Mind, Body and Immunity - Research Paper Example

? Psychoneuroimmunology and Stress submitted Psychoneuroimmunology and Stress Introduction Psychoneuroimmunology (PNI) is a theoretical branch of medical investigation that examines the relationship between the manifestations of clinical disease and how the brain effects such manifestations (Reddy, 2010). To break this analysis down further, PNI constitutes the analysis of the dynamic coalescence of “consciousness (psycho)”, the “brain and central nervous system (neuro)”, and the body’s protection from “infection and internal aberrant cell division (immunology)” (Reddy, 2010). As a part of every day life and an acknowledged catalyst of illness, this discourse will seek to examine the psychoneuroimmunological effects of stress on overall human health (Lorentz, 2006). Through an exhaustive literature review and analysis of relevant research regarding PNI, stress, and the relational determinants that affect health, this paper will attempt to illustrate how stress can negatively impact overall health and how measures to directly counteract every day stressors can improve health and the quality of life. Literature Review Mind, Body, & Immunity While the study of “mind-body interactions” have been of interest in philosophical studies since the times of the ancient Greeks, the direct effects of stress, specifically on the immune system is a relatively new science (Benowitz, 1996; Glaser, 2004; Tausk, Elenkov, & Moynihan, 2008). The study of ‘‘psychoneuroimmunology’’ did not exist prior to 1981 and the first dedicated psychoneuroimmunology summit was not held until 1986 (Tausk, Elenkov, & Moynihan, 2008). At this first assembly, the primary goals to be addressed through exploration of this theoretical approach to to medicinal practice were declared in these proposed research questions: “Are there interactions between the brain and the immune system? If so, how are they mediated? Are they bi-directional? and Are they trivial or important to understanding health and disease?” (Tausk, Elenkov, & Moynihan, 2008, p.645) Examination of the linkage between the immunoregulatory process and stress levels facilitated the introduction of psychoneuroimmunology and the investigation of the immune system, not as the body’s autonomous defense system, but as responses that are subjectively caused by the brain (Ader, 2000). Furthermore, studies have shown that stress changes the fragile equilibrium forging the barrier between health and disease (Tausk, Elenkov, & Moynihan, 2008). As Tausk, Elenkov, & Moynihan (2008) present, the multitude of studies indicating that non-pharmacologic methods like PNI can successfully alleviate an abundance of various skin ailments diseases can only serve to provide healthcare providers with better ways to treat their patients. For the purpose of this paper, we will use the definition of stress as follows: “Stress generally refers to demands placed on the body that threaten homeostasis” (Bauer-Wu, 2002, p.3). Neural and endocrine functions and behavior are all aspects affected by the immune system and psychoneuroimmunology seeks to study the relational reactions between the function of the immune system and endocrine, neural, and behavioral processes (Ader, 2000). Furthermore, the connection between the immune system and the nervous system can allow stress factors to directly alter human behavior, thought and mood, which can cause physically illness (Azar, 2001). These determinations have stimulated research into the exact proportions of the influences stress factors can have on human physical well-being and the precise dimensions of these affects through the scientific examination of psychoneuroimmunology and stress. The theory of psychoneuroimmunology is continually being examined in a wide ranging and ever increasing array of medical specifications, including cancer, heart disease, and mental health venues such as depression, inflammatory disorders, HIV/AIDS, and many other aspects of healthcare (Hodo, 2001; McCain, Gray, Walter, & Robinsons, 2005). The development of procedures and practices using PNI techniques is not only being developed by doctors and scientists, but also by nurses and many others within the medical community (Bauer-Wu, 2002). Establishing the relationships between various functions of the physical body, their immunological reactions, and cognitive reactions will allow medical professionals and the scientific community to design more effective treatment methods that treat the body on a holistic level rather that simply treating the illness (Tausk, Elenkov, & Moynihan, 2008). Essentially, the basic function of the endocrine system involve neurotransmitters, hormones, and neuropeptides regulating immune cells, and these communicate with nervous tissue through the secretion of various cytokines (Tausk, Elenkov, & Moynihan, 2008). However, the depth and overall impact of the effect of these aspects are also determined by individual physical and environmental characteristics in addition to biological, although it is duly noted that individual perceptions of contributory stress factors are constantly changing, and this can affect established PNI relationships (McCain, Gray, Walter, & Robinsons, 2005). External stress (e.g., death of a loved one) is a cognitive sensory stimulus with initial processing through the peripheral and central nervous systems. Internal sensory input, or noncognitive stress (e.g., viral infection), is received by the immune system, which relays this information to the neuroendocrine system (Bauer-Wu, 2002). The variations in the terms and parameters of what constitutes as stress has facilitated demands for solid delineations of this primary constituent in establishing its import in relation to PNI (Apanius, 1998). This factor is especially vital to proper relational identification since stress can cause different immunological reactions with short term and long term exposure to stressors (Apanius, 1998). The bidirectional pathways that link the brain and the immune system are the core venues that enable response stimulation and the duration of the stress factors on the conditioned reactions that occur between the brain and the nervous system can cause variations in the immunological responses stimulated (Ader, 2001). Lymphocytic reactions are translated into hormonal excretions that produce physical effect to the immunological stimulation (Ader, 2001). The nervous and endocrine systems sustain widespread communication with the immune system by manipulating hormones, neurotransmitters, and the function of the sympathetic and parasympathetic nerves to the lymphoid organs (Briones, n.d.). Effectually, the stronger and longer the duration of the stimuli, the more intensely the immune system will react, which can manifest in mild to severe illnesses (Halldorsdottir, 2007). PNI & Emotions Science is further breaking down the relationship between stress and PNI by providing evidence of the negative emotions commonly generated by anxiety, which can intensify the detrimental effects of a variety of health threats and result to sustained infection and delay the wound healing process, fueling the continuation of prointiammatory cytokine production (Halldorsdottir, 2007). According to Caine (2003), studies indicate that: “…depressed and anxious mood states are associated with decreases in lymphocyte proliferation and the activity of natural killer cells and with changes in the number of white blood cells and the quantity of antibody circulating in the blood. Moreover, stress is associated with changes in the functioning of immune cells. Links between negative [stress factors] and psychological states such as anxiety, depression, hopelessness, and grief and the immune system have been explored” (p.65). Results suggest that depressed and anxious mood states are associated with decreases in lymphocyte proliferation and the activity of natural killer cells and with changes in the number of white blood cells and the quantity of antibody circulating in the blood (Caine, 2003). These determinations have been noted as far back as 1993 in similar research conducted by Ader & Cohen, who deduced that the nervous and immune systems, which are the two most multifaceted systems that play a significant role in the regulation of human homeostasis, are broader functions of an interconnected causative system that ensures the ability of the individual or the species to assimilate. Langley, Fonesca, & Iphofen (2006) define homeostasis as “the ability of the body to maintain internal stability, despite environmental fluctuations” (p.1128). This allows the body to adapt accord with their diverse needs through alteration of body functions (Langley, Fonesca, & Iphofen, 2006). In essence, “homeostasis is not a static balance but a dynamic equilibrium in which continuous change occurs and yet relatively uniform conditions prevail” (Langley, Fonesca, & Iphofen, 2006, p.1128). Psychoneuroimmunology highlights the purpose and significance of this correlation in conjunction with the more traditional analysis of immunology as an independent mechanism regulating functions within a solitary organism (Ader & Cohen, 1993). Numerous evidentiary studies support a coherent affiliation between stress, associated conditions, and immune system changes, as surmised by Goodkin & Visser (2000), and more recently, by Irwin (2002), who states that psychological stress and depressive symptoms are thought to result in greater instances of the presence of illness or disease and death. This prevalence was particularly observed in patients with cardiovascular disease and, in older adults where chronic medical disease was already a dominating factor, clinical depression remains persistent with discernible recurrent and remitting episodes (Irwin, 2002). Furthermore, Leonard & Myint have also concluded that chronic stress can instigate augmentations in the hypothalamic-pituitary-adrenal (HPA) axis, causing the immune system to trigger physical symptoms of anxiety and depression (2009). There are a number of collaborative examinations that coincide with the determination that the rise in the abundance of pro-inflammatory cytokines and glucocorticoids, as is the case when encountering a persistently stressful situation and is also exhibited in cases of depression, play a part in the changes in characteristics commonly observed in those suffering from depression (Leonard & Myint, 2009). PNI & Pregnancy Christian (2011) indicated that psychological stress “promotes immune dysregulation in non-pregnant humans and animals” (p.1). Corwin & Pajer (2008) noted that the fluctuations of the bidirectional HPA and innate immune system during the post-partum period are most likely responsible for the mental disorder known as post-partum depression (PPD, which concurs with Christian’s deduction. It is also well-established that the immune system goes through substantial changes to support a healthy pregnancy, by reducing inflammatory responses and destruction of cell-mediated immunity (Christian, 2011). This adjustment is thought to guard the fetus from elimination by the maternal immune system (Christian, 2011). For this reason, Christian (2011) indicates that “stress-induced immune dysregulation during pregnancy has unique implications for both maternal and fetal health, particularly preterm birth” (p.1). In another observation, Wong, (2002) noted that post-traumatic stress disorder (PTSD) can hasten the development of pre-existing health conditions and medical and psychiatric illnesses can present with various immunological profiles based on their pathophysiology. In a study containing participants with and without PTSD suffering from periodontal disease, it was determined that the subjects with PTSD had a more advanced type of the disease related to an inflammatory immune pattern that was not present in the non-PTSD group (Wong, 2002). It has additionally been noted that PTSD may be associated with inflammatory conditions, like inflammatory bowel disorders, cardiovascular disease, and rheumatoid arthritis (Wong, 2002). Concurrent with this determination, Christian (2011) indicated that stress encourages inflammation, stunts antibody reactions to vaccination, diminishes the natural capacity for wounds to heal, and represses cell-mediated immune function. Asthma is a chronic inflammatory pulmonary disorder that is characterized by reversible airway obstruction. Psoriasis is an inflammatory condition of the skin and joints. Irritable bowel syndrome (IBS) and non-specific inflammatory bowel disease (IBD) have both been linked to stress Mailoo (2006). These conditions were shown to aggravate with the exacerbation of the following stressors: “Obsessive-compulsive behavior Worrying Sensitivity to others' opinions of the self Inability to express anger or aggression Histories of domineering parents Limited capacity to develop warm friendships Dependence on conflict ridden relationships Emotional conflict revolving around inability to express anger or hostility Trait anxiety Neuroticism Suspiciousness High intelligence Timidity Inadequate coping skills Emotional instability” (Mailoo,2006, p.505). The negative impact these life situations can have on the immune system PNI & Skin Disorders Diseases of the skin more than any other organ appear to be influenced by emotional factors, and most dermatologists encounter patients who report a temporal relationship between disease flares and stressful life events. Emotional stressors have been linked to the development or evolution of a variety of cutaneous diseases including acne, vitiligo, alopecia areata, lichen planus, seborrheic dermatitis, herpes simplex infections, pemphigus, urticaria, psoriasis, and atopic eczema (Mailoo, 2006). Two chemicals thought to play key roles in psoriasis are substance- P and Nerve Growth Factor (NGF). Substance-P is chemotactic to neutrophils, activates T-cells and releases interleukin-1 from keratinocytes. NGF stimulates increased keratinocyte numbers and activity and promotes inflammation via a cytokine chain reaction. Stress increases blood NGF levels in humans, and has been shown to increase adrenal gland substance-P levels in an animal model (Segerstrom, 2010, p.114) Furthermore, Mailoo (2006) determined that PNI care has been particularly helpful for patients with a wide array of inflammatory skin disorders, like alopecia areata, hyperhidrosis, psoriasis, urticaria., eczema (atopic dermatitis), pruritus, acne vuigaris, and trichotiilomania, which are acknowledged to be stress-related skin diseases associated with psychological stress, anxiety and depression. Recent studies propose that immune dysregulation may be one central mechanism for a spectrum of conditions linked with aging, including arthritis, cardiovascular disease, osteoporosis, certain cancers, Type 2 diabetes, and frailty and functional decline; production of pro-inflammatory cytokines that influence these and other conditions can be stimulated directly by negative emotions and indirectly by prolonged infection (Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002a). Although intensely stressful situations have been proven to increase immune responses, persistent stress frequently leads to immuno-suppressive reactions (Shi et al., 2003). In the examination conducted by Shi et al. (2003), following exposure to chronic stress, the reduction in lymphocyte mitogenic response and lymphocyte cellularity were assessed and correlated to the findings later indicated by Ho et al (2010) in a later study, which determined that “psychological stressors change endothelial function and lead to chemotaxis” (p.192). In lay terms, chronic stress releases endotoxins in the body that allows illness to occur due to reduction in the body’s natural ability to deflect infections. Partially responsible for this reaction is the fact that keen “mental stressors lead to leukocytosis, increased natural killer cell cytotoxicity, and reduced proliferative response to mitogens” although incessant psychosomatic stressors can bring about to adverse health effects that may produce alteration in cardiovascular function, causing the onset of coronary artery disease (CAD) (Ho et al., 2010, p.192). During normal body functions, cortisol, which is a glucocorticoid, initiate the release of glucose from the stored glycogen in the liver and from the conversion of amino acids and fats, but stress causes the increase of cortisol (Lusk & Lash, 2006). Increased levels of cortisol suppress the inflammatory and immune responses and the cortisol decrease the number of active leukocytes, or white blood cells, and prevent the movement of leukocytes to the site of infectivity by diminishing capillary permeability and hindering chemotaxis (Lusk & Lash, 2006). Cortisol also stabilizes lysosomal membranes, thus preventing release of their infection-fighting proteolytic enzymes. Furthermore, “cortisol inhibits the release of inflammatory substrates, such as histamine and prostaglandins, decreases fibroblast proliferation and functions at the site of injury, and depresses phagocytosis” (Lusk & Lash, 2006, p.26). In addition, Ho et al. (2010) found that severe, continual emotional stress will enhance haemostatic aspects and “acute phase proteins”, which can lead to “thrombus formation and myocardial infarction” (p.192). The verification regarding the consequences of severe and unceasing psychological stress on the start and development of CAD is steady and compelling (Ho et al., 2010). Cohen & Williamson (1991) indicated that stress is associated with increases in symptoms of illness and may be similarly associated with increased onset and reactivation of verified infectious disease. The conclusions drawn in the study conducted by Sheridan, Dobbs, Brown, & Zwilling (1994) support these conclusions, providing evidence for a correlation between stress and the pathogenesis of infectious disease and proposes that “the effects of stress on infectious disease are mediated through the neuroendocrine-immune interactions” (p.200). More recent studies support these determinations, indicating that the immune system and the central nervous system (CNS) play a major role in a wide series of disorders characterized by a hypo-responsive or hyper-responsive immune reactions (Kern & Ziemssen, 2008). In multiple sclerosis (MS), which is a debilitating inflammatory and neurodegenerative disease, an overload of inflammatory processes is the primary symptom and there is increasing proof that this is due to a breach in effective communication between the CNS and the immune system as a critical pathogenic issue (Kern & Ziemssen, 2008). Additionally, Suarez, Feramisco, Koo, & Steinhoff (2011) indicated that the event of atopic dermatitis is frequently related to emotional and mental stress. The body then increases the degree of neuropeptide mediators in the brain, endocrine organs, and peripheral nervous system that have an immediate affect on the immune system and resident cells in the skin in response to stress (Suarez, Feramisco, Koo, & Steinhoff, 2011). Another aspect concerns the findings that longer-term stressors that are also associated with changes in immuno-responsiveness, which includes conditions like job burnout, unemployment, job strain, and isolation (Glaser & Keicolt-Glaser, 2005). Unfavorable immunological augmentations have also been acknowledged for weeks or months following natural catastrophes like earthquakes and hurricanes, with more persistent immune dysregulation occurring in individuals who suffered the most private losses (Glaser & Keicolt-Glaser, 2005). Stress factors that are considered to be unpredictable and uncontrollable can also be connected with increases in stress hormone levels (Glaser & Keicolt-Glaser, 2005). The capacity to release tension following stressful situations allows the person to revert to their normal neuroendocrine baseline in a reasonably short time which is considered influential to the total burden that stressors place on an individual (Glaser & Keicolt-Glaser, 2005). Some behavioral disparities that have been noticed in relation to the PNI effects of stress was that individuals displayed diminished activity, loss of interest in their surroundings, less food intake, and, based on the individual, illness is accompanied by depressed mood, fatigue, and amplified sensations of pain (Zachariae, 2009). These differences can be caused by injections of pro-inflammatory cytokines like interleukin-1, which is usually secreted when immune cells are activated in reaction to bacterial or viral contagion (Zachariae, 2009). However, Zachariae (2009) speculates that the reaction of sickness triggered by the immune system is induced as a motivational tactic rather than a response to weakness. It has also been theorized that such a reaction incites a reaction that encourages behaviors that are more conducive to the physiological changes that are occur due to the illness (Zachariae, 2009). For this reason, the symptoms, such as the increase in body temperature that signals a fever, disallows activities that could cause additional symptoms to develop or activities do not help the body fight infection (Zachariae, 2009). Thus, the characteristics of sickness behavior can be interpreted as an extremely controlled stratagem critical to the continued existence of the individual (Zachariae, 2009). Further studies by Segerstrom (2010) corroborate these determinations and present the perspective on “phenotypic plasticity in immunity”, which refers to changes associated with the significance of immunity across different situations, particularly stressful ones (p.114). Their findings determined that that ecological immunology offers a broad hypothetical viewpoint that indicates sickness behaviors are reflex mechanisms designed to preserves energy for use by the immune system and intense stress activates the body’s primary immune protectors while restraining stronger responses in order to preserve power to offset the energy loss resulting from the stress (Segerstrom, 2010). Unexpected relationships between stress “buffers” and immune functions demonstrate phenotypic plasticity related to resource pursuit or preservation (Segerstrom, 2010, p.114). Benefits Methods of PNI Therapy Healthcare providers can become powerful in facilitating patient recovery with the use of PNI to reduce stress, which would in turn reduce the incidences of stress-related illnesses, like cancer, heart disease, PTSD, mental disorders, skin irritations and subcutaneous diseases, and a host of other sicknesses discussed in this brief analysis (Halldorsdotter, 2007). Curing illness would, undoubtedly increase the patients' sense of well-being, health, and healing and it is apparent from the data that the healthcare worker/patient relationship can be therapeutic and healing (Halldorsdotter, 2007). PNI tools include the use of homeopathy remedies, like acupuncture. Initiating precisely cadenced electrical impulses a little more intense than what the nervous system already produces using the practice of medical acupuncture can therapeutically modify anomalous signals caused by stressors(Walling, 2005). This can trigger the release of neuropeptides and initiate the stabilization of homeostatic regulations so that health outcomes are improved (Walling, 2005). As neurological activity is changed, the pattern of nerve activity is changed, causing a change in the electrical pattern, which produces a change in the biochemical pattern (Walling, 2005). As indicated by Walling (2005), techniques like these will not modify the quantity of stressors an individual is exposed to but it will adjust their physiological reaction to them (Walling, 2005). When the nervous system is in homeostatic balance, individuals will report enhanced feelings of well-being, be more effective in coping with their conditions of living, and therefore be less susceptible to illness (Walling, 2005). According to the examination conducted by Keicolt-Glaser, McGuire, Roubles, & Glaser (2002b), an adequate amount of empirical research supports the conclusion that immune augmentation through the use of psychosocial stressors or interventions can result in actual health changes, and the largest compilation of undeviating confirmation has been conducted to examine the effects of PNI on infectious diseases and wound healing. Furthermore, Keicolt-Glaser, McGuire, Roubles, & Glaser (2002b) have identified a vast continuum of illnesses “…whose onset and course may be influenced by pro-inflammatory cytokines, from cardiovascular disease to frailty and functional decline; pro-inflammatory cytokine production can be directly stimulated by negative emotions and stressful experiences and indirectly stimulated by chronic or recurring infections (p.15). Consequently, “distress-related immune dysregulation” can be one main aspect behind a sundry set of health risks linked with “negative emotions” (Keicolt-Glaser, McGuire, Roubles, & Glaser, 2002b, p.15). Professional healthcare can make healing more profound, expedient, and better internalized if it is provided with skill and care (Halldorsdotter, 2007). The use of PNI in patient recovery procedures will allow the profession to use physiological measures of the effects of occupational interventions to gauge the efficacy of this method of intervention (Mailoo, 2002). As detailed by Mailoo (2002), “…such measures could include hormonal levels or immune cell activity, which may increase the inter-professional credibility of occupational therapy when working alongside other professions which use reductionist reasoning”, (p.507). A close link between stressful life events and both physical and mental health has revealed that stress factors have a strong impact on the “immune, circulatory and nervous system and it may affect immunological, cardiovascular and neurodegenerative diseases as well as mental disorders” (Mailoo, 2002, p.507). While PNI investigations thus far are inconclusive in pinpointing the exact relational dimensions of various stressors and immuno-reactionary measures, it is also unclear whether mixed changes affect disease process, vice-versa, or both (Mailoo, 2002). Additionally, the psychosomatic force of sickness could change temperament and individuality or physiological transformations relating to disease may affect the CNS (Mailoo, 2002). Some mental and behavioral changes associated with inflammatory diseases are thought to be the product of the presence of pro-inflammatory cytokines on the CNS (Mailoo, 2006). PNI examinations have produced confirmation for all-encompassing bidirectional messages between the brain and the immune system (Zachariae, 2009). Research into early animal studies signifies that left- and right-brain lesions generate dissimilar patterns of repression and commencement of an assortment of immune measures (Zachariae, 2009). Furthermore, Zachariae (2009) indicated that “…the existence of an extensive brain-immune network suggests that the immune system should be under at least partial influence by psychological processes”, (p.646). Unfortunately, this does not clarify how the associations between psychosocial aspects, physical condition, and sicknesses are “…mediated by the identified brain-immune pathways…” requiring additional research in this area (Zachariae, 2009, p.646). PNI research has also exposed the elevated extent by which the intricacy of the brain-immune interactions and the assimilative role of many of these interactions remain misunderstood (Zachariae, 2009). This makes it hard to understand an assortment of immune outcomes in studies of psychosocial dimensions and immunity and also accentuates the promises of a ‘‘strengthened immune system’’ frequently supported by advocates of balancing and unconventional health management (Zachariae, 2009). “Although the field of psychoneuroimmunology has provided promising results, the critical question of whether behavioral manipulation, like stressors or intervention, can affect immunity so as to influence health and survival, still remains to be answered” (Zachariae, 2009, P.549-550). According to Ader (2000) “…the neural and endocrine changes that accompany changes in behavioral states and the network of brain–immune system connections that have already been elaborated provide numerous pathways through which behavioral processes could influence immune responses” (p.174). These augmentations will probably be based on the nature of the responses obtained by the unique nature of the empirical dynamics divergent from the ordinary appurtenances of a nonspecific stress response like corticosteroid elevations (Ader, 2000). This would be in addition to the detailed nature of the defensive responses elicited by the “immunogenic challenge to which the individual is exposed” (Ader, 2000, p.174). Overall, the quantifiable repercussions of PNI will be better respected when interacting variables that govern immunoregulatory processes are identifiable and easily manipulated (Ader, 2000). The central premise underlying psychoneuroimmunology is that the nervous, endocrine, and immune system are components of an integrated system of defenses (Ader, 2000. p.174). To help people manage their own stress by facilitating lifestyle changes, PNI intervention will de designed to decrease psychological stress and may require a move away from reductionist clinical reasoning towards holistic approaches such as: “Psycho-spiritual integration Reverse therapy Yoga Life coaching” (Mailoo, 2002, p.507) “Psycho-spiritual integration is the use of occupations to create a sense of meaning and purpose in life” (Mailoo, 2002, p.507). Additional presumptions indicate that behavioral, neural, and endocrine interference is highly relevant in regards to the efficacy of PNI as a treatment for various immune-deficiencies and diseases (Ader, 2001). Furthermore, it is postulated that the immune system may be a contributory aspect to gaining further comprehension concerning the treatment of behavioral, neural, and endocrine-related mental disorders, like depression (Ader, 2001). Although we research has yet to yield answers to questions regarding the mechanisms mediating the effects of the various life situations on immune response, it is certain that neural and endocrine changes are associated with changes in behavior and that there is a network of bidirectional connections between the brain and the immune system (Ader, 2001). References Ader, R. (2000, June 28). On the development of psychoneuroimmunology. European Journal of Pharmacology, Center for Psychoneuroimmunology Research, Department of Psychiatry, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA, 405, pp.167–176. retrieved from www.elsevier.nlrlocaterejphar Ader, R. (2001, June). Psychoneuroimmunology. Current Directions in Psychological Science, 10(3), pp.94-101. Ader, R. & Cohen, N. (1993). Psychoneuroimmunology: Conditioning and stress. Department of Psychiatry and Microbiology a d Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York, Annu. Rev. Psychol, 44, pp.53-85. Retrieved from www.annualreviews.org/aronline Apnius, V. (1998). Stress and immune defense. Advances in the Study of Behavior, 27, pp.133-153. Azar, B. (2001, December). A new take on psychoneuroimmunology. American Psychological Association, 32(11). Print version: page 34 Bauer-Wu, S.M. Psychoneuroimmunology Part I: Physiology. Georgia M. Decker (Associated Editor). Clinical Journal of Oncology Nursing, Integrated Care 6(3), pp.1-4. Benowitz, S. (1996, August 19). Psychoneuroimmunology finds acceptance as science adds evidence. The Scientist, 10(16), p.14. Retrieved from www.Britannica.com, http://www.jewishealing.com/psychoneuroimmunology.html Briones, T.L.. (n.d.). Psychoneuroimmunology and Related Mechanisms in Understanding Health Disparities in Vulnerable Populations Caine, R.M. (2003). Psychological influences in critical care: Perspectives from psychoneuroimmunology. Critical Care Nurse, April, 23(2), pp.60-70. Christian, L.M. (2011). Psychoneuroimmunology in pregnancy: Immune pathways linking stress with maternal health, adverse birth outcomes, and fetal development. Neurosci. Biobehav. Rev. Retrieved from EBSCOhost, doi:10.1016/j.neubiorev.2011.07.005 Cohen, S. & Williamson, G.M. (1991). Stress and infectious disease in humans. Carnegie Mellon University and Center for Pittsburgh, Pennsylvania. American Psychological Association, Inc., Brain, Behavior, and Immunity 109(l), pp.5-24. Corwin, E.J. & Pajer, K. (2008). The Psychoneuroimmunology of Postpartum Depression Journal of Women’s Health, Mary Ann Liebert, Inc 17(9), pp.1529-1534. Retrieved from EBSCOhost, doi: 10.1089/jwh.2007.0725. Glaser, R. (2005). Presidential address: Stress-associated immune dysregulation and its importance for human health: a personal history of psychoneuroimmunology. Brain, Behavior, and Immunity, 19, 3–11. Retrieved from www.elsevier.com/locate/ybrbi Goodkin, K. & Visser, A.P. (2000). American Psychiatric Press. Progress in Psychiatry, 59, Washington, DC, 444 pages, Glaser R. & Kiecolt-Glaser, J.K. (2005, March). Stress-induced immune dysfunction: implications for health. Nature Reviews Immunology, 5, pp.243-251. Halldorsdottir, S. (2007). A psychoneuroimmunological view of the healing potential of professional caring in the face of human suffering. International Journal for Human Caring, 11(2), pp.32-37. Ho, R.C.M. et al. (2010, March). Research on Psychoneuroimmunology: Does stress influence immunity and cause coronary artery disease? Annals Academy of Medicine, 39(3), pp.191-196. Hodo, D.W. (2001, October 01). Psychoneuroimmunology: Stress, Mental Disorders, and Health. Am J Psychiatry, 158, pp.1753-1753. Irwin, M. (2002). Presidential Address: Psychoneuroimmunology of depression- Clinical Implications. Brain, Behavior, and Immunity, Cousins Center for Psychoneuroimmunology, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, California, 16, pp.1–16. Retrieved from EBSCOhost, doi:10.1006/brbi.2001.0654, Retrieved from: http://www.idealibrary.com on Kern, S. & Ziemssen, T. (2008). Brain–immune communication psychoneuroimmunology of multiple sclerosis. Multiple Sclerosis, 14, pp. 6–21. Retrieved from SAGE Publications, doi: 10.1177/1352458507079657 Kiecolt-Glaser, J.K., McGuire, L., Robles, T.F., & Glaser, R. (2002a). Psychoneuroimmunology: Psychological influences on immune function and health. Journal of Consulting and Clinical Psychology Copyright by the American Psychological Association, Inc, 70(3), pp.537–547. Retrieved from EBSCOhost, doi: 10.1037//0022-006X.70.3.537 Kiecolt-Glaser, J.K., McGuire, L., Robles, T.F. & Glaser, R. (2002b) Psychoneuroimmunology and psychosomatic medicine: Back to the future. Psychosomatic Medicine, 64, pp.15–28. Retrieved fron EBSCOhost, doi: 0033-3174/02/6401-001 Langley, P., Fonseca, J., & Iphofen, R. (2006). Psychoneuroimmunology and health from a nursing perspective. British Journal of Nursing, 15(20), pp.1126-1129. Leonard, B.E. & Myint, A. (2009, February11). The psychoneuroimmunology of depression human psychopharmacology. Hum. Psychopharmacol Clin Exp, Wiley Inter Science, 24, pp.165–175. Retrieved from www.interscience.wiley.com, doi: 10.1002/hup.1011. Lorentz, M.M. (2006, July). Alternative stress and psychoneuroimmunology revisited: using mind-body interventions to reduce stress. Journal of Nursing, 11, pp.1-11. Lusk B. & Lash, A.A. (2005, January/February). The stress response, psychoneuroimmunology, and stress among ICU Patients. Dimensions of Critical Care Nursing, 24(1), pp.25-31. Mailoo, V.J. (2006, November). Psychoneuroimmunology and occupational therapy for inflammatory disorders. International Journal of Therapy and Rehabilitation, 13(11), pp.503-10. McCain, N.L., Gray, D.P., Walter, J.M., & Robins, J.L. (2005). Implementing a comprehensive approach to the study of health dynamics using the psychoneuroimmunology paradigm. Advances in Nursing Science, Lippincott Williams & Wilkins, Inc., 28(4), pp.320-332. Reddy, S. (2010, October 25). Psycho-neuro-immunology or how stress causes illness. Retrieved from http://www.cancerawakens.com/blog/2010/10/psycho-neuro-immunology-or-how-stress-causes-illness/ Segerstrom, S.C. (2010, June 5). Resources, Stress, and Immunity: An Ecological Perspective on Human Psychoneuroimmunology. Ann. Behav. Med., The Society of Behavioral Medicine, 40, pp.114–125, doi: 10.1007/s12160-010-9195-3 Sheridan, J.F., Dobbs, C., Brown, D., & Zwilling, B. (1994). Psychoneuroimmunology: stress effects on pathogenesis and immunity during infection. Clin. Microbiol. Rev., 7(2), pp.200. Retrieved from EBSCOhost, doi: 10.1128/CMR.7.2.200. Shi, Y. et al. (2003) Stressed to death: Implication of lymphocyte apoptosis for psychoneuroimmunology. Brain, Behavior, and Immunity, 17, pp.S18–S26. Retrieved from www.elsevier.com/locate/ybrbi Suarez, A.L., Feramisco, J.D., Koo, J. & Steinhoff. M. (2002). Psychoneuroimmunology: Psychological influences on immune function and health. Journal of Consulting and Clinical Psychology, American Psychological Association, Inc., 70(3), pp.537–547. Retrieved from EBSCOhist, doi: 10.1037//0022-006X.70.3.537 Tausk, F. Elenkov, I. & Moynihan, J. (2008). Psychoneuroimmunology. Dermatologic Therapy, Blackwell Publishing Inc., ISSN 1396-0296 21, 22–31. Walling, A. (2006). Therapeutic modulation of the psychoneuroimmune system by medical acupuncture creates enhanced feelings of well-being. Journal of the American Academy of Nurse Practitioners, 18 135–143, doi:10.1111/j.1745-7599.2006.00115.x Wong, C.M. (2002). Post-traumatic stress disorder: Advances in psychoneuroimmunology. Department of Psychiatry, Mount Sinai School of Medicine, Bronx VAMC, OOMH 130 West Kingsbridge Road, Bronx, NY Psychiatr Clin N Am, 25, pp.369–383. Zachariae, R. (2009). Health and disability psychoneuroimmunology: A bio-psycho-social approach to health and disease. Scandinavian Journal of Psychology, 50, pp.645–651. doi: 10.1111/j.1467-9450.2009.00779.x Read More