after sexual and physical abuse in childhood. Journal of the American Medical Association, 284
  47. Cicchetti, D., & Rogosch, F. A. (2001). The impact of child maltreatment and psychopathology upon neuroendocrine functioning. Development and Psychopathology, 13, 783-804.
  48. Fries, A.B., Shirtcliff, E.A., & Pollak, S.D. (2008). Neuroendocrine dysregulation following early social deprivation in children. Developmental Psychobiology, 50(8), 588-599.
  49. Chen, E., Cohen, S., & Miller, G.E. (2010). How low soceioeconomic status affects 2-year hormonal trajectories in children. Psychological Science, 21, 31-37.
  50. Evans, G.W., & Kim, P. (2007). Childhood poverty and health: Cumulative risk exposure and stress dysregulation. Psychological Science, 18, 953-957.
  51. McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338, 171–179.
  52. Niskanen, L., Laaksonen, D. E., Nyyssonen, K., Punnonen, K., Valkonen, V., Fuentes, R., Tuomainen, T., Salonen, R., & Salonen, J. (2004). Inflammation, abdominal obesity, and smoking as predictors of hypertension. Hypertension, 44, 859-865.
  53. Amar, J., Fauvel, J., Drouet, L., Ruidavets, J.B., Perret, B., Chamontin, B., Boccalon, H., & Ferrieres, J. (2006). Interleukin 6 is associated with subclinical atherosclerosis: a link with soluble intercellular adhesion molecule 1. Journal of Hypertension, 24, 1083-1086.
  54. Cesari, M., Penninx, B. W., Newman, A. B., Kritchevsky, S. B., Nicklas, B. J., Sutton-Tyrrell K., Rubin, S. M., Ding, J., Simonsick. E. M., Harris, T.B., & Pahor, M. (2003). Inflammatory markers and onset of cardiovascular events: results form the Health ABC study. Circulation, 108, 2317-2322.
  55. Ridker, P. M., Rifai, N., Stampfer, M. J., & Hennekens, C. H. (2000). Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men. Circulation, 101, 1767-1772.
  56. Raison, C. L., Capuron, L., & Miller A. H. (2006). Cytokines sing the blues: Inflammation and the pathogenesis of depression. Trends in Immunology, 27(1), 24-31.
  57. Wellen, K. E., & Hotamisligil, G. S. (2005). Inflammation, stress, and diabetes. Journal of Clinical Investigation, 115(5), 1111-1119.
  58. Coussens, L. M. & Werb, Z. (2002). Inflammation and cancer. Nature, 420, 860-867.
  59. Rakoff-Nahoum. (2006). Why cancer and inflammation? Yale Journal of Biology and Medicine, 79(3-4), 123-130.
  60. Kiecolt Glaser, Preacher, MacCallum, Atkinson, Malarkey, and Glaser, 2003
  61. Steptoe, A., Hamer, & Chida, Y. (2007). The effects of acute psychological stress on circulating inflammatory factors in humas: A review and meta-analysis. Brain, Behavior, and Immunity, 21, 901-912.
  62. Slavich, G. M., Way, B. M., Eisenberger, N. I., & Taylor, S. E. (2010). Neural sensitivity to social rejection is associated with inflammatory responses to social stress. Proceedings of the National Academy of Sciences, 107(33), 14817-14822.
  63. Dickerson, S. S., Gable, S. L., Irwin, M. R., Aziz, N., & Kemeny, M. E. (2009). Social-evaluative threat and proinflammatory cytokine regulation: An experimental laboratory investigation. Psychological Science, 20, 1237-1244.
  64. Miller, G. E., Rohleder, N., Stetler, C., & Kirschbaum, C. (2005). Clinical depression and regulation of the inflammatory response during acute stress. Psychosomatic Medicine, 67, 679-687.
  65. Miller, G. E., Rohleder, N., & Cole, S. W. (2009). Chronic interpersonal stress predicts activation of pro- and anti-inflammatory signaling pathways 6 months later. Psychosomatic Medicine, 71, 57-62.
  66. Taylor, S.E., Lehman, B.J., Kiefe, C.I., & Seeman, T.E. (2006) Relationship of early life stress and psychological functioning of C-reactive protein in the coronary artery risk development in young adults study. Biological Psychiatry, 60, 819-824.
  67. Miller, G.E., Chen, E., Sze, J., Marin, T. Arevalo, J.M., Doll, R., Ma, & Cole, S.W. (2008). A functional genomic fingerprint of chronic stress in humans: blunted glucocorticoid and increase NF-kappaB signaling. Biological Psychiatry, 64(4), 266-272.
  68. Stark, J.L., Avitsur, R., Padgett, D.A., Campbell, K.A., Beck, F.M., & Sheridan J.F. (2001). Social stress induces glucocorticoid resistance in macrophages. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 280(6), 799-805.
  69. Jan, B.U., Coyle, S.M., Macor, M.A., Reddell, M., Calvano, S.E., & Lowry, S.F. (2010). Relationship of basal heart rate variability to in vivo cytokine responses after endotoxin exposure. Shock, 33(4), 363-368.
  70. Marsland, A.L., Gianaros, P.J., Prather, A.A., Jennings, J.R., Neumann, S.A., & Manuck, S.B. (2007). Stimulated production of proinflammatory cytokines covaries inversely with heart rate variability. Psychosomatic Medicine, 69(8), 709-716.