Social stress is stress that stems from one's relationships with others and from the social environment in general. A person experiences stress when he or she does not have the ability or resources to cope when confronted with an external stimulus (stressor), or when they fear they do not have the ability or resources. An event which exceeds the ability to cope does not necessarily have to occur in order for one to experience stress, as the threat of such an event occurring can be sufficient. This can lead to emotional, behavioral, and physiological changes that can put one under greater risk for developing a mental disorder and physical illness.
Humans are social beings by nature, as they typically have a fundamental need and desire to maintain positive social relationships. Thus, they usually find maintaining positive social ties to be beneficial. Social relationships can offer nurturance, foster feelings of social inclusion, and lead to reproductive success. Anything that disrupts or threatens to disrupt their relationships with others can result in social stress. This can include low social status in society or in particular groups, giving a speech, interviewing with potential employers, caring for a child or spouse with a chronic illness, meeting new people at a party, the threat of or actual death of a loved one, divorce, and discrimination. Social stress can arise from one's micro-environment (e.g., family ties) and macro-environment (e.g., hierarchical societal structure). Social stress is typically the most frequent type of stressor that people experience in their daily lives and affects people more intensely than other types of stressors.
- 1 Measurement
- 2 Mental health
- 3 Physical health
- 4 Physiology
- 5 See also
- 6 References
Social stress is typically studied by asking people about their social experiences and relationships or by inducing social stress in the laboratory.
Questionnaires used to assess stressful social experiences include the Test of Negative Social Exchange, Marital Adjustment Test, and the Risky Families Questionnaire. More detailed information can be gathered by asking open-ended questions. For instance, the UCLA Life Stress Interview includes questions about romantic partners, closest friendships, other friendships, and family relationships.
In rodent models, social disruption and social defeat are two common social stress paradigms. In the social disruption paradigm, an aggressive rodent is introduced into a cage housing male rodents that have already naturally established a social hierarchy. The aggressive "intruder" disrupts the social hierarchy, causing the residents social stress. In the social defeat paradigm, an aggressive "intruder" and another non-aggressive male rodent fight.
In human research, the Trier Social Stress Task (TSST) and conflict discussions are common inductions of social stress. In the TSST, participants have to give an impromptu speech and then perform mental arithmetic as quickly and accurately as possible. Both tasks are completed in front of a judging panel that is trained to provide nonverbal negative feedback. 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.
Research has consistently demonstrated that social stress increases risk for developing negative mental health outcomes. One prospective study asked over fifteen hundred Finnish employees whether they had "considerable difficulties with [their] coworkers/superiors/inferiors during the last 6 months, 5 years, earlier, or never". Information on suicides, hospitalizations due to psychosis, suicidal behavior, alcohol intoxication, depressive symptoms, and medication for chronic psychiatric disorders was then gathered from the national registries of mortality and morbidity. Those who had experienced conflict in the workplace with coworkers or supervisors in the last five years were more likely to be diagnosed with a psychiatric condition.
Risk for developing clinical depression significantly increases after experiencing social stress; depressed individuals often experience interpersonal loss before becoming depressed. One study found that depressed individuals who had been rejected by others had developed depression about three times more quickly than those who had experienced stress not involving social rejection. In non-clinically depressed populations, people with friends and family who make too many demands, criticize, and create tension and conflict tend to have more depressive symptoms. Conflict between spouses also leads to more psychological distress and depressive symptoms, especially for wives. In particular, unhappy married couples are 10–25 times more at risk for developing clinical depression. Similarly, social stress arising from discrimination is related to greater depressive symptoms. In one study, African-Americans and non-Hispanic whites reported on their daily experiences of discrimination and depressive symptoms. Regardless of race, those who perceived more discrimination had higher depressive symptoms.
Social stress occurring early in life can have psychopathological effects that develop or persist in adulthood. One longitudinal study found that children were more likely to have a psychiatric disorder (e.g. anxiety, depressive, disruptive, personality, and substance use disorders) in late adolescence and early adulthood when their parents showed more maladaptive child-rearing behaviors (e.g., loud arguments between parents, verbal abuse, difficulty controlling anger toward the child, lack of parental support or availability, and harsh punishment). Child temperament and parental psychiatric disorders did not explain this association. 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.
Relapse and recurrence
Social stress can also exacerbate current psychopathological conditions and compromise recovery. For instance, patients recovering from depression or bipolar 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. Similarly, outpatients with schizophrenia or schizoaffective disorder show greater psychotic symptoms if the most influential person in their life is critical and are more likely to relapse if their familial relationships are marked by tension. In regard to substance abuse, cocaine-dependent individuals report greater cravings for cocaine following exposure to a social stressor.
Research has also repeatedly found a robust relationship between various social stressors and aspects of physical health.
Social status, a macro social stressor, is a robust predictor of death. In a study of over 1700 British civil servants, socioeconomic status (SES) was inversely related to mortality. Those with the lowest SES have worse health and greater mortality rats than those with the greatest SES. Other studies have replicated this relationship between SES and mortality in a range of diseases, including infectious, digestive, and respiratory diseases. Similarly, social stressors in the microenvironment are also linked to increased mortality. A seminal longitudinal study of nearly 7,000 people found that socially isolated people had greater risk of dying from any cause.
Social stress also makes people sicker. People who have fewer social contacts are at greater risk for developing illness, including cardiovascular disease. The lower one’s social status, the more likely he or she is to have a cardiovascular, gastrointestinal, musculoskeletal, neoplastic, pulmonary, renal, or other chronic diseases. These links are not explained by other, more traditional risk factors such as race, health behaviors, age, sex, or access to health care. In one laboratory study, researchers interviewed participants to determine whether they had been experiencing social conflicts with spouses, close family members and friends. They then exposed the participants to the common cold virus and found that participants with conflict-ridden relationships were two times more likely to develop a cold than those without such social stress.
Exposure to social stress in childhood can also have long-term effects, increasing risk for developing diseases later in life. In particular, adults who were maltreated (emotionally, physically, sexually abused or neglected) as children report more disease outcomes, such as stroke, heart attack, diabetes, and hypertension or greater severity of those outcomes. The Adverse Childhood Experiences study (ACE), which includes over seventeen thousand adults, also found that there was a 20% increase in likelihood for experiencing heart disease for each kind of chronic familial social stressor experienced in childhood, and this was not due to typical risk factors for heart disease such as demographics, smoking, exercise, adiposity, diabetes, or hypertension.
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% increased risk for mortality when there was more relationship negativity with their spouse even when controlling for severity of disease and treatment. 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.
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.
Sympathetic nervous system
The sympathetic nervous system (SNS) becomes activated in response to stress. Sympathetic arousal stimulates the medulla of the medulla to secrete epinephrine and norepinephrine into the blood stream, which facilitates the fight-or-flight response. 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 SNS activity. Studies of rodents show that social stress causes hypertension and atherosclerosis. Studies of non-human primates also show that social stress clogs arteries.[clarification needed] 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. 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.
Hypothalamic-pituitary adrenocortical axis (HPA)
In response to stress, the hypothalamus releases corticotropin-releasing hormone (CRH), stimulating the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH then stimulates the adrenal cortex to secrete glucocorticoids, including cortisol. It is thought that social stress can lead to adverse health outcomes by chronically activating the HPA axis or disrupting the HPA system. There are a number of studies that link social stress and indications of a disrupted HPA axis; for instance, monkey infants neglected by their mothers show prolonged cortisol responses following a challenging event. In humans, abused women exhibit a prolonged elevation in cortisol following a standardized psychosocial laboratory stressor compared to those without an abuse history. Maltreated children not only show higher morning cortisol values than non-maltreated children, but their HPA systems also fail to recover after a stressful social interaction with their caregiver. Over time, low-SES children show progressively greater output of cortisol. Although these studies point to a disrupted HPA system accounting for the link between social stress and physical health, they did not include disease outcomes. Nevertheless, a dysfunctional HPA response to stress is thought to increase risk for developing or exacerbating diseases such as diabetes, cancer, cardiovascular disease, and hypertension.
Inflammation is an immune response that is critical to fighting infections and repairing injured tissue. Although acute inflammation is adaptive, chronic inflammatory activity can contribute to adverse health outcomes, such as hypertension, atherosclerosis, coronary heart disease, depression, diabetes, and some cancers.
Research has elucidated a relationship between different social stressors and cytokines (the markers of inflammation). Chronic social stressors, such as caring for a spouse with dementia, lead to greater circulating levels of cytokine interleukin-6 (IL-6), whereas acute social stress tasks in the laboratory have been shown to elicit increases in proinflammatory cytokines. Similarly, when faced with another type of social stress, namely social evaluative threat, participants showed increases in IL-6 and a soluble receptor for tumor necrosis factor-α. Increases in inflammation may persist over time, as studies have shown that chronic relationship stress has been tied to greater IL-6 production 6 months later and children reared in a stressful family environment marked by neglect and conflict tend to show elevated levels of C-reactive protein, a marker of IL-6, in adulthood.
Interactions of physiological systems
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, and proinflammatory cytokines can also activate the HPA system. Sympathetic activity can also upregulate inflammatory activity. Given the relationships among these physiological systems, social stress may also influence health indirectly via affecting a particular physiological system that in turn affects a different physiological system.
- Slavich, George M; O'Donovan, Aoife; Epel, Elissa S; Kemeny, Margaret E (September 2010). "Black sheep get the blues: a psychobiological model of social rejection and depression". Neuroscience and Biobehavioral Reviews 35 (1): 39–45. doi:10.1016/j.neubiorev.2010.01.003. PMC 2926175. PMID 20083138.
- Baumeister, R F; Leary, M R (May 1995). "The need to belong: desire for interpersonal attachments as a fundamental human motivation". Psychological Bulletin 117 (3): 497–529. doi:10.1037/0033-2909.117.3.497. PMID 7777651.
- Almeida, D.M. (2005). "Resilience and vulnerability to daily stressors assessed via diary methods". Current Directions in Psychological Science 14 (2): 64–68. doi:10.1111/j.0963-7214.2005.00336.x.
- Ruehlman, Linda S.; Karoly, Paul (1991). "With a little flak from my friends: Development and preliminary validation of the Test of Negative Social Exchange (TENSE)". Psychological Assessment 3 (1): 97–104. doi:10.1037/1040-35184.108.40.206.
- Locke, Harvey J.; Wallace, Karl M. (August 1959). "Short Marital-Adjustment and Prediction Tests: Their Reliability and Validity". Marriage and Family Living 21 (3): 251. doi:10.2307/348022. JSTOR 348022.
- Taylor, Shelley E; Lerner, Jennifer S; Sage, Rebecca M; Lehman, Barbara J; Seeman, Teresa E (December 2004). "Early environment, emotions, responses to stress, and health". Journal of Personality 72 (6): 1365–1393. doi:10.1111/j.1467-6494.2004.00300.x. PMID 15509286.
- Kirschbaum, C; Pirke, K M; Hellhammer, D H (1993). "The 'Trier Social Stress Test'—a tool for investigating psychobiological stress responses in a laboratory setting". Neuropsychobiology 28 (1-2): 76–81. doi:10.1159/000119004. PMID 8255414.
- Romanov, K; Appelberg, K; Honkasalo, M L; Koskenvuo, M (February 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. doi:10.1016/0022-3999(95)00577-3. PMID 8778399.
- Monroe, S.M.; Slavich, G.M.; Georgiades, K. (23 October 2008). "The social environment and life stress in depression editor-last=Gotlib". Handbook of Depression, Second Edition. Guilford Press. pp. 340–360. ISBN 9781606238028.
- Paykel, E. S. (2003). "Life events and affective disorders". Acta Psychiatrica Scandinavica 108: 61–66. doi:10.1034/j.1600-0447.108.s418.13.x.
- Mazure, Carolyn M. (1998). "Life Stressors as Risk Factors in Depression". Clinical Psychology: Science and Practice 5 (3): 291–313. doi:10.1111/j.1468-2850.1998.tb00151.x.
- Slavich, GEORGE M.; Thornton, Tiffany; Torres, Leandro D.; Monroe, Scott M.; Gotlib, Ian H. (1 February 2009). "Targeted Rejection Predicts Hastened Onset of Major Depression". Journal of Social and Clinical Psychology 28 (2): 223–243. doi:10.1521/jscp.2009.28.2.223. PMC 2847269. PMID 20357895.
- Schuster, T L; Kessler, R C; Aseltine, R H, Jr (June 1990). "Supportive interactions, negative interactions, and depressed mood". American Journal of Community Psychology 18 (3): 423–438. doi:10.1007/bf00938116. PMID 2264558.
- Finch, J F; Okun, M A; Pool, G J; Ruehlman, L S (August 1999). "A comparison of the influence of conflictual and supportive social interactions on psychological distress". Journal of Personality 67 (4): 581–621. doi:10.1111/1467-6494.00066. PMID 10444852.
- Pinquart, Martin; Sörensen, Silvia (March 2003). "Associations of stressors and uplifts of caregiving with caregiver burden and depressive mood: a meta-analysis". The Journal of Gerontology: Psychological and Social Sciences 58b (2): 112–128. PMID 12646594.
- Horwitz, A V; McLaughlin, J; White, H R (June 1998). "How the negative and positive aspects of partner relationships affect the mental health of young married people". Journal of Health And Social Behavior 39 (2): 124–136. JSTOR 2676395. PMID 9642903.
- Weissman, M M (April 1987). "Advances in psychiatric epidemiology: rates and risks for major depression.". American Journal of Public Health 77 (4): 445–451. doi:10.2105/ajph.77.4.445. PMC 1646931. PMID 3826462.
- Daniel, K.; Christian, Jennifer L.; Mendell, Nancy R. (1994). "A closer look at the link between marital discord and depressive symptomatology". Journal of Social and Clinical Psychology 13 (1): 33–41. doi:10.1521/jscp.19220.127.116.11.
- Taylor, John; Jay, R. (2002). "Perceived discrimination, social stress and depression in the transition to adulthood: Racial contrasts". Social Psychology Quarterly 65 (3): 213–225. doi:10.2307/3090120.
- Johnson, J G; Cohen, P; Kasen, S; Smailes, E; Brook, J S (May 2001). "Association of maladaptive parental behavior with psychiatric disorder among parents and their offspring". Archives of General Psychiatry 58 (5): 453–460. doi:10.1001/archpsyc.58.5.453. PMID 11343524.
- Repetti, Rena L; Taylor, Shelley E; Seeman, Teresa E (March 2002). "Risky families: family social environments and the mental and physical health of offspring". Psychological Bulletin 128 (2): 330–366. doi:10.1037/0033-2909.128.2.230. PMID 11931522.
- Butzlaff, R L; Hooley, J M (June 1998). "Expressed emotion and psychiatric relapse: a meta-analysis". Archives of General Psychiatry 55 (6): 547–552. doi:10.1001/archpsyc.55.6.547. PMID 9633674.
- Docherty, Nancy M.; St-Hilaire, Annie; Aakre, Jennifer M.; Seghers, James P.; McCleery, Amanda; Divilbiss, Marielle (1 May 2011). "Anxiety Interacts With Expressed Emotion Criticism in the Prediction of Psychotic Symptom Exacerbation". Schizophrenia Bulletin 37 (3): 611–618. doi:10.1093/schbul/sbp123. PMID 19892819.
- Back, Sudie E; Hartwell, Karen; DeSantis, Stacia M; Saladin, Michael; McRae-Clark, Aimee L; Price, Kimber L; Moran-Santa Maria, Megan M; Baker, Nathaniel L; Spratt, Eve; Kreek, Mary Jeanne; Brady, Kathleen T (1 January 2010). "Reactivity to laboratory stress provocation predicts relapse to cocaine". Drug and Alcohol Dependence 106 (1): 21–27. doi:10.1016/j.drugalcdep.2009.07.016. PMC 2815094. PMID 19726138.
- Marmot, M G; Rose, G; Shipley, M; Hamilton, P J (December 1978). "Employment grade and coronary heart disease in British civil servants". Journal of Epidemiology and Community Health 32 (4): 244–249. doi:10.1136/jech.32.4.244. PMC 1060958. PMID 744814.
- Adler, N E; Boyce, T; Chesney, M A; Cohen, S; Folkman, S; Kahn, R L; Syme, S L (January 1994). "Socioeconomic status and health. The challenge of the gradient". The American Psychologist 49 (1): 15–24. doi:10.1037/0003-066x.49.1.15. PMID 8122813.
- Kaplan, G A; Keil, J E (October 1993). "Socioeconomic factors and cardiovascular disease: a review of the literature". Circulation 88 (4, part 1): 1973–1998. doi:10.1161/01.cir.88.4.1973. PMID 8403348.
- Berkman, L F; Syme, S L (February 1979). "Social networks, host resistance, and mortality: a nine-year follow-up study of Alameda County residents". American Journal of Epidemiology 109 (2): 186–204. PMID 425958.
- Seeman, T E (August 2000). "Health promoting effects of friends and family on health outcomes in older adults". American Journal of Health Promotion 14 (6): 362–370. doi:10.4278/0890-1171-14.6.362. PMID 11067571.
- 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 United States population". Journal of Chronic Diseases 40 (9): 865–874. doi:10.1016/0021-9681(87)90186-x. PMID 3597688.
- Cohen, S; Frank, E; Doyle, W J; Skoner, D P; Rabin, B S; Gwaltney, J M, Jr (May 1998). "Types of stressors that increase susceptibility to the common cold in healthy adults". Health Psychology 17 (3): 214–223. doi:10.1037/0278-618.104.22.168. PMID 9619470.
- Rich-Edwards, Janet W; Spiegelman, Donna; Lividoti Hibert, Eileen N; Jun, Hee-Jin; Todd, Tamarra James; Kawachi, Ichiro; Wright, Rosalind J (December 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. doi:10.1016/j.amepre.2010.09.007. PMC 3003936. PMID 21084073.
- Wegman, Holly L; Stetler, Cinnamon (October 2009). "A meta-analytic review of the effects of childhood abuse on medical outcomes in adulthood". Psychosomatic Medicine 71 (8): 805–812. doi:10.1097/PSY.0b013e3181bb2b46. PMID 19779142.
- Dong, Maxia; Giles, Wayne H; Felitti, Vincent J; Dube, Shanta R; Williams, Janice E; Chapman, Daniel P; Anda, Robert F (28 September 2004). "Insights Into Causal Pathways for Ischemic Heart Disease: Adverse Childhood Experiences Study". Circulation 110 (13): 1761–1766. doi:10.1161/01.CIR.0000143074.54995.7F. PMID 15381652.
- 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 (August 2000). "Dyadic relationship conflict, gender, and mortality in urban hemodialysis patients". Journal of the American Society of Nephrology 11 (8): 1518–1525. PMID 10906166.
- Orth-Gomér, K; Wamala, S P; Horsten, M; Schenck-Gustafsson, K; Schneiderman, N; Mittleman, M A (20 December 2000). "Marital stress worsens prognosis in women with coronary heart disease: The Stockholm Female Coronary Risk Study". The Journal Of the American Medical Association 284 (23): 3008–3014. doi:10.1001/jama.284.23.3008. PMID 11122587.
- McEwen, B S; Stellar, E (27 September 1993). "Stress and the individual: Mechanisms leading to disease". Archives of Internal Medicine 153 (18): 2093–2101. doi:10.1001/archinte.153.18.2093. PMID 8379800.
- Sgoifo, A; Koolhaas, J; De Boer, S; Musso, E; Stilli, D; Buwalda, B; Meerlo, P (November 1999). "Social stress, autonomic neural activation, and cardiac activity in rats". Neuroscience and Biobehavioral Reviews 23 (7): 915–923. doi:10.1016/s0149-7634(99)00025-1. PMID 10580306.
- Manuck, S B; Marsland, A L; Kaplan, J R; Williams, J K (June 1995). "The pathogenicity of behavior and its neuroendocrine mediation: an example from coronary artery disease". Psychosomatic Medicine 57 (3): 275–283. PMID 7652128.
- Gerin, W; Pieper, C; Levy, R; Pickering, T G (June 1992). "Social support in social interaction: a moderator of cardiovascular reactivity". Psychosomatic Medicine 54 (3): 324–336. PMID 1620808.
- Tomfohr, Lianne; Cooper, Denise C; Mills, Paul J; Nelesen, Richard A; Dimsdale, Joel E (April 2010). "Everyday discrimination and nocturnal blood pressure dipping in black and white americans". Psychosomatic Medicine 72 (3): 266–272. doi:10.1097/PSY.0b013e3181d0d8b2. PMC 2894630. PMID 20124424.
- Smart Richman, Laura; Pek, Jolynn; Pascoe, Elizabeth; Bauer, Daniel J (July 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. doi:10.1037/a0019045. PMID 20658828.
- Dettling, A; Pryce, C R; Martin, R D; Döbeli, M (July 1998). "Physiological Responses to parental separation and a strange situation are related to parental care received in juvenile Goeldi's monkeys (Callimico goeldii)". Developmental Psychobiology 33 (1): 21–31. doi:10.1002/(sici)1098-2302(199807)33:1<21::aid-dev3>3.0.co;2-u. PMID 9664169.
- Heim, C; Newport, D J; Heit, S; Graham, Y P; Wilcox, M; Bonsall, R; Miller, A H; Nemeroff, C B (2 August 2000). "Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood". Journal of the American Medical Association 284 (5): 592–597. doi:10.1001/jama.284.5.592. PMID 10918705.
- Cicchetti, D; Rogosch, F A (2001). "The impact of child maltreatment and psychopathology on neuroendocrine functioning". Development and Psychopathology 13 (4): 783–804. PMID 11771908.
- Wismer Fries, Alison B.; Shirtcliff, Elizabeth A.; Pollak, Seth D. (September 2008). "Neuroendocrine dysregulation following early social deprivation in children". Developmental Psychobiology 50 (6): 588–599. doi:10.1002/dev.20319. PMC 2673795. PMID 18683181.
- Chen, Edith; Cohen, Sheldon; Miller, Gregory E. (1 January 2010). "How Low Socioeconomic Status Affects 2-Year Hormonal Trajectories in Children". Psychological Science 21 (1): 31–37. doi:10.1177/0956797609355566. PMID 20424019.
- Evans, Gary W; Kim, Pilyoung (November 2007). "Childhood poverty and health: cumulative risk exposure and stress dysregulation". Psychological Science 18 (11): 953–957. doi:10.1111/j.1467-9280.2007.02008.x. PMID 17958708.
- McEwen, B S (15 January 1998). "Protective and damaging effects of stress mediators". The New England Journal of Medicine 338 (3): 171–179. doi:10.1056/NEJM199801153380307. PMID 9428819.
- Niskanen, Leo; Laaksonen, David E; Nyyssönen, Kristiina; Punnonen, Kari; Valkonen, Veli-Pekka; Fuentes, Ricardo; Tuomainen, Tomi-Pekka; Salonen, Riitta; Salonen, Jukka T (December 2004). "Inflammation, abdominal obesity, and smoking as predictors of hypertension". Hypertension 44 (6): 859–865. doi:10.1161/01.HYP.0000146691.51307.84. PMID 15492131.
- Amar, Jacques; Fauvel, Josette; Drouet, Ludovic; Ruidavets, Jean Bernard; Perret, Bertrand; Chamontin, Bernard; Boccalon, Henri; Ferrieres, Jean (June 2006). "Interleukin 6 is associated with subclinical atherosclerosis: a link with soluble intercellular adhesion molecule 1". Journal of Hypertension 24 (6): 1083–1088. doi:10.1097/01.hjh.0000226198.44181.0c. PMID 16685208.
- Cesari, Matteo; Penninx, Brenda W J H; Newman, Anne B; Kritchevsky, Stephen B; Nicklas, Barbara J; Sutton-Tyrrell, Kim; Rubin, Susan M; Ding, Jingzhong; Simonsick, Eleanor M; Harris, Tamara B; Pahor, Marco (11 November 2003). "Inflammatory markers and onset of cardiovascular events: results from the Health ABC study". Circulation 108 (19): 2317–2322. doi:10.1161/01.CIR.0000097109.90783.FC. PMID 14568895.
- Ridker, P M; Rifai, N; Stampfer, M J; Hennekens, C H (18 April 2000). "Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men". Circulation 101 (15): 1767–1772. doi:10.1161/01.cir.101.15.1767. PMID 10769275.
- Raison, Charles L; Capuron, Lucile; Miller, Andrew H (January 2006). "Cytokines sing the blues: inflammation and the pathogenesis of depression". Trends in Immunology 27 (1): 24–31. doi:10.1016/j.it.2005.11.006. PMC 3392963. PMID 16316783.
- Wellen, Kathryn E; Hotamisligil, Gökhan S (May 2005). "Inflammation, stress, and diabetes". The Journal of Clinical Investigation 115 (5): 1111–1119. doi:10.1172/JCI25102. PMC 1087185. PMID 15864338.
- Coussens, Lisa M; Werb, Zena (19 December 2002). "Inflammation and cancer". Nature 420 (6917): 860–867. doi:10.1038/nature01322. PMC 2803035. PMID 12490959.
- Rakoff-Nahoum, Seth (December 2006). "Why Cancer and Inflammation?". The Yale Journal of Biology and Medicine 79 (3-4): 123–130. PMC 1994795. PMID 17940622.
- Kiecolt-Glaser, Janice K; Preacher, Kristopher J; MacCallum, Robert C; Atkinson, Cathie; Malarkey, William B; Glaser, Ronald (22 July 2003). "Chronic stress and age-related increases in the proinflammatory cytokine IL-6". Proceedings of the National Academy of Sciences of the United States of America 100 (15): 9090–9095. doi:10.1073/pnas.1531903100. PMC 166443. PMID 12840146.
- Steptoe, Andrew; Hamer, Mark; Chida, Yoichi (October 2007). "The effects of acute psychological stress on circulating inflammatory factors in humans: a review and meta-analysis". Brain, Behavior, and Immunity 21 (7): 901–912. doi:10.1016/j.bbi.2007.03.011. PMID 17475444.
- Slavich, George M.; Way, Baldwin M.; Eisenberger, Naomi I.; Taylor, Shelley E. (17 August 2010). "Neural sensitivity to social rejection is associated with inflammatory responses to social stress". Proceedings of the National Academy of Sciences of the United States of America 107 (33): 14817–14822. doi:10.1073/pnas.1009164107. PMC 2930449. PMID 20679216.
- Dickerson, Sally S; Gable, Shelly L; Irwin, Michael R; Aziz, Najib; Kemeny, Margaret E (October 2009). "Social-evaluative threat and proinflammatory cytokine regulation: an experimental laboratory investigation". Psychological Science 20 (10): 1237–1244. doi:10.1111/j.1467-9280.2009.02437.x. PMC 2761517. PMID 19754527.
- Miller, Gregory E; Rohleder, Nicolas; Stetler, Cinnamon; Kirschbaum, Clemens (October 2005). "Clinical depression and regulation of the inflammatory response during acute stress". Psychosomatic Medicine 67 (5): 679–687. doi:10.1097/01.psy.0000174172.82428.ce. PMID 16204423.
- Miller, Gregory E; Rohleder, Nicolas; Cole, Steve W (January 2009). "Chronic interpersonal stress predicts activation of pro- and anti-inflammatory signaling pathways 6 months later". Psychosomatic Medicine 71 (1): 57–62. doi:10.1097/PSY.0b013e318190d7de. PMC 2720615. PMID 19073750.
- Taylor, Shelley E; Lehman, Barbara J; Kiefe, Catarina I; Seeman, Teresa E (15 October 2006). "Relationship of early life stress and psychological functioning to adult C-reactive protein in the coronary artery risk development in young adults study". Biological Psychiatry 60 (8): 819–824. doi:10.1016/j.biopsych.2006.03.016. PMID 16712805.
- Wilder, R L (1995). "Neuroendocrine-immune system interactions and autoimmunity". Annual Review of Immunology 13: 307–338. doi:10.1146/annurev.iy.13.040195.001515. PMID 7612226.
- Jan, Badar U; Coyle, Susette M; Macor, Marie A; Reddell, Michael; Calvano, Steve E; Lowry, Stephen F (April 2010). "Relationship of basal heart rate variability to in vivo cytokine responses after endotoxin exposure". Shock 33 (4): 363–368. doi:10.1097/SHK.0b013e3181b66bf4. PMC 2980578. PMID 20407404.
- Marsland, Anna L; Gianaros, Peter J; Prather, Aric A; Jennings, J Richard; Neumann, Serina A; Manuck, Stephen B (November 2007). "Stimulated production of proinflammatory cytokines covaries inversely with heart rate variability". Psychosomatic Medicine 69 (8): 709–716. doi:10.1097/PSY.0b013e3181576118. PMID 17942840.