Acute Stress Disorder and Posttraumatic Stress Disorder

Whereas traumatic stress in acute stress disorder (ASD) persists for at least two days to four weeks, the stress associated with post traumatic stress disorder (PTSD) is longer term and the repercussions from the trauma are ongoing and become chronic (Laureate Education, Inc., 2012). The symptoms of ASD and PTSD are similar in that the experiences of the incident or event are frightening or fear inducing. The primary difference between these two stress disorders is the biological component of PTSD and the sequelae associated with the trauma, specifically the dysfunction of the HPA axis stress response, an overactive amygdala, and the reduction in size of the hippocampus (Laureate Education, Inc., 2012). The ramifications of these brain changes are dysruptions in the normal functioning of emotions and memory, incapacitating stress, the chronic revisiting of the stressful event(s).

Potential PTSD Symptoms in Military Health Worker

Although an abundance of contemporary research exists on PTSD, there is a paucity of research on the post traumatic stress of military healthcare professionals (Akbayrak et al., 2006; Gibbons, Hickling, & Watts, 2012; Ikin, 2004). Military health workers are as apt to experience psychological trauma as anyone in any other occupation (Akbayrak et al., 2005). Kolkow (2007) found that up to 9% of military health workers fill the criteria for PTSD. Biological changes in the brain can cause these workers to continue to recall the memories of their experiences inaccurately, recalling the stress and trauma of the death of many individuals, rather than the helping element of their role in the military. The potential exists for them to consider medical professionals as ineffectual in their roles as doctors and nurses because of the skewed perception of their own distressing experiences (Akbayrak et al., 2005).

Female nurses working in the Vietnam war experienced a chronic ongoing danger to themselves because of ongoing attacks and explosions close by to where they worked (Gibbons, Hickling, & Watts, 2012). A common experience for military health workers with PTSD is to feel unsafe even in safe circumstances, and to feel the constant pressure of threat to one's personal safety (Kolkow, 2007). Protective for this group of nurses working in Vietnam was social support, having a sense of purpose, and keeping a positive outlook (Gibbons et al., 2012). Another symptom of nurses was a general sense of inadequacy from being on the frontlines of disaster without effective means to mediate the needs of their patients (Akbayrak et al., 2005). Because the female gender experiences a higher rate of the symptoms associated with post traumatic stress, these feelings may be gender specific (Akbayrak et al., 2005).

Whatever the trauma, and whoever experiences it, the ramifications of these experiences should be taken seriously despite whether the individual fills the criteria of PTSD (Akbayrak et al., 2005). Experiences post trauma can cause a range of psychological and social problems (Akbayrak et al., 2005). Biological ramifications of trauma include permanent biological alterations in the brain (Laureate Education, Inc., 2012). It may not be unreasonable to believe that traumas that may not cause a diagnosable case of PTSD, can cause damage, and should be attended.

Effective Intervention Techniques

Joseph (2004) found incidences of post-traumatic growth, however, for many individuals, the effects of traumatic events after the fact can cause chronic symptoms (Laureate Education, Inc., 2012). Proactive interventions such as self-care and social support groups have been proven effective for female military personnel in health care positions, although in these circumstances, women seem to be more resilient than men (Gibbons et al., 2012).

It may be effective to teach military personnel about PTSD, and teach them techniques to manage stress and anxiety (Hourani, Council, Hubal, & Strange, 2011). Coping skills training may be effective for military personnel and has been successful in secular populations. Psychoeducation, for example, providing information on psychological symptoms experienced after traumatic events, may encourage these workers to seek help, rather than to remain reticent about stress, depression, and chronic feelings of fear, which are common experiences in PTSD (Hourani et al., 2011). However, there is a paucity of research on psychoeducational interventions and little empirical evidence that it is helpful overall in encouraging military personnel to seek help (Hourani et al., 2011).

Stress inoculation training (SIT) has been effective when implemented during pre- and post-deployment. SIT has been effective for reducing stress and increasing coping skills in military personnel by preparing them psychologically and fostering resilience against the stress of wartime (Houdini et al., 2011). In addition, developing peer and social support systems prior to deployment may be as effective as it was for nurses in Vietnam (Gibbons et al., 2012). For example, creating a buddy system or small groups of workers who meet for the sole purpose of discussing stress and the trauma of war settings may create a valuable social support system.

References

Akbayrak, N., Oflaz, F., Aslan, O., Ozcan, C., Tastan, S., & Ciçek, H. (2005). Post-traumatic stress disorder symptoms among military health professionals in Turkey. Military Medicine, 170(2), 125-129.

Dougall, A. L., & Swanson, J. N. (2011). Physical health outcomes of trauma. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (pp. 373–384). New York, NY: Springer Publishing Company.

Gibbons, S. W., Hickling, E. J., & Watts, D. D. (2012). Combat stressors and post-traumatic stress in deployed military healthcare professionals: an integrative review. Journal Of Advanced Nursing, 68(1), 3-21. doi:10.1111/j.1365-2648.2011.05708.x

Hourani, L. L., Council, C. L., Hubal, R. C., & Strange, L. B. (2011). Approaches to the primary prevention of posttraumatic stress disorder in the military: A review of the stress control literature. Military Medicine, 176(7), 721–730.

Ikin, J. F. (2004). War-related psychological stressors and risk of psychological disorders in Australian veterans of the 1991 Gulf War. The British Journal of Psychiatry, 185(2), 116-126. doi: 10.1192/bjp.185.2.116

Joseph, S. (2004). Client-centered psychotherapy, post-traumatic stress, and post-traumatic growth: theoretical perspectives and practical implications. Psychology and Psychotherapy: Theory, Research and Practice. 77(1), 101-119.

Kolkow, T., Spira, J., Morse, J., & Grieger, T. (2007). Post-traumatic stress disorder and depression in health care providers returning from deployment to Iraq and Afghanistan. Military Medicine, 172(5), 451-455.

McCauley, M., Hughes, J., & Liebling-Kalifani, H. (2010). Wellbeing of military mental health staff. Mental Health Practice, 14(4), 14-19.

Depression and Chronic and Autoimmune Diseases

                                   Depression and Chronic and Autoimmune Diseases

Depression has a powerful affect on the immune and inflammatory response systems. It increases cortisol and other inflammatory cytokines such as IL-6, and an enzyme called IDO (Müller & Schwarz, 2007). These substances decrease the body's ability to heal, which can increase vulnerability to autoimmune diseases such as systemic lupus erythematosus (SLE). The goal of this paper is to describe the association between depression and SLE, explain the factors of the disease that account for its high co-occurrence with depression, and discuss the role of stress hormones and inflammation in SLE. Further, it will explain three teaching strategies that might reduce the effects of SLE and effective methods to encourage the adoption of strategies to reduce the effects of SLE.

                                         Depression and Systemic Lupus Erythematosus

High levels of inflammatory factors and depression are characteristic of many autoimmune diseases (Laureate Education, Inc., 2012). For example, depression is highly comorbid with systemic lupus erythematosus (SLE). More than 65% of patients with chronic rheumatological disorders, such as SLE suffer from depression (Maes et al., 2011). Patients with SLE have several comorbidities including hypertension, gall bladder disorders, cataracts, cardiovascular disease, and neurologic and endocrine disorders (Wolfe et al., 2010). Almost 40% of patients with SLE are diagnosed with depression, which, has been linked to a lower life quality (Wolfe et al., 2010). Palagini et al., (2013) claimed SLE is co-occuring with depression in 14% to 89% of patients. Women with SLE have at least a 47% chance of being diagnosed with depression. Further, anxiety and depression have been associated to permanent deformation of the joints and active inflammation in SLE patients (Waheed, Hameed, Khan, Syed, & Mirza, 2006). Depression is, however, the most prevalent comorbidity associated with SLE (Wekking, 1993).

                                   The Role of Stress Hormones and Inflammation in SLE

Depression associated with SLE may be mediated by an autoimmune mechanism (Palagini et al., 2013). Bachen, Chesney, and Criswell (2009) hypothesized proinflammatory cytokines play a role in SLE's inflammatory response. The body's cytokine immune response has been implicated in depression as well as in some autoimmune diseases (Wilson & Warise, 2008). Cytokines are immune proteins that regulate the immune system, especially during a stress response (Wilson & Warise, 2008). Cytokines, have an inflammatory effect on the neurotransmission of serotonin, a neurotransmitter that has been known to have a profound effect on psychological health and well-being (Dabhar, 2011; Salih & Feyza, 2012; Wilson & Warise, 2008).

SLE and other chronic inflammatory diseases are associated with depression (Wilson & Warise, 2008). It is well known that stress exacerbates symptoms of SLE (Peralta-Ramirez, Jimenez-Alonso, Godoy-Garcia, & Perez-Garcia, 2004). Further, cytokine imbalances are characteristic of autoimmune diseases, such as SLE, especially during its beginning stages as well as during disease progression (Freiri, 2003). When an excess of cytokines are flushed into the blood stream during stress, an enzyme called IDO is activated, and this enzyme degrades serotonin (Müller & Schwarz, 2007). This inflammatory process degrades the body's serotonergic system, which decreases the body's ability to manufacture serotonin. The lowered level of serotonin leaves the individual more susceptible to depression.

Maes (2010) found depression shares the same inflammatory pathways with other diseases, and rather than the existence of two separate degenerative processes, for example, one for SLE, and one for depression, these comorbidities may be symptoms of one degenerative process. Inflammatory processes may have a variety of causes, such as diet, lifestyle, and genetic predispositions, but the biological process may be singular (Maes, 2010). In addition, Maes (2010) found that this shared biological process is bidirectional, and cyclical, in that inflammation provoked degeneration and vice versa.

                                             Teaching Strategies to Reduce Anxiety
Cognitive-Behavioral Stress Management

Cognitive-behavioral stress management (CBSM) has been proven effective in ameliorating stress that accompanies chronic illness and has been shown to help individuals cope effectively with disease-related treatment and manage social resources (Nezu, Nezu, & Xanthopoulos, 2011). CBSM increased individuals' ability to find benefit in their illness as well as their ability to remain optimistic amid the challenge of chronic disease (Nezu et al., 2011). Stress and anxiety are common in SLE patients, and in general, they are not as aware of effective coping strategies as the general population, and the strategies they tend to use are inadequate and less effective than other strategies such as CBSM (Peralta-Ramirez et al., 2004). Patients who implemented CBSM perceived themselves less likely to have a flare of symptoms, felt confident about their future, experienced significant improvement in their psychological health and well-being, felt more vital, and experienced significantly less pain (Peralta-Ramirez et al., 2004).

Exercise

Exercise has been shown to be a possible antidepressant and it exercise also generates neurons in adults (National Institute on Mental Health, 2010). Home-based exercise made a significant difference in a group of sedentary women with SLE (Yuen et al., 2013). Physical exercise was proven useful and successful in improving symptoms of SLE without provoking disease activity (Reis-Neto, Silva, Monteiro, Camargo, & Sato, 2013). Similarly, Ayán and Martín (2007) concluded SLE patients can benefit from exercise.

Relaxation Techniques

Smith and Balaban (1983) found behavioral therapy that included deep relaxation, hypnosis and psychodynamic psychotherapy was effective for pain management, coping, and negative emotions associated with the stress of SLE. Torem (2007) postulated the immune system interacts with the central nervous system, and believed hypnosis and imagery could affect the immune system. Torem found this treatment effective in patients with autoimmune diseases. Zhang, Wei, and Wang (2013) discovered psychological interventions had the potential to help patients with SLE manage negative emotions and reduce stress.

Encouraging Health Behavior Change
Changing health behaviors is a complex undertaking, and effective interventions must consider the individual (Glanz, Rimer, & Viswanath, 2008). The Transtheoretical Model (TTM) of behavior change is concerned with individually tailored interventions (Brug, 2004). When encouraging behavior change, it seems important to account for various individual factors in patients, especially their stage of understanding and their readiness for education. The TTM takes into account patients' attitudes and beliefs, which will have an effect on whether they can make changes in their health behavior (Glanz et al., 2008). Because this model of behavior change accommodates individual needs, it may be a salient component in developing effective interventions (Velicer, Redding, Sun, & Prochaska, 2007). This may be especially true in patients with SLE because this population has fewer effective stress management strategies than the general population (Peralta-Ramirez et al., 2004). Lack of awareness, education, and experience, may contribute to this deficiency, and understanding their personal experience and readiness may be important in establishing durable behavior change.

                                                                     Conclusion

Depression is commonly found in a significant number of individuals diagnosed with SLE. The body's inflammatory immune response to stress has been implicated in depression and autoimmune diseases, such as SLE (Wilson & Warise, 2008). In particular, proinflammatory cytokines play a role in depression as well as in SLE's inflammatory response (Bachen, Chesney, & Criswell, 2009). Maes (2010) hypothesized that depression and illnesses such as SLE may share inflammatory pathways and a foundational cause. Since lifestyle and stress have the potential to cause inflammation, exercise, CBSM, and relaxation techniques may provide relief and decrease symptoms of depression and SLE (Zhang, Wei, & Wang, 2012). Utilizing the TTM, effective coping and stress management strategies that account for personal readiness can be developed for positive health outcomes and to instigate durable behavior change (Glanz et al., 2008).

References

Ayán, C., & Martín, V. (2007). Systemic lupus erythematosus and exercise. Lupus, 16(1), 5-9. Bachen, E., Chesney, M., & Criswell, L. (2009). Prevalence of mood and anxiety disorders in women with systemic lupus erythematosus. Arthritis & Rheumatism: Arthritis Care & Research, 61(6), 822-829. doi:10.1002/art.24519

Brug, J. (2004). The Transtheoretical Model and stages of change: A critique: Observations by five Commentators on the paper by Adams, J. and White, M. (2004) Why don't stage- based activity promotion interventions work? Health Education Research, 20(2), 244- 258. doi: 10.1093/her/cyh005

Dhabhar, F. S. (2011). Effects of stress on immune function: Implications for immunoprotection and immunopathology. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (pp. 47–63). New York, NY: Springer Publishing Company.

Frieri, M. (2003). Neuroimmunology and inflammation: Implications for therapy of allergic and autoimmune diseases. Annals of Allergy, Asthma, & Immunology, 90(6, Suppl. 3), 34-40.

Glanz, K., Rimer, B. K., & Viswanath, K. (Eds.). (2008). Health behavior and health education: Theory, research, and practice (4th ed.). San Francisco, CA: Jossey-Bass.

Laureate Education, Inc. (2012). Stress, the immune system, chronic illness, and your body. [Handout].

Maes, M. (2010). An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways. Progress in Neuro-Psychopharmacology and Biological Psychiatry. doi: 10.1016/j.pnpbp.2010.06.023

Maes, M. M., Kubera, M. M., Obuchowiczwa, E. E., Goehler, L. L., & Brzeszcz, J. J. (2011). Depression's multiple comorbidities explained by (neuro) inflammatory and oxidative & nitrosative stress pathways. Neuroendocrinology Letters, 32(1), 7-24.

Müller, N., & Schwarz, M. J. (2007). The immune-mediated alteration of serotonin and glutamate: Towards an integrated view of depression. Molecular Psychiatry, 12(11), 988- 1000. doi: 10.1038/sj.mp.4002006

National Institute of Mental Health. (Producer). (2010, November 23). NIMH investigators talk about new evidence that suggests exercise and positive environment can help hedge against stress related depression [Audio podcast]. NIH Radio. Retrieved from http://www.nimh.nih.gov/media/audio/nih-radio-nimh-investigators-talk-about-new- evidence-that-suggests-exercise-and-positive-environment-can-help-hedge-against-stress- related-depression.shtml

Nezu, A. M., Nezu, C. M., & Xanthopoulos, M. S. (2011). Stress reduction in chronically ill patients. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (p. 475-500). New York, NY: Springer Publishing Company.

Palagini, L., Mosca, M., Tani, C., Gemignani, A., Mauri, M., & Bombardieri, S. (2013). Depression and systemic lupus erythematosus: a systematic review. Lupus, 22(5), 409- 416. doi:10.1177/0961203313477227

Peralta-Ramírez, M., Jiménez-Alonso, J., Godoy-García, J., & Perez-García, M. (2004). The effects of daily stress and stressful life events on the clinical symptomatology of patients with lupus erythematosus. Psychosomatic Medicine, 66(5), 788-794.

Reis-Neto, E., Silva, A., Monteiro, C., Camargo, L., & Sato, E. (2013). Supervised physical exercise improves endothelial function in patients with systemic lupus erythematosus. Rheumatology (Oxford, England), [serial online].

Salih, G., & Feyza, A. (2012). Inflammation in depression: the role of cytokines. Journal Of Marmara University Institute Of Health Sciences, 2(3), 103-107.

Smith, S. J., & Balaban, A. B. (1983). A multidimensional approach to pain relief: Case report of a patient with Systemic Lupus Erythematosus. International Journal Of Clinical And Experimental Hypnosis, 31(2), 72-81. doi:10.1080/00207148308406594

Torem, M. S. (2007). Mind-Body Hypnotic Imagery in the Treatment of Auto-Immune Disorders. American Journal of Clinical Hypnosis, 50(2), 157-170. doi: 10.1080/00029157.2007.10401612

Velicer, W. F., Redding, C. A., Sun, X., & Prochaska, J. O. (2007). Demographic variables, smoking variables, and outcome across five studies. Health Psychology, 26, 278-287.

Wilson, D. R., & Warise, L. (2008). Cytokines and their role in depression. Perspectives in Psychiatric Care, 44(4), 285–289.

Waheed, A., Hameed, K., Khan, A., Syed, J., & Mirza, A. (2006). The burden of anxiety and depression among patients with chronic rheumatologic disorders at a tertiary care hospital clinic in Karachi, Pakistan. JPMA. The Journal Of The Pakistan Medical Association, 56(5), 243-247.

Wolfe, F., Michaud, K., Li, T., & Katz, R. (2010). Chronic conditions and health problems in rheumatic diseases: comparisons with rheumatoid arthritis, noninflammatory rheumatic disorders, systemic lupus erythematosus, and fibromyalgia. Journal Of Rheumatology, 37(2), 305-315. doi:10.3899/jrheum.090781

Wekking, E. (1993). Psychiatric symptoms in systemic lupus erythematosus: an update. Psychosomatic Medicine, 55(2), 219-228.

Yuen, H., Breland, H., Vogtle, L., Holthaus, K., Kamen, D., & Sword, D. (2013). The process associated with motivation of a home-based Wii Fit exercise program among sedentary African American women with systemic lupus erythematosus. Disability And Health Journal, 6(1), 63-68. doi:10.1016/j.dhjo.2012.08.003

Zhang, J., Wei, W., & Wang, C. (2012). Effects of psychological interventions for patients with systemic lupus erythematosus: a systematic review and meta-analysis. Lupus, 21(10), 1077-1087. doi:10.1177/0961203312447667

The Relationship between Stress and Depression

The relationship between stress and depression is complex (Laureate Education, Inc., 2012). It is bidirectional in that stress can cause depression and depression can cause and exacerbate stress (Laureate Education, Inc., 2012; Wilson & Warise, 2008). In an effort to understand the inextricable interconnectedness of the immune system and depression, one might wonder if depression, like other diseases, is a product of inflammation. In any event, inflammation and the immune response are implicated in depression. Although depression may lead to inflammation (Wilson & Warise, 2008) but inflammation can lead to depression (Musselman et al., 2001).

Factors that Influence Depression

One of the body's primary responses to stress is the surge of cytokines, specifically interleukins and interferons, through the blood to defend the body against pathogenic invaders. The body's cytokine immune response has been implicated in depression as well as in some autoimmune diseases (Wilson & Warise, 2008).

Cytokines Causing Symptoms of Sickness

Cytokines are immune proteins that regulate the immune system, especially during a stress response (Wilson & Warise, 2008). This dispatch can cause overall feelings of fatigue and malaise that can contribute to depression. When stress forces this immune response, the resulting fatigue and reduced motivation can cause frustration, anxiety, and additional stress. Stress has been defined as the increasing incongruence between the needs of the individual and his or her environment (Storch, Gaab, Küttel, Stüssi, & Fend, 2007). For example, if an individual's stress level has positioned her on the brink of depression, the growing difference between her ability to accomplish her daily responsibilities with her suboptimal level of physical energy and decreased motivation could cause further frustration and problems at work, exacerbating her level of stress, and contributing to the development of depression. This is an example of the bidirectional character of the relationship between the stress and depression.

Cytokines Affect on Serotonin

Another influence of cytokines is their inflammatory effect on the neurotransmission of serotonin, which plays an important role in psychological health and well-being (Dabhar, 2011; Salih & Feyza, 2012; Wilson & Warise, 2008). Inflammation has an effect on the body's ability to manufacture serotonin. Further, cytokines have an influence on the other neurotransmitters dopamine and norepinephrine, both of which are integral to well-being. When cytokines are flushed into the blood stream by the immune system, they activate an enzyme called IDO, which degrades serotonin (Müller & Schwarz, 2007). In addition, this enzyme has an effect on tryptophan, which is the precursor to serotonin. With lower levels of serotonin in the system, the individual is more susceptible to depression. In effect, the inflammation from the immune response destroys serotonin (Müller & Schwarz, 2007). When cytokines are administered as a medical treatment for disease, side effects are known to cause social problems, insomnia, and a decline in cognitive functioning, all of which are symptomatic in depression (Raison, Demetrashvili, Capuron, & Miller, 2005).

Depression and the Immune and Inflammatory Response Systems

Depression has a powerful affect on the immune and inflammatory response systems. It increases stress hormones such as cortisol and other inflammatory cytokines such as IL-6, and the aforementioned IDO (Müller & Schwarz, 2007). These substances decrease the body's ability to heal, which can increase vulnerability to other diseases, even some types of cancer and autoimmune diseases such as lupus and osteoporosis. IL-6 has been implicated in decreased immune functioning and chronic inflammation and has been frequently studied in depression (Salih & Feyza, 2012). High levels of IL-6 have been found in depressed patients as well as in cancer patients. In effect, an increase in cytokines typically induces sickness behaviors, and the same increase has been found in depressed individuals (Müller & Schwarz, 2007; Salih & Feyza, 2012).

On a personal note, it is somewhat exciting to learn about the implications of inflammation in depression. However, my excitement is tempered by considering the complex relationship between the environment, individual genetics and perceptions, and biology, and the fact that likely there is not a sole cause of depression. Maintaining a holistic perspective continues to benefit research, individual case conceptualization, and the development of interventions for depression (Gutman, & Nemeroff,, 2011; Raison et al., 2005).

References

Dhabhar, F. S. (2011). Effects of stress on immune function: Implications for immunoprotection and immunopathology. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (pp. 47–63). New York, NY: Springer Publishing Company.

Gutman, D. A., & Nemeroff, C. B. (2011). Stress and depression. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (pp. 345–357). New York, NY: Springer Publishing Company.

Laureate Education, Inc. (2012). Stress, the immune system, chronic illness, and your body. [Handout].

Müller, N., & Schwarz, M. J. (2007). The immune-mediated alteration of serotonin and glutamate: Towards an integrated view of depression. Molecular Psychiatry, 12(11), 988-1000. doi: 10.1038/sj.mp.4002006

Musselman, D. L., Miller, A. H., Porter, M. R., Manatunga, A., Gao, F., Penna, S., & ... Nemeroff, C. B. (2001). Higher Than Normal Plasma Interleukin-6 Concentrations in Cancer Patients With Depression: Preliminary Findings. American Journal of Psychiatry, 158(8) 1252-1257.

Salih, G., & Feyza, A. (2012). Inflammation in depression: the role of cytokines. Journal Of Marmara University Institute Of Health Sciences, 2(3), 103-107.

Wilson, D. R., & Warise, L. (2008). Cytokines and their role in depression. Perspectives in Psychiatric Care, 44(4), 285–289.

Zhang, S. (2012). A biological explanation for depression: The role of interleukin-6 in the aetiology and pathogenesis of depression and its clinical implications. Australian Medical Student Journal, 3(2), 24-26.

Stress and Illness

Brief Description of Breast Cancer

The illness I have chosen for this discussion is breast cancer. Breast cancer has become a common disease affecting 12% of women (American Cancer Society, 2013). More than 230,000 new cases of breast cancer are diagnosed each year, and approximately 40,000 women will die this year from breast cancer. Although the number of women being diagnosed with breast cancer has declined during the last two decades, this disease continues to affect a significant number of women (ACS, 2013). It remains the second leading cause of death for women (ACS, 2013). Although a significant number of women have no known risk factors, some women are more susceptible than others. Some research has implicated stress as a risk factor for this cancer type (Pudrovska, Carr, McFarland, & Collins, 2013). Other research, however, found women who experienced job strain were less inclined to utilize mammographic screening, but found no association between job stress and breast cancer (Achat, Kawachi, Byrne, Hankinson & Colditz, 2000).

Susceptibility and Vulnerability

The two populations used for this discussion are women in lower socioeconomic occupational positions and women in higher socioeconomic occupational jobs and positions of authority. The latter group, who have the ability to determine the compensation of other employees and the authority to hire and fire workers has a higher risk of being diagnosed with breast cancer than women in the former group (Pudrovska, Carr, McFarland, & Collins, 2013; Pudrovska, 2013). In a longitudinal 54-year study, women exposed to the job stress of positions of authority had an increased risk of breast cancer.

These findings are paradoxical to the idea that individuals in higher socioeconomic life positions and socioeconomic status groups have increased health advantages compared to individuals from lower socioeconomic groups (Jannings & Reibert, 2012; Williams, Mohammed, Leavell, & Collins, 2010). Chandola and Marmot (2011) explained that lower socioeconomic status has been linked to increased stress in the work environment, and further that lower socioeconomic groups might be more susceptible to an increase in biological stress responses. Needham et al., (2013) found leukocyte telomere length, which is a marker of cell aging, and associated with stressful life experiences, was shorter in individuals who failed to complete high school, compared to individuals who were college educated. This augments the body of contemporary scholarship that demonstrates a link between lower socioeconomic status and cell aging, conveying an intrinsic biological benefit to higher socioeconomic groups. However, Pudrovska et al. (2013) found contradictory evidence that suggests high-powered women were more susceptible to breast cancer.

Stress and Coping in Both Populations

Women in higher socioeconomic groups, such as those in positions of occupational power are known to have greater accessibility to resources that enable them to manage stress and cope more effectively in stressful situations (Jannings & Reibert, 2012). Because of more easily accessible resources, the higher socioeconomic group might appraise stress as manageable (Lazarus, 1991). In any event, because of their high-powered positions, they are exposed to long-term stress that affects and causes dysregulation of the clucocorticoid system. Subsequent exposure of breast tissue to chronically elevated cortisol levels explains the higher risk of professional women to breast cancer (Pudrovska et al., 2013).

Women in higher paying jobs may have an increased accessibility to resources and subsequently the ability to appraise stress as more manageable than women without adequate resources. The former group, however, was continually exposed to the stress of occupational positions traditionally reserved for men, and this stress was not experienced by housewives and workers in lower socioeconomic positions to the same extent (Ridgeway, 2001). Chronic social stress and the subsequent exposure to stress hormones has been proven to be at least partly culpable in breast cancer. Stress hormones, specifically cortisol exposure has been shown to be an underlying psychophysiological pathway to breast cancer (Antonova et al., 2011). The higher powered women were chronically exposed to higher cortisol levels (Pudrovska et al., 2013).

Conclusion

Women in higher socioeconomic positions may have the potential to resolve stress in ways less accessible to women in lower socioeconomic positions. However, these benefits do not appear to extend to chronic stress specific to their high powered positions and the subsequent exposure to high levels of cortisol that may lead to breast cancer. Women in positions of authority may be exposed to chronic stress that is less easily mitigated by the resources available to them. Housewives and women in lower socioeconomic occupational settings may have fewer resources for mitigating stress, however, they may not be exposed to the higher intensity chronic stress that may lead to breast cancer.

References

Achat, H., Kawachi, I., Byrne, C., Hankinson, S., & Colditz, G. (2000). A prospective study of job strain and risk of breast cancer. International Journal of Epidemiology, 29(4), 622-628. doi: 10.1093/ije/29.4.622

Antonova, L., Aronson, K., & Mueller, C. (2011). Stress and breast cancer: from epidemiology to molecular biology. Breast Cancer Research, 13(2).

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Jannings, A., & Reibert, S. (2012). Socioeconomic Status and Health Implications. Hauppauge, N.Y.: Nova Science Publisher's.

Chandola, T., & Marmot, M. G. (2011). Socioeconomic status and stress. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (pp. 185–193). New York, NY: Springer Publishing Company.

Davis, M. C., Burleson, M. H., & Kruszewski, D. M. (2011). Gender: Its relationship to stressor exposure, cognitive appraisal/coping processes, stress responses, and health outcomes. In R. J. Contrada & A. Baum (Eds.), The handbook of stress science: Biology, psychology, and health (pp. 247–261). New York, NY: Springer Publishing Company.

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