CENTER ON BEHAVIORAL MEDICINE
graciously given by the author to reproduce this paper
The Impact of Stress on the Immune System
Mark R. Zuccolo
The study of the physiology of stress as a discipline of scientific inquiry began in 1936 with a Canadian investigator, Hans Selye, who adopted the term "stress", used until then only in engineering to describe forces acting on metals, to characterize the response of the human body to a strong stimulus (Jerram, 2003). Today, stress is invoked with increasing frequency as the cause of or contributing factor to physical and mental disorders.
Stress, per se, is not a scourge of the human body but a necessary and vital defense mechanism. The physiological response we call stress allows the healthy body to face immediate threats, real or perceived. In essence, stress prepares the organism for "fight or flight". Problems arise when the stress response becomes maladaptive. Now classic clinical studies have demonstrated that the chronic activation or the chronic repression of the normal stress response can compromise the state of health and cause diseases that can be directly traced to stress (Eysenck, 1997). The normative or maladaptive stress response is conditioned by personal, psychological and social characteristics. Some individuals are more vulnerable than others to diseases from stress since they may be daily and chronically exposed to stressor that put an unusual burden on their physiological coping abilities (Noriyuki, Yoshiharu, & Nozomu, 2001).
At the most fundamental level, the natural stress response may be induced by a physical change (physical inducer) such a sensation of cold or warmth, or by a thwarted expectation or intense mental activity (psychological inducer) (Gorski, 2002). When the body’s natural stress response is activated by a real or perceived threat, glucose, which is the principal source of energy of the body, is mobilized from its normal storage locations. The blood, transporter of glucose and oxygen, diverts it from essential organs such as the skin and the intestine, and quickly ferries it to organs essential to face the emergency: the heart, the muscles, and the brain. The variation of the blood flow is put into effect in part through the constriction of some vessels, the expansion of others and the increase in heart beat. At the same time, cognitive processes are enhanced (to facilitate the elaboration of information relative to the threat) and the perception of pain is attenuated by the secretion of endorphin (Firdaus, 2002). All physiological activities that are not of immediate benefit are delayed; growth, reproduction, and digestion, among others, which are processes requiring much energy and of no immediate value against the threat, are inhibited.
In addition to the mobilization of glucose to provide energy, the body’s response to stress causes the secretion of certain hormones and the inhibition of others. Certain alterations of T and Natural Killer (NK) cells have been observed and associated with hypothalamic and hippocampus lesions (Vivier, Nunès, & Vély, 2004); the functionality of the lymphatic cells is influenced by hormones and neurotransmitters released under stress (Pardoll, 2001); the lymphocytes, through the release of cytokine and interleukin 1, influence the neuroendocrine system; the well documented effects of interleukin 1 are fever, increase of the level of the glycocorticoids, stimulus of the hypothalamic secretion of CRH, hypothalamic secretion stimulus of ACTH and endorphin; the thymus secretes at least four substances (humoral thymic factor, thymopoietin, thymulin, thymusin) that have an effects on the immune system and on the neuroendocrine system (Cooney, 1998); peptides of central nervous system and peripheral nervous system are mobilized to enhance or inhibit the body’s immune functions. Finally, at the cellular level, in conditions of stress, certain proteins are synthesized whose physiological function is to repair any damages that the impending threat may cause to the body (Glaser, 2000).
This complex response to adverse changes or stressors represents a fundamental mechanism of defense and is intended to be temporary. After the threat passes, the body gradually returns to its pre-stress condition, and hormone levels are reduced accordingly. The inescapable unity of body, spirit and psyche, and their intimate correlation, point to the need to maintain the equilibrium that naturally exists between the endocrine system, the autonomous nervous system and the immune system. This implies that when the stress response is triggered, it arises, peaks and normalizes in a natural ebb and flow. This optimal capacity for arousal, action and return to homeostasis is the epitome of well-being.
The immune system appears to be the most reactive to stress-inducing stimuli and unexpected changes (stressors) that come from the outside (Segerstrom & Miller, 2004) and the most susceptible to damage from a sustained and unremitting stress response. The stress-inducing or stress-maintaining stimuli or changes may be of an acute nature (death of a loved one, loss of a job) or more long-lasting (living in an unpleasant atmosphere, interpersonal difficulties with colleagues, or difficulty in adjusting to a new school).
Research studies have shown that continue exposure to stressors and a chronically activated stress response can have the effect of lowering the immune defense of the human body (Courtnenay, 2000). This effect is mediated by the response to those stressors of the autonomous nervous system, which causes the endocrine system to secrete hormones such as cortisol and the catecholamines. The individual whose immune system is impaired is more sensitive to the effect of stressful stimuli and is more vulnerable to disease. The opposite is also true. For example, women who suffer from breast cancer respond better to therapies and exhibit a higher life expectancy correlated with an increase in immune defenses, if they are more optimistic about their own recovery, trust their doctors more, and believe that a complete remission is possible (Wein, 2000). Stress, whether brought about by an acute or chronic event or continuously maintained, can negatively affect various organs of the human body: an increase in heart beat and blood pressure, disturbances of the gastrointestinal apparatus, perspiration, tension and often pain of the muscular fascia, genital problems (erectile dysfunction or absence of one or more menstrual cycles). The psychological effects of stress manifest themselves in nervousness, agitation, anxiety, depression, sleep disturbances, difficulty in maintaining concentration, and many more.The mechanisms through which somatopsychic stress is converted into psychosomatic disease are multiple and new connection between stress and diseases such asthma and rheumatoid arthritis and many others are continually established by research (Segerstrom & Miller, 2004). For example, recent discoveries show that the levels of glycocorticoids, typical hormones released in presence of stress, when chronically elevated can become neurotoxins capable of damaging cells in rapid multiplication in the region of the hippocampus, which is an important center for memory processes (Lupien & Gillin, 1999; Scoville & Milner, 2000). Research has also shown that all phenomena characteristic of somatopsychic decline, characteristic of the aging process, may be accelerated by stress (McEwen, 1998).
Basile, K. C., Arias, I., Desai, S., & Thompson, M. P. (2004). The differential association of intimate partner physical, sexual, psychological, and stalking violence and posttraumatic stress symptoms in a nationally representative sample of women. Journal of Traumatic Stress, 17(5), 413.
Beck, K. D., & Servatius, R. J. (2003). Stress and cytokine effects on learning: What does sex have to do with it? Integrative Physiological & Behavioral Science, 38(3), 179-188.
Cohen, S., & Rabin, B. S. (1998). Psychological stress, immunity, and cancer. Journal of the National Cancer Institute, 90(1), 3.
Cooney, J. M. (1998). Stress, stress hormones and the immune system. The International Journal of Social Psychiatry, 44(2), 156.
Copenhaver, M. M., Lash, S. J., & Eisler, R. M. (2000). Masculine gender-role stress, anger, and male intimate abusiveness: Implications for men's relationships. Sex Roles, 42(5/6), 405.
Courtnenay, W. H. (2000). Behavioral factors associated with disease, injury, and death among men: Evidence and implications for prevention. Journal of Men's Studies, 9(1), 81.
Eysenck, H. J. (1997). Stress, the immune system and psychiatry. Behaviour Research and Therapy, 35(5), 486.
Firdaus, S. D. (2002). A hassle a day may keep the doctor away: Stress and the augmentation of immune function. Integrative and Comparative Biology, 42(3), 556.
Glaser, R. M. (2000). Stress, immune function, and health: The connection. The Quarterly Review of Biology, 75(1), 88.
Gorski, A. (2002). Seasonal patterns of stress, immune function and disease. British Medical Journal, 325(7364), 603.
Heslop, P. E. T. (2001). Perceived stress and coronary heart disease risk factors. British Journal of Health Psychology, 6(Part 2), 167-178.
Jerram, L. (2003). More about periodization. The Physician and Sports Medicine, 31(8), 42.
Lupien, S. J., & Gillin, C. J. (1999). Working memory is more sensitive than declarative memory to the acute effects of stress. Behavioral Neuroscience, 113(3), 420.
McCabe, M. P. (2005). The role of performance anxiety in the development and maintenance of sexual dysfunction in men and women. International Journal of Stress Management, 12(4), 379-388.
McEwen, B. S. (1998). Protective and damaging effects of stress mediators. The New England Journal of Medicine, 338(3), 171.
Miller, G. E., Dopp, J. M., Myers, H. F., Stevens, S. Y., & Fahey, J. L. (1999). Psychosocial predictors of natural killer cell mobilization during marital conflict. Health Psychology, 18(3), 262-271.
Noriyuki, K., Yoshiharu, K., & Nozomu, A. (2001). Suppression of cellular immunity in men with a past history of posttraumatic stress disorder. The American Journal of Psychiatry, 158(3), 484.
Pardoll, D. M. (2001). Stress, NK
and immune surveillance. Science, 294(5542), 534.
Phillips-Miller, D. L., Campbell, N. J., & Morrison, C. R. (2000). Work and family: Satisfaction, stress, and spousal support. Journal of Employment Counseling, 37(1), 16.
Scoville, W. B., & Milner, B. (2000). Loss of recent memory after bilateral hippocampal lesions. Journal of Neuropsychiatry & Clinical Neuroscience, 12(1), 103-a-113.
Segerstrom, S. C., & Miller, G. E. (2004). Psychological stress and the human immune system: A meta-analytic study of 30 years of inquiry. Psychological Bulletin, 130(4), 601.
Segerstrom, S. C., Taylor, S. E., Kemeny, M. E., & Fahey, J. L. (1998). Optimism is associated with mood, coping, and immune change in response to stress. Journal of Personality and Social Psychology, 74(6), 1646.
Stowell, J. R., Kiecolt-Glaser, J. K., & Glaser, R. (2001). Perceived stress and cellular immunity: When coping counts. Journal of Behavioral Medicine, 24(4), 17-34.
Strauman, T. J., Lemieux, A. M., & Coe, C. L. (1993). Self-discrepancy and natural killer cell activity: Immunological consequences of negative self-evaluation. Journal of Personality & Social Psychology, 64(6), 1042-1052.
Vivier, E., Nunès, J. A.,
Vély, F. (2004). Natural killer cell signaling pathways.
Wein, H. (2000). Stress and
perspectives. Word on Health Retrieved October 10, 2005,