Stress and Health Research Paper

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1. Introduction

1.1 The Origin Of Stress Research

Stress is a term that is often related to a psychological or physical state of health (cf. Sapolsky 1994) and is used by many psychological, sociological, and medical scientists as well as laymen. A first definition of the term stress was proposed by Cannon (1935). He postulated that passing a critical stress level, triggered by physical and emotional stimuli, endangers the homeostatic control of an organism. However, the name that is most closely associated with stress is Hans Selye, who defined stress as a nonspecific response of the body to any demand characterized by the secretion of glucocorticoids. Selye developed the concept of the general adaptation syndrome (GAS), which encompasses the alarm reaction, the stage of resistance, and finally the stage of exhaustion. The bodily responses to massive or ongoing stress are summarized in the stress triad, including (a) the enlargement and hyperactivity of the adrenal cortex, (b) the shrinking or atrophy of the thymus, spleen, lymph nodes, and the lymphatic system, and (c) the appearance of gastrointestinal and bowel ulcers (Selye 1936, 1937). Regarding health consequences, Selye argued that stress plays a role in the development of every disease. According to Selye, there is always a particularly weak organ or system (due to heredity or external conditions) that is thus likely to break down under stress, which is why he concluded that individuals can develop different types of diseases under the influence of the same kind of stressor.

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In the concept of four basic variations of stress, Selye (1983) emphasized that stress can be based on overstress (hyperstress) as well as understress (hypostress). He also contrasts harmful, damaging stress (distress) from good stress (eustress).

Selye’s idea of an unspecific stress response to all kinds of stimuli was challenged by Mason (1968, 1975), who underlines the importance of specific emotional reactions that determine a specific endocrine stress response. Mason showed that specific situational characteristics, such as novelty, uncontrollability, unpredictability, ambiguity, anticipation of negative consequences, and high ego-involvement, lead to specific hormonal stress responses.

1.2 Definitions Of Stress

To date, a large number of definitions of stress are available. Some researchers have even proposed to drop the term stress. Levine and Ursin (1991) have offered a comprehensive definition of stress, distinguishing between (a) input (stress stimuli), (b) (individual) processing, and (c) outcome (stress reaction). In this concept, those stimuli that require processing are defined as loads. An individual appraisal process determines whether a load becomes a stressor. Differences in processing are based for example on genetic, ontogenetic, and social factors, and early life as well as lifelong experiences. A related idea has been introduced earlier by Lazarus and Folkman (1984). According to the cognitive transactional model by Lazarus and Folkman, stress is experienced as a process that is initially triggered by situational demands, but then mainly by the cognitive appraisal of these demands. The characteristics of a situation (primary appraisal) are evaluated simultaneously in line with the available coping capacities or resources (secondary appraisal). This results in a cognitive appraisal of challenge, threat, or harm loss, and, subsequently, in emotions, coping attempts, and adaptational outcomes. This process can be cyclical, and it may lead to a number of reappraisals that change the nature of the stress episode.

At the level of stress responses, physiological, behavioral, and subjective/verbal reactions could be distinguished. Physiological responses primarily include the sympathetic–adrenal–medullary (SAM) axis, hypothalamic–pituitary–adrenal (HPA) axis, and immune system. Behavioral responses, among others, cover attention, arousal, and vigilance; subjective verbal reactions are interpretations, cognitions, and emotions. The stress reactions to physical and psychological stimuli are primarily determined by the individual interpretation, but also by the social context, the social status, genetic factors, gender, developmental stage, and individual lifelong experiences.

Finally, Levine and Ursin (1991) contrast an unspecific stress response (general alarm) and a specific individual stress reaction. With this idea they offer an integrational view of Selye’s (1983) and Mason’s (1968) approaches to a definition of stress.

2. The Model Of Allostatic Load

2.1 Introduction

While homeostatic regulation reflects the stability of constants, allostatic regulation means stability through change. Homeostatic systems (e.g., body temperature, blood oxygen, blood pH, glucose levels) must be maintained within a narrow range. That means that deviations in a homeostatic system trigger a restorative response to correct the changes. In contrast, the regulation of allostatic (adaptive) systems can operate in a relatively broad range of regulation. Following Sterling and Eyer (1988), allostasis is the regulation of the internal milieu through dynamic change in hormonal and physical parameters. Allostasis is defined as the ability of the body to increase or decrease vital functions to a new steady state on challenge.

McEwen and Stellar (1993) concluded that the concept of homeostasis is not helpful for explaining the hidden costs of chronic stress on the organism. Therefore, they extended the concept of allostasis over the dimension of time and introduced the idea of allostatic load. Allostatic load is defined as the cost of chronic exposure to elevated or fluctuating endocrine or neural responses resulting from chronic or repeated challenges that the individual experiences as stressful. Stress, for instance psychological demands, physical threat/danger, or adverse life experiences, activates various adaptive (allostatic) systems, initiating adaptation and coping processes. The SAM and the HPA axes are the main endocrine stress systems of the organism involved in an allostatic response.

In the face of an internal or external challenge, these systems are activated. (a) Catecholamines are released from the sympathetic nerves and the adrenal medulla. (b) Corticotropin-releasing factor (CRF) from the nucleus paraventriculares (PVN) of the hypothalamus triggers the discharge of adrenocorticotrophic hormone (ACTH) from the anterior pituitary gland. ACTH stimulates the secretion of glucocorticoids (e.g., cortisol) from the adrenal cortex. These hormones serve as mediators of adaptational processes. Besides the sympathetic nervous system and the HPA axis, the cardiovascular, metabolic, and immune system play a crucial role in allostatic processes.

In sum, allostatic systems enable the body to respond adequately to changes in social and physical conditions and therefore protect the body in the short run. In the long run, however, the bodily responses to stress can cause damage and finally promote several diseases. The organism’s ‘hidden toll’ of short-term adaptation to challenges is described as allostatic load, which constitutes a wear and tear on the body from chronic overactivity or underactivity of allostatic systems.

2.2 Types Of Allostatic Load

Four different scenarios can cause allostatic load: (1) frequent exposure to stress, (2) inability to habituate to repeated challenges, and (3) inability to terminate a stress response. In these three types, allostatic load is promoted by an organism’s increased exposure to stress hormones and other allostatic mediators. Finally, (4) an inadequate allostatic response in one allostatic system could be related to an increased activation of another allostatic system. An inadequate response of one allostatic system could trigger an inadequate (compensatory) response in another allostatic system.

The model emphasizes that allostatic load reflects not only the impact of lifelong experiences (wear and tear), but also covers early life experiences, genetic predispositions, environmental factors, as well as psychological and behavioral parameters. The cascading relationships between these factors could explain individual differences in the susceptibility to stress and, in some cases, to disease.

For example, Meaney and co-workers (1994) showed in animal studies that early life experiences can calibrate the lifelong pattern of physiological stress responses. Whereas unpredictable stress in newborn rodents led to an overactivity of HPA and SAM axis responsiveness, neonatal handling resulted in a reduced reactivity of the stress systems for the entire lifespan. Concerning the impact of genes on HPA axis functioning, Wust et al. (2000) report on a mediumsized yet distinct genetic influence on cortisol levels after awakening. The role of genes in the regulation of stress systems is discussed in detail by Koch and Stratakis (2000). Psychological factors, such as anticipating negative consequences, pessimism, anxiety, or worry also contribute to allostatic load. While the origin of allostatic load can be based on an individual psychological appraisal process, psychological factors can prolong, intensify, expand, or aggravate the amount of existing allostatic load. Finally, there seems to be a bidirectional influence of stress and lifestyle factors, for example nutrition, physical exercise, sleeping habits, alcohol, caffeine, and nicotine consumption, with significant effects on the extent of allostatic load (cf. Steptoe 2000).

3. Stress And Health

3.1 Types Of Allostatic Load And Health

The four different types of allostatic load may possibly be related to increased risks of the development of different health problems. Repeated ups and downs of physiological responses or a heightened activity of physiological systems due to internal or external challenges result in allostatic load, which could predispose the organism to disease. There is evidence that acute and chronic stress are significant risk factors for cardiovascular, immunological, and psychological health problems as well as impairments in the central nervous system (CNS). However, it has to be taken into consideration that evidence for stress effects on health are mainly based on correlational analyses.

Animal and human data point to the idea that allostatic load of type 1 and type 3 may possibly be related to the risk of myocardial infarction. Repeated blood pressure elevation (allostatic load type 1), for instance, could promote atherosclerosis. The failure to recover from blood pressure increase following an acute stressor (allostatic load type 3) may lead to hypertension, which also increases the risk of atherosclerosis. Furthermore, heightened cortisol levels promote an increase in insulin secretion, resulting in an endocrine condition that may also accelerate atherosclerosis. Atherosclerosis itself appears to increase the risk of myocardial infarction.

Allostatic load type 2 covers the failure to habituate or the extent of habituation to repeated stress exposure. After repeated speaking and mentally solving arithmetic problems in front of an audience (Trier Social Stress Test), most participants showed habituation in their cortisol response, but about one-third of them still had high cortisol increases every time they were exposed to the stressor. The relationship between the inability of the HPA axis to habituate to repeated exposure to this psychosocial laboratory stress protocol and various health parameters is currently being investigated.

Chronically elevated SAM and HPA axis activity can lead to decreased bone mineral density, body weight loss, amenorrhea and/or anorexia nervosa, as observed in depressed patients or high-performance athletes (allostatic load type 3). Concerning bone mineral density, Michelson et al. (1996) showed that moderately elevated glucocorticoid levels over a prolonged period were associated with reduced levels of osteocalcin in depressed women, therefore inhibiting bone formation (allostatic load type 3).

Allostatic load type 4 is illustrated by observing that a hyporeactive HPA axis (decreased release of glucocorticoids after stress) could lead to an increased response of the immune system. In case one system does not show an adequate stress response, another system increases its activity because the underactive system does not provide the normal counter-regulatory control. For instance, lewis rats, which are known to have an HPA axis hyporeactivity, show increased susceptibility for autoimmune and inflammatory disturbances, and those rats which developed an HPA axis hyporeactivity due to a subordinate position in their social network are believed to die earlier than their counterparts (allostatic load type 4) (cf. McEwen 2000).

3.2 Stress And The Cardiovascular System

Animal and human studies indicate that a relationship exists between stress and cardiovascular disturbances. Stress plays a crucial role in cardiovascular diseases as a risk factor in the progressive development of hypertension and atherosclerosis and as a trigger of acute incidences, such as myocardial infarction, stroke, or even death. While stress provokes cardiovascular and endocrine changes that could be beneficial even in healthy human beings, the same stimuli can be detrimental to patients with coronary artery disease.

Manuck et al. (1988) observed that socially subordinate female primates and dominant male primates in unstable social hierarchies have an increased risk of developing atherosclerosis. In humans, occupational strain, for example, jobs with high psychological demands and low control, leads to elevated blood pressure, increased progression of atherosclerosis, and increased risk of coronary heart disease (CHD) (cf. McEwen 2000). Allen and colleagues (1993) concluded that women are more likely to be cardiac reactors, whereas men are more prone to be vascular reactors, suggesting a gender-specific allostatic load within the cardiovascular system.

3.3 Stress And The Immune System

A large amount of literature shows the impact of stress on changes in immune system functioning (cf. Biondi 2001). Chronic psychological stress or increased allostatic load is generally shown to be associated with decreased immune responses as well as enhanced severity of infections. Consequently, a stress-related suppression of cellular immune system functioning can, for instance, lead to increased susceptibility to or severity of the common cold (Cohen et al. 1991). While chronic stress seems to precede blunted immune response, acute stress may be potentially beneficial: experiencing acute stress can enhance the trafficking of immune cells to the site of acute challenge, resulting in an immune-enhancing effect over several days (cf. McEwen 2000). Acute stress may call immune cells ‘to their battle stations,’ thus enhancing short-term immunity (cf. Dhabar 2000, Dhabar and McEwen 1997).

Possible mechanisms involved in the relationship between psychological stress and immune function changes, covering the stress–disease connection, are discussed in Biondi (2001). There seems to be a complex connection between emotional stress and the development of cancer. In sum, human data on psychological factors and cancer are controversial, but apparently there is support that psychological stress may contribute to disease manifestation and progression. Concerning infectious diseases, some studies have reported negative findings. However, human data point to a possible role that stress plays in increasing the risk of tuberculosis, influenza, upper respiratory infections in children and adults, as well as recurrences of herpes labialis virus and genital herpes virus, or HIV progression. Biondi (2001) summarizes that psychological stress could act as a cofactor in the pathogenesis, course, and outcome of infectious diseases in animals and humans. The exact role of psychological factors in the pathogenesis and course of specific autoimmune diseases (e.g., rheumatoid arthritis, systemic lupus erythematosis, multiple sclerosis, ulcerative colitis, Crohn’s disease, joint inflammation, psoriasis) is still poorly understood. In view of the clinical complexity of these illnesses, a simple connection between psychological stress and the status of an autoimmune disease cannot be presumed. For asthma bronchiale, there appears to be some support for the assumption that this illness could be exacerbated by psychological stress via immune–inflammatory mechanisms. Finally, the process of wound healing appears to be impaired under chronic as well as minor psychological stress, a process which may be mediated by proinflammatory cytokines (Glaser et al. 1999).

3.4 Stress And The Central Nervous System

Besides numerous peripheral effects of stress, stressinduced secretion of adrenal steroids can also affect the central nervous system (CNS). For example, elevated glucocorticoid levels can impair hippocampal and temporal lobe functioning, brain areas which are involved in declarative, episodic, and short-term memory. While acute stress can profoundly impair memory (effects reversible and relatively short-lived; Kirschbaum et al. 1996), repeated stress can end up in atrophy of the dendrites of pyramidal neurons in the CA3 region of the hippocampus, causing long-term cognitive impairments. Besides its role in memory and cognition, the hippocampus is most important for the negative feedback regulation of the HPA axis. Allostatic load during a lifetime may cause loss of resilience of HPA axis function, resulting in an attenuation of the negative feedback signal that may lead to hyperactivity of this stress system. The connection between the wear and tear on this region of the brain and the dysregulation of the HPA axis is elaborated in detail in the glucocorticoid cascade hypothesis (Sapolsky et al. 1986).

Animal data show that in aged rats, impairments of declarative, episodic, and spatial memory are associated with HPA axis hyperactivity. In elderly humans, Lupien et al. (1998) observed that hippocampal atrophy and cognitive impairment were related to progressive elevations of cortisol levels over a four- year interval.

In sum, animal as well as human data support the idea that elevated glucocorticoid levels could lead to a reduction in hippocampal functioning. Consequences may include the dysregulation of the HPA axis as well as cognitive impairments.

3.5 Stress And Psychological Diseases

Stress is said to be one important parameter, among others, in the manifestation or aggravation of several psychological disturbances, psychosomatic illnesses, and psychiatric disorders, including burnout, anorexia nervosa, chronic fatigue syndrome (CFS), asthma, neurodermatitis, major depression, schizophrenia, or post-traumatic stress disorder (PTSD), which are sometimes referred to as stress-related disorders. The notion that stress contributes somehow to onset or progression of these disorders does not indicate how strong the influence of stress is compared to other important contributing factors, such as genetic predisposition or organic diseases.

However, changes in the regulation of the HPA axis can be related to several stress-related disorders. For example, chronic stress, major depression, schizophrenia, or anorexia nervosa seem to be associated with a hyperactive HPA axis, whereas a hyporeactive HPA axis is found more often in CFS, autoimmune processes, or PTSD. Since there are only few longitudinal data available to date on the relationship between HPA activity and stress-related disorders, the question of cause and effect remains to be answered in future research.

4. Gender Differences In Stress Responses And Health

Gender-specific prevalence rates reveal that men and women are at differential risk for a number of illnesses. Whereas women suffer more often from autoimmune diseases (e.g., multiple sclerosis or systemic lupus erythematosus), men are more prone to develop coronary heart diseases and appear to be more susceptible to infectious diseases. Also, the incidence of psychiatric disorders is not equally distributed between men and women. Diagnoses such as major depression, anxiety, phobia, panic disorder, and obsessive compulsive disorder are more common in women, whereas men more often develop antisocial behavior, abuse substances, or commit suicide. Life expectancy is about seven years higher for women compared to men, although women consistently appear to report more physical as well as somatoform symptoms than men.

Besides this clear gender–disease dimorphism, gender differences also exist in subjective and biological aspects of the human stress response (cf. Kudielka et al. 2000). Concerning subjective verbal reactions to stress, several studies (ranging from everyday hassles to posttraumatic stress reactions) show that women experience and/or report more stress than men. As to HPA axis responses to psychological stress, men showed repeatedly higher ACTH and free, bioavailable, cortisol responses compared to women, but similar total cortisol increases. Only in the luteal phase of the menstrual cycle did women show similar free cortisol responses to those of men (Kirschbaum et al. 1999). There is evidence that these differences are, at least partly, explained by gender differences in the availability of gonadal steroids, especially estrogens.

The finding that men have higher blood pressure changes and higher elevations in epinephrine concentrations under psychological stress parallels the observation that some women seem to be protected from CHD. Estrogen availability is discussed as being a preventive agent for the onset or progression of CHD, but the use of hormone replacement therapy (HRT) for prevention of heart disease is more complex than initially believed. The heart and estrogen progestin replacement study (HERS) was a first large randomized, blind, placebo-controlled secondary prevention trial to evaluate the efficacy and safety of estrogen and progesterone replacement therapy in reducing CHD risk (cf. e.g., Hulley et al. 1998). It was conducted from January 1993 through July 1998, with a mean follow-up of 4.1 years at 20 centers. However, in sum, the results of the HERS study could not support the notion that HRT is a protective measure against CHD.

5. Summary And Conclusion

This research paper has dealt with the origin of stress research, briefly describing the basic aspects of the stress concepts of Cannon, Selye, and Mason. Then, a comprehensive definition of stress by Levine and Ursin (1991) was offered, distinguishing between stress stimuli, individual processing, and stress reactions on three different levels (physiological, behavioral, subjective verbal).

The relationship between stress and health was elucidated using the allostatic load model introduced by McEwen and Stellar (1993): the body’s cost of short-term adaptation to internal and external challenges is allostatic load, which constitutes a wear and tear on the organism. Four different types of allostatic load were presented and related to different health problems, including the cardiovascular system, the immune system, and the CNS. Finally, gender differences in stress responses and health outcome, including psychosomatic and psychiatric diseases, were briefly discussed, with the conclusion that the gender– disease dimorphism could be associated with genderspecific stress responses.


  1. Allen M T, Stoney C M, Owens J F, Matthews K A 1993 Hemodynamic adjustments to laboratory stress: The influence of gender and personality. Psychosomatic Medicine 55: 505–17
  2. Biondi M 2001 Effects of stress on immune functions: An overview. In: Ader R, Felten D L, Cohen N (eds.) Psychoneuroimmunology, 3rd edn. Academic Press, San Diego, CA, Vol. 2, pp. 189–226
  3. Cannon W B 1935 Stresses and strains of homeostasis. American Journal of the Medical Sciences 189(1): 1–14
  4. Cohen S, Tyrrell D A, Smith A P 1991 Psychological stress and susceptibility to the common cold. New England Journal of Medicine 325: 606–12
  5. Dhabar F S 2000 Stress-induced enhancement of immune function. In: Fink G (ed.) Encyclopedia of Stress. Academic Press, San Diego, CA, Vol. 2, pp. 515–23
  6. Dhabar F S, McEwen B S 1997 Acute stress enhances while chronic stress suppresses immune function in vivo: A potential role for leukocyte traffi Brain Behavior and Immunity 11: 286–306
  7. Glaser R, Kiecolt-Glaser J K, Marucha P T, MacCullum R C, Laskowski B F, Malarkey W B 1999 Stress-related changes in proinflammatory cytokine production in wounds. Archives of General Psychiatry 56: 450–6
  8. Hulley S, Grady D, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E 1998 Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen progestin replacement study HERS) research group. Journal of the American Medical Association 280(7): 605–13
  9. Kirschbaum C, Kudielka B M, Gaab J, Schommer N C, Rohleder R, Hellhammer D H 1999 Impact of gender, menstrual cycle phase and oral contraceptives on the activity of the hypothalamic–pituitary–adrenal axis. Psychosomatic Medicine 61(2): 154–62
  10. Kirschbaum C, Wolf O T, May M, Wippich W, Hellhammer D H 1996 Stressand treatment-induced elevations of cortisol levels associated with impaired declarative memory in healthy adults. Life Sciences 58(17): 1475–83
  11. Koch C A, Stratakis C A 2000 Genetic factors and stress. In: Fink G (ed.) Encyclopedia of Stress. Academic Press, San Diego, CA, Vol. 2, pp. 205–12
  12. Kudielka B M, Hellhammer D H, Kirschbaum C 2000 Sex differences in human stress response. In: Fink G (ed.) Encyclopedia of Stress. Academic Press, San Diego, CA, Vol. 3, pp. 424–9
  13. Lazarus R S, Folkman S 1984 Stress, Appraisal, and Coping. Springer, New York
  14. Levine S, Ursin H 1991 What is stress? In: Brown M R, Koob G F, Rivier C (eds.) Stress—Neurobiology and Neuroendocrinology. Marcel Dekker, New York, Chap. 1
  15. Lupien S J, de Leon M, de Santi S, Convit A, Tarshish C, Nair N P, McEwen B S, Hauger R L, Meaney M J 1998 Cortisol levels during human aging predict hippocampal atrophy and memory deficits [published erratum appears in Nature Neuroscience 1998, 1(4): 329]. Nature Neuroscience 1: 69–73
  16. Manuck S B, Kaplan J R, Adams M R, Clarkson T B 1988 Studies of psychosocial influences on coronary artery atherogenesis in cynomolgus monkeys. Health Psychology 7: 113–24
  17. Mason J W 1968 A review of psychoendocrine research on the sympathetic–adrenal medullary system. Psychosomatic Medicine 30: 631–53
  18. Mason J W 1975 A historical view of the stress field. Journal of Human Stress 1: 6–12
  19. McEwen B S 2000 Allostasis and allostatic load. In: Fink G (ed.) Encyclopedia of Stress. Academic Press, San Diego, CA, Vol. 1, pp. 145–50
  20. McEwen B S, Stellar E 1993 Stress and the individual. Archives of Internal Medicine 153: 2093–101
  21. Meaney M J, Tannenbaum B, Francis D, Bhatnagar S, Shanks N, Viau V, O’Donnell D, Plotsky P M 1994 Early environmental programming hypothalamic pituitary–adrenal responses to stress. Seminars in Neuroscience 6: 247–59
  22. Michelson D, Stratakis S, Hill L, Reynolds J, Galliven E, Chrousos G, Gold P 1996 Bone mineral density in women with depression. New England Journal of Medicine 335: 1176–81
  23. Sapolsky R M 1994 Why Zebras Don’t Get Ulcers. W H Freeman, New York
  24. Sapolsky R M, Krey L C, McEwen B S 1986 The neuroendocrinology of stress and aging: The glucocorticoid cascade hypothesis. Endocrine Review s 7: 284–301
  25. Selye H 1936 A syndrome produced by diverse nocuous agents. Nature 32
  26. Selye H 1937 Studies on adaptation. Endocrinology 21(2): 169–88
  27. Selye H 1983 The stress concept: past, present, and future. In: Cooper C L (ed.) Stress Research. Wiley, Chichester, UK, pp. 1–20
  28. Steptoe A 2000 Health behavior and stress. In: Fink G (ed.) Encyclopedia of Stress. Academic Press, San Diego, CA, Vol. 2, pp. 322–6
  29. Sterling P, Eyer J 1988 Allostasis: A new paradigm to explain arousal pathology. In: Fisher S, Reason H S (eds.) Handbook of Life Stress, Cognition and Health. Wiley, New York, pp. 629–49
  30. Wust S, Federenko I, Hellhammer D H, Kirschbaum C 2000 Genetic factors, perceived chronic stress, and the free cortisol response of awakening. Psychoneuroendocrinology 25: 707–20
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