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There is considerable research interest overlap between biological anthropology and psychoneuroimmunology (PNI), particularly given recent anthropological interest in endocrine and immune system functioning over the life span and in different environmental contexts. In this chapter, I argue that conducting research on non-WEIRD populations and applying an anthropological, evolutionary approach to PNI can greatly strengthen our understanding of immune-endocrine-behavior connections. This chapter reviews population-level variation in the human immune and endocrine systems, as well as genetic and environmental contributions to this variation. The effects of culture on shaping health outcomes and stress responses are also considered. Finally, this chapter discusses some noninvasive sampling methodologies appropriate to field research and alternatives to laboratory-based research designs. By confronting variable social and environmental contexts, PNI can greatly expand on its existing contributions to the treatment and understanding of depression, mood disorders, stress, and other aspects of health and well-being.

Accumulating evidence has made clear that experience-the knowledge an individual acquires during a lifetime of sensing and acting-is of fundamental biological relevance. Experience makes an impact on all adaptive systems, including the endocrine, immune, and nerve systems, and is of the essence, not only for the unfolding of an organisms' healthy status, but also for the development of malfunctional traits. Nevertheless, experience is often excluded from empirical approaches. A variety of complex interactions that influence life histories are thereby neglected. Such ignorance is especially detrimental for psychoneuroimmunology, the science that seeks to understand how the exquisite and dynamic interplay between mind, body, and environment relates to behavioral characteristics. This chapter reviews claims for incorporating experience as a member of good explanatory standing in biology and medicine, and more specifically claims that experiential knowledge is required to enable meaningful and relevant explanations and predictions in the psychoneuroimmunological realm.

Objective: Despite considerable research into associations between the effort reward imbalance (ERI) model and various health outcomes over the past 20years, the underlying mechanisms responsible for the association remain unclear. Recently, ERI investigations have examined associations with immune sub-systems (e.g., leukocytes, cytokines and immunoglobulins). Synthesis of the amalgamated research evidence will aid clarity to this field of enquiry. We conducted a meta-analysis and reviewed the associations of ERI and over-commitment (OC) in the workplace with immunity., Method: Electronic databases were searched with the phrase 'effort reward imbalance' which initially yielded 319 studies leading to 57 full text studies being screened. Seven studies that met inclusion criteria were combined using mixed and random effects models., Results: Greater ERI was associated with lower immunity (r=-0.09, CI -0.14, -0.05, p<0.001). Sub-group analyses revealed the effect with mucosal immunity was stronger (r=-0.33, CI -0.47 to -0.18) than trends between both cytokine (r=-0.04, CI -0.07, -0.01) and leukocyte sub-groups (r=-0.02 CI -0.04, 0.01) respectively (k=7, N=9952). Over-commitment was also associated with lower immunity (r=-0.05, CI -0.09, 0.01, p=0.014); subgroup (leukocytes, cytokines, mucosal immunity) associations, however, were homogenous (Q=1.83, df=2, p=0.400, k=6, N=2358)., Conclusions: Greater ERI and OC were both associated with lower immunity. The association between mucosal immunity and ERI was stronger than the cytokine and leukocyte sub-groups. OC moderated the relationship between ERI and immunity., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Psychological factors have long been assumed to be involved in the pathogenesis of allergic skin diseases. The effects of psychological stress on allergic contact dermatitis (ACD) have been experimentally well investigated; however, the effects of ACD on stress responses are largely unknown. Here, we report that preceding chronic ACD dramatically affects the behavioral and physiological stress responses to social isolation (a psychological stressor). In male BALB/c mice, social isolation combined with long-standing (>2 months) ACD by repeated hapten application caused characteristic symptoms, including chronic dermatitis from persistent self-scratching, behavioral changes related to fear/anxiety, and elevated serum IgE levels. The symptoms were maintained by social isolation alone without further hapten application after the onset, and were improved by resocialization. Treatment with topical corticosteroids exacerbated chronic scratch dermatitis, whereas it was effective for chronic ACD. These results show that the symptoms represent a de novo development of a specific disease state and not a mere exacerbation of a preexisting allergic inflammation. With this experimental protocol, similar results were obtained in several other strains of mice. This murine model provides a tool for investigating the pathogenesis and treatment of allergic skin disease with psychodermatological aspects.

Cytokines are coordinators of immune homeostasis. Evidence for the participation of cytokines in neurogenic inflammation, peripheral and central sensitization and hyperalgesia as well as for induction of inflammatory immune responses by pain-related catastrophizing is well documented. A disproportion of proinflammatory and anti-inflammatory cytokines is known to be a contributory cause of pain and pain behavior. Embedded into psychoneuroendocrine immunological feedback control systems cytokines are able to perpetuate a virtuous circle between local inflammation and systemic pain behavior (pain/sickness behavior) thus contributing to chronification of nonspecific musculoskeletal pain.In this model avoidance and pain-related nonrecognition as key components of systemic pain behavior lead to maintenance of the virtuous circle by generating of a local inflammation with local and systemic consequences. This model can explain the success of established therapy concepts from the point of view of psychoneuroimmunology, such as fear avoidance, which are effectively used as principal components in multimodal pain therapy.

Background: Comorbidity studies have shown that depression and somatization (multiple somatoform symptoms) often overlap. Therefore it has been suggested to classify at least some patients with somatization syndromes under the category of depressive disorders. We wanted to investigate whether psychobiological investigations confirm the lumping of somatization and depression, or whether psychobiological pathways favor distinguishing these disorders., Method: An overview is presented summarizing psychobiological studies including patients with depression and/or somatization-associated syndromes. We focus on the following topics: heritability, polymorphisms in special candidate genes, immune activation, hypothalamic-pituitary-adrenal (HPA) axis reactivity, serotonergic pathways, monoamino acids, and fatty acid concentrations., Results: Immunological activation seems to be associated with specific features of somatoform disorders, namely, sickness behavior and pain thresholds. Genetic factors can also contribute to somatic complaints, e.g., via serotonergic pathways, HPA-axis response, immune activation, and other biological systems that contribute to the self-description of not being healthy. Some results indicate that psychobiological aspects of depression and somatization overlap in part (e.g., the relevance of serotonergic pathways), but there is clearly more evidence for discrepancies of psychobiological pathways in depression and somatization (e.g., the relevance of proinflammatory immune processes; HPA-axis activity; monoamino acid availability; omega-3-concentration; the role of triallelic subtypes of 5-HTTLPR)., Conclusion: Many psychobiological pathways act differently in depression and somatization. These differences in psychobiology favor the distinction of these syndromes in classification approaches., (Copyright 2010 Elsevier Inc. All rights reserved.)

Psychoneuroimmunology (PNI) is closely associated with the bidirectional pathways between mind/brain and the immune system. PNI research represents a rapidly growing area within psychosomatic research. Recent studies in PNI are based mainly on the immunological concepts of Th1/Th2 dichotomy and inflammation. This review covers human PNI studies dealing with stress-associated changes in cytokine (Th1, Th2) levels in immune-related processes such as wound healing, atopic diseases as well as autoimmune and other inflammatory diseases. It is shown that PNI studies measuring immune activity near the site of the disease (e. g. woundhealing) and dealing with objective stressors show more consistent findings (stress-associated Th1/Th2 shift, stress-associated proinflammatory activation) than those dealing with chronic and complex diseases (e. g., autoimmune disease). This warrants the expansion of the methodological repertoire in future PNI research toward designs allowing for the investigation of complex psychosomatic phenomena.

Purpose of Review: Recent research findings into putative psychobiological mechanisms of emotional disorders as the future development of psychosomatic medicine are discussed., Recent Findings: Recent studies reinforce the communication between the immune and central nervous systems and identify the large set of peptide and nonpeptide neurotransmitters and ligands they share. Cytokines are seen as humoral mediators that may explain the interaction between endocrine and immune systems. The hypothalamic-pituitary axis has been investigated as part of the regulatory circuits that interact with autonomic regulation to expose immunologic processes related to stress or depression, and also to several diseases. Immune dysregulation and psychological distress have been linked to each other in disease, chronic stress, bereavement and other major life events. Research findings in depressive disorders and cancer may generate new theoretical paradigms in psychosomatic medicine., Summary: The clinical understanding and management of distress or emotional disorders associated with physical illness may change in future because of the results of interdisciplinary research, where environmental factors will be integrated with psychological and biological systems, mainly of endocrine or neuroimmunological nature. The ultimate goal of psychosomatic medicine may be the integration of different levels of individual functioning on a systemic basis.

Objective: To examine the association of changes in current negative mood and long-term daily hassles with changes in lung function and airway inflammation in patients suffering from asthma and in healthy controls. Associations between psychological factors and asthma symptoms have been documented, but the relationship between airway inflammation and psychological factors has been largely unexplored., Method: Data were analyzed from 46 asthma patients and 25 controls who completed questionnaires on current mood and daily hassles at two assessments 3 months apart. Lung function was measured by spirometry (forced expiratory volume in the first second (FEV(1))) and airway inflammation by the fraction of nitric oxide in exhaled air (FeNO). Regression analyses controlling for allergen load and air pollution (ozone) were calculated to study the association between changes in psychological factors and changes in lung function and airway inflammation, and to examine the mediational role of airway inflammation in the stress-lung function association., Results: In patients with asthma, increases in negative affect were associated with decreases in FEV(1) and increases in FeNO. For daily hassles, a reverse pattern of associations was found, with decreases in daily hassles linked to decreases in FEV(1) and increases in FeNO. Mediation analyses showed that FeNO was a significant mediator of the association of both negative affect and daily hassles with lung function changes. No significant associations were found for healthy controls., Conclusion: Psychological variables are consistently associated with spirometric lung function and airway inflammation in asthma patients. For asthma patients, effects of acute negative affect must be distinguished from more chronic distress due to daily hassles.

The field of psychoneuroimmunology has witnessed an explosion of empirical findings during the last two decades. Research has documented the mechanisms through which stressful emotions alter white blood cell function. Stress diminishes white blood cell response to viral infected cells and to cancer cells. Moreover, vaccination is less effective in those who are stressed and wounds heal less readily in those who are stressed. While stress decreases the activity of some white blood cells, stress does not compromise the function of all types of white blood cells. Indeed, some types of autoimmune disease, which involve particular subsets of white blood cells, are exacerbated by stress. The literature documents the efficacy of talk-therapy interventions in altering immune system parameters and enhancing the body's ability to combat disease. The literature also documents the impact of the chronic stress of poverty on immune system function.

For the precise coordination of systemic functions, the nervous system uses a variety of peripherally and centrally localized receptors, which transmit information from internal and external environments to the central nervous system. Tight interconnections between the immune, nervous, and endocrine systems provide a base for monitoring and consequent modulation of immune system functions by the brain and vice versa. The immune system plays an important role in tumorigenesis. On the basis of rich interconnections between the immune, nervous and endocrine systems, the possibility that the brain may be informed about tumorigenesis is discussed in this review article. Moreover, the eventual modulation of tumorigenesis by central nervous system is also considered. Prospective consequences of the interactions between tumor and brain for diagnosis and therapy of cancer are emphasized.

The reaction of blood lymphocytes on adaptive irradiation in vitro (0.05 Gy) and challenge irradiation (1.0 Gy) 5 h after has been studied among 320 children 3-16 years old by micronuclei test with cytochalasin B cytokinetic block. The adaptive response or the hypersensitivity phenomenon (HS) has been determined by the calculation of the number of binucleated cells with micronuclei (MN) in 1000-2000 binucleated cells. For each individual by the chi2 criteria significant differences between the frequencies of damaged cells by irradiation in challenge dose and by combined action of adaptive and challenge doses have been detected. On the base of the results obtained the connection between AR or HS and the somatic diseases of different type and the disturbancies in systems of humoral and cell immunity has been studied. It was shown that in the row of allergic diseases and tuberculous infection among the significant part of the children (approximately 50%) the HS phenomenon was registered. The connection between the HS phenomenon and inflammatory processes (without allergic components), the logopedic disturbancies wasn't observed. It was shown in the group of HS children the deviation in the cell immunity system is registered. Significant deviations in HS group in the system of the humoral immunity is observed. So by the HS phenomenon significant number of the children have the somatic diseases and the deviation in the systems of cell and humoral immunity.

Chornobyl APS--after--effects liquidators were examined. While objective examination the following changes were registered in the patients: slowing down the rate of psychical activity (51%), lowering of mental labor efficiency; the patients spent a lot of time to carry out some kind of work. As the severity of the disease aggravated, the immune disturbances were growing.

Objective: Although psychological modulation of immune function is now a well-established phenomenon, much of the relevant literature has been published within the last decade. This article speculates on future directions for psychoneuroimmunology research, after reviewing the history of the field., Methods: This review focuses on human psychoneuroimmunology studies published since 1939, particularly those that have appeared in Psychosomatic Medicine. Studies were clustered according to key themes, including stressor duration and characteristics (laboratory stressors, time-limited naturalistic stressors, or chronic stress), as well as the influences of psychopathology, personality, and interpersonal relationships; the responsiveness of the immune system to behavioral interventions is also addressed. Additionally, we describe trends in populations studied and the changing nature of immunological assessments. The final section focuses on health outcomes and future directions for the field., Results: There are now sufficient data to conclude that immune modulation by psychosocial stressors or interventions can lead to actual health changes, with the strongest direct evidence to date in infectious disease and wound healing. Furthermore, recent medical literature has highlighted a spectrum of diseases whose onset and course may be influenced by proinflammatory cytokines, from cardiovascular disease to frailty and functional decline; proinflammatory cytokine production can be directly stimulated by negative emotions and stressful experiences and indirectly stimulated by chronic or recurring infections. Accordingly, distress-related immune dysregulation may be one core mechanism behind a diverse set of health risks associated with negative emotions., Conclusions: We suggest that psychoneuroimmunology may have broad implications for the basic biological sciences and medicine.

Objective: The objective of this study was to determine the effects of spaceflight duration on immune cells and their relationship to catecholamine levels., Methods: Eleven astronauts who flew aboard five different US Space Shuttle flights ranging in duration from 4 to 16 days were studied before launch and after landing., Results: Consistent with prior studies, spaceflight was associated with a significant increase in the number of circulating white blood cells (p <.01), including neutrophils (p <.01), monocytes (p <.05), CD3+CD4+ T-helper cells (p <.05), and CD19+ B cells (p <.01). In contrast, the number of CD3-CD16+56+ natural killer cells was decreased (p <.01). Plasma norepinephrine levels were increased at landing (p <.01) and were significantly correlated with the number of white blood cells (p <.01), neutrophils (p <.01), monocytes (p <.01), and B cells (p <.01). Astronauts who were in space for approximately 1 week showed a significantly larger increase on landing in plasma norepinephrine (p =.02) and epinephrine (p =.03) levels, as well as number of circulating CD3+CD4+ T-helper cells (p <.05) and CD3+CD8+ T-cytotoxic cells (p <.05) as compared with astronauts in space for approximately 2 weeks., Conclusions: The data suggest that the stress of spaceflight and landing may lead to a sympathetic nervous system-mediated redistribution of circulating leukocytes, an effect potentially attenuated after longer missions.

Top down central nervous system (CNS) influences on the immune system and bottom up immune system influences on the CNS take part in a complex feedforward and feedback loop which may be responsible for initiating events and perpetuating circumstances in the course of neuropsychiatric as well as immune system diseases. In this paper the authors examine the neuroendocrine-neuroimmune stress response system, the concept of autoimmunoregulation, and recent studies of immune and pharmacological dysregulation in neuropsychiatric and psychosomatic illnesses. The authors review the recent English language literature on these subjects. Support for the hypothesis that macrophages play an important role in neurodevelopment and in the pathophysiology of various neuropsychiatric conditions is found. The interplay between neurologic and immune systems may help to uncover the pathophysiologies of certain neuropsychiatric systems. This may provide new strategies for pharmacologic anti inflammatory treatments. The monocyte /macrophage, which crosses the blood brain barrier is an essential candidate cell in the study of psychoneuroimmunology.

This study examined the interactive effects of job demands, control, and individual characteristics on upper respiratory illnesses and immune function. Having high job control appeared to lessen the linkage between job demands and poor health among individuals with high self-efficacy and those who perceived that they were not often responsible for negative job outcomes. Conversely, having high job control exacerbated the association between job demands and poor health among inefficacious individuals. Implications for promoting more healthful work environments and facilitating employee coping are discussed.

We investigated how the progressive function of the metaphor, the model world of signs, language and culture, link the cell's immunological knowledge with a perceivable concept of the body. Using ethnomethodologically oriented, partly interpretative text analysis, we examined the lymphocyte stimulation test, word clusters in immunology and other medical specialties, the linguistic presentation of the body in German, American and the internet, the presentation of the "self" of the cell in biology and immunology, and protocols of oncological out-patient interviews and chatrooms. When an abstract sign model is created, then the existence of a "negotiable", "competent" and "tolerant" immune cell is predominated by the concept of a cell and much less by elements of the body. Thus, the passive, spatial-anatomical concept of the body can be overcome and the position of the microscopically describable inner observer achieved. This is related to the American concept of a body that can be formed at will from animated individual parts. This model immune system impresses upon physical life and also provides a new metaphor for human interaction in accordance with the pattern of immunocompetent cells.

Objective: Study 1: Introduce and validate a method for measuring EBV p18-VCA antibodies in whole blood spots to provide a minimally invasive marker of cell-mediated immune function. Study 2: Apply this method to a large community-based study of psychopathology in children and adolescents., Methods: The EBV antibody method was evaluated through analysis of precision, reliability, stability, and comparisons with plasma and indirect immunofluorescence methods. The effects of life events on p18-VCA antibody level were considered in a subsample of 9, 11, and 13 year-old children participating in the Great Smoky Mountains Study in North Carolina. The subsample was stratified by age, sex, and degree of overall life strain., Results: Dried blood spots provided a convenient, sensitive, precise, and reliable method for measuring EBV p18-VCA antibody titer. Life events were positively associated with p18-VCA antibodies in girls but not in boys., Conclusions: The validity of the blood spot EBV p18-VCA antibody assay, as well as the ease of sample collection, storage, and transportation, may provide an opportunity for psychoneuroimmunology to explore a wider range of stress models in larger, community-based studies.

Forty-four patients with bronchial asthma, aside from clinical and functional evaluation, were studied for the psychological profile (MMPI-test) and the presence of antibodies to the lung tissue. The correlations established were as follows: normal titers of antibodies to the lung tissue--more agreeable and satisfactory psychological profile of the patients, the lower or higher the antibody titer, the less acceptable is the psychological profile.

Objective: The cell adhesion molecule, L-selectin (CD62L), serves a crucial role in the migration of naive T lymphocytes and is typically shed on cell activation. The objective of this study was to determine the effects of chronic stress on L-selectin expression on peripheral lymphocytes in elderly spousal caregivers of patients with Alzheimer's disease., Methods: Twenty caregivers (mean age, 73.5 years) had their lymphocytes and catecholamine levels sampled at rest and in response to an acute psychological stressor. Ten of the caregivers were classified as susceptible or "vulnerable" based on the large amount of care required by the patient relative to the amount of respite the caregiver received during the previous 6 months., Results: At rest, vulnerable caregivers had 60% fewer L-selectin negative CD8+ T cells (CD8+CD62L-) (p=.01) but no difference in CD8+CD62L+ cells. Vulnerable caregivers also showed significantly fewer CD4+CD62L- T lymphocytes (p=.04) but no difference in CD4+CD62L+ lymphocytes. Resting plasma epinephrine levels were 44% higher in vulnerable caregivers as compared with nonvulnerable caregivers (p=.01). The acute stressor increased circulating levels of CD8+CD62L- and CD8+CD62L+ lymphocytes and catecholamines similarly in both groups., Conclusions: The findings suggest that caregivers who are more vulnerable to the chronic stress of caregiving show a decrement in circulating CD62L- T lymphocytes, possibly by adrenomedullary activation. The data also suggest the identity of lymphocyte subsets that may underlie prior observations of immunologic decrements associated with the chronic stress of caregiving.

The dynamics of stress-related decrease of salivary Immunoglobulin A (sIgA) were examined with respect to whether an increase of upper respiratory tract (URT) symptoms can be observed concurrently with or subsequent to sIgA alterations and whether one can use students' studying behavior during academic examinations to predict changes in sIgA. From a 2-part medical examination of 42 students, daily measures of sIgA were obtained, and symptoms of URT infections and studying behavior were determined by means of questionnaires. Assessment periods began 7 days before each part of the academic examination began and lasted until the 6th day afterward. A control group of 24 medical students who were not undergoing examinations also responded to all questionnaires. A progressive suppression of sIgA, outlasting the examination period by more than 6 days, was observed. Time spent studying explained a significant proportion in sIgA variation. However, no relationship between sIgA and URT symptoms was observed, nor did students who took academic examinations differ from untested controls in symptom rates.

Objective: To examine the impact of and relationship between exposure to Hurricane Andrew, a severe stressor, posttraumatic stress symptoms and immune measures., Methods: Blood draws and questionnaires were taken from community volunteer subjects living in the damaged neighborhoods between 1 and 4 months after the Hurricane., Results: The sample exhibited high levels of posttraumatic stress symptoms by questionnaire (33% overall; 76% with at least one symptom cluster), and 44% scored in the high impact range on the Impact of Events (IES) scale. A substantial proportion of variance in posttraumatic stress symptoms could be accounted for by four hurricane experience variables (damage, loss, life threat, and injury), with perceived loss being the highest correlate. Of the five immune measures studied Natural Killer Cell Cytotoxicity (NKCC) was the only measure that was meaningfully related (negatively) to both damage and psychological variables (loss, intrusive thoughts, and posttraumatic stress disorder (PTSD). White blood cell counts (WBCs) were significantly positively related with the degree of loss and PTSD experienced. Both NKCC (lower) and WBC were significantly related to retrospective self-reported increase of somatic symptoms after the hurricane. Overall, the community sample was significantly lower in NKCC, CD4 and CD8 number, and higher in NK cell number compared to laboratory controls. Finally, evidence was found for new onset of sleep problems as a mediator of the posttraumatic symptom-NKCC relationship., Conclusions: Several immune measures differed from controls after Hurricane Andrew. Negative (intrusive) thoughts and PTSD were related to lower NKCC. Loss was a key correlate of both posttraumatic symptoms and immune (NKCC, WBC) measures.

This study evaluated the initial promise of a dual-pathway conceptual model linking daily event stressors to rheumatoid arthritis (RA) disease activity through changes in immune system activation and mood. Fifty individuals, who were studied on five occasions two weeks apart, reported daily event stressors on the Daily Life Experience Checklist, daily mood on an abbreviated version of the Profile of Mood States-B, and daily joint pain on the Rapid Assessment of Disease Activity in Rheumatology. Serial clinical examinations comprised ratings of joint tenderness and swelling, and blood drawn during exams was analyzed for sedimentation rate (an indicator of systemic inflammation) and soluble interleukin-2 receptors (a marker of immune system activation known to correlate with RA disease activity). Across-person analyses failed to establish links from daily event stressors to either disease activity or composites of joint pain and joint inflammation when associations were adjusted for the effect of neuroticism on self-report measures. Pooled within-person analyses, however, were generally consistent with the relations predicted by the dual-pathway model. Increases in daily event stressors during the week preceding each clinical exam were associated with increased joint pain (regardless of changes in mood). At the same time, increased daily stressors were indirectly associated with decreased joint inflammation through reduction in levels of soluble interleukin-2 receptors. The dual-pathway model, which may be limited to short-term psychological and psychoimmunologic processes, underscores the importance of distinguishing potentially opposing effects of stress on pain versus inflammation in individuals with rheumatoid arthritis.

Objective: The 1994 Northridge earthquake created life disruption and psychological distress for employees of the nearby Sepulveda VA Medical Center. We were interested in the immunologic correlates of disruption and distress under these stressful circumstances., Method: Sixty-eight employees were examined beginning 11 days post-earthquake and were observed until about 4 months after the earthquake, during which time three psychological and immunologic assessments were done. Subjects experienced life disruption from the earthquake itself, damage to home and possessions, injury to self and others, and damage to and functional disruption of workplace. Questionnaires assessed degree of life disruption (personal and work-related), mood, earthquake-specific distress, and repression (alexithymia, coping style or "Type C", and "immunosuppression-prone" traits). Immune measures included lymphocyte subsets-total T (CD3+), helper T (CD4+), cytotoxic T (CD3 + CD8+), B (CD19+), and natural killer (NK; CD3 - CD16 + CD56+)-as well as lymphoid cell mitogenesis (PHA and PWM), and NK cell cytotoxicity., Results: Along with a lessening degree of distress over time, a number of immunologic measures declined over the assessment period (CD3+, CD8+, CD16 + 56+ cells. T cell blastogenesis, and NK cell cytotoxicity). Furthermore, subjects reporting low distress had higher numbers of CD3+ and CD8+ cells and a higher proliferative response to PHA. Those with distress corresponding to life disruption had highest levels of CD3+ and CD8+ cells. Measures of repression did not relate directly to immunity., Conclusion: These results suggest that appropriateness of psychological reaction to the realistic degree of life stress was least disruptive of an aspect of immunity.

Alexithymia is not infrequent among psychosomatic patients. The incapacity to decode one's own emotional experience implies an exacerbation of the physiological response through a recursive loop. If this vicious circle is maintained it can increase the risk of psychosomatic diseases which could be in this way regarded as functions of external meaningful events mediated by the central nervous system. The meaning varies from one individual to another and depends on his cognitive-emotional organisation. In order to study such an organisation, it can be useful to classify his mental state regarding his attachment. The authors, who previously observed an association between psychosomatic skin disease and the "non-free" mental state with regard to attachment, suggest that further studies on psychosomatic patients should be conducted applying the principles and methods of the attachment theory.

The relationship between stress and immunity is not a hot topic of psychoneuroimmunology. The review outlines the main aspects of these interrelations; stress sensitive immunological markers, experimental research and studies on humans which underline the prevailing immunosuppressive effects of stress are discussed. A classification of stress-related diseases comprises autoimmune, acute, psychosomatic and neuroendocrine diseases. Besides the hypothalamopituitary-adrenocortical axis and the symparthoadrenal system, newer information points to the role of cytokines, opioids and other mediators in the complex mechanisms involved. Several data from the physiological laboratory in Cluj are included. The final consideration outlines some unclarified aspects and new research directions.

This article reviews research on the role of psychological stress, personality, social support and other psychosocial factors in bacterial, viral and parasitic infections. After 100 years of research on man and animals, psychological stress is considered as a potential cofactor in the pathogenesis of infectious disease. Psychological stress seems able to alter the susceptibility of animals and man to infectious agents, influencing the onset, course and outcome of certain infectious pathologies. Many experiments have identified in neuroimmunomodulation the principal mediator of the alterations associated with conditions of stress. The development of psychoneuroimmunology has fostered in-depth study of the complex relationship between psychosocial factors, the central nervous system, the immune system and infectious disease. Although antimicrobial drugs have certainly remained the basis of all anti-infective therapy, this type of study has already led some authors to propose and experiment protocols of psychological intervention or psychoimmunotherapy in pathologies such as tuberculosis, or herpes simplex virus or human immunodeficiency virus infections. The psychoneuroimmunological approach to infectious diseases will probably grow in importance in the future not only in the setting of research in psychosomatic medicine but also in that of clinical microbiology.

Results of psychophysiological, psychoendocrinological, and psychoneuroimmunological research on the skin in patients with atopic dermatitis were evaluated. 11 investigations were selected and analysed with respect to both design and results. In 6 instances, healthy or ill control groups were included, rarely did the sample size exceed 30. With respect to physiology, blood pressure, heart rate and EDA were most commonly assessed; with respect to immunology, number of leucocytes and differential blood count and with respect to psychology, anxiety, neuroticism and stress perception. The results involving stress induction, itching induction and the relationship of personality and skin parameters were not consistent. The best established relationship is that between skin reactivity (flare, wheal size and pruritus) on the one hand and cognitive appraisal of stress-stimuli and the experimental situation on the other hand. Psychoendocrinological and even more psychoimmunological indicators of the stress of reaction-unlike psychophysiological indicators-were correlated with the skin response. Only half of the studies found an elevated physiological stress reaction in patients with atopic dermatitis.

This review addresses the importance of studies of human psychoneuroimmunology in understanding the role of psychological factors in physical illness. First, it provides psychologically and biologically plausible explanations for how psychological factors might influence immunity and immune system-mediated disease. Second, it covers substantial evidence that factors such as stress, negative affect, clinical depression, social support, and repression/denial can influence both cellular and humoral indicators of immune status and function. Third, at least in the case of the less serious infectious diseases (colds, influenza, herpes), it considers consistent and convincing evidence of links between stress and negative affect and disease onset and progression. Although still early in its development, research also suggests a role of psychological factors in autoimmune diseases. Evidence for effects of stress, depression, and repression/denial on onset and progression of AIDs and cancer is less consistent and inconclusive, possibly owing to methodological limitations inherent in studying these complex illnesses, or because psychological influences on immunity are not of the magnitude or type necessary to alter the body's response in these cases. What is missing in this literature, however, is strong evidence that the associations between psychological factors and disease that do exist are attributable to immune changes.

It is widely accepted that abnormal personality factors play an important role in the etiology and maintenance of myofascial-type temporomandibular disorder, or M/TMD. However, the foundation on which this belief rests is based largely on clinical lore, rather than on any evidence. The continued belief in the stress theory has important implications. Clinicians continue to be trained in unproven but traditionally sanctioned treatments. Such approaches not only may lead to problems of patient care, they may forge an unstable foundation for future research. Two theories are examined in this article: the psychosomatic and psychophysiological models. The findings show that both theories lack evidence, and further research is warranted because definitive studies are unavailable. The data from this study do not support the contention that M/TMD cases are characterized by a specific premorbid personality.

Traditional aetiological models in neuropsychiatry have placed little emphasis on the abnormal behavioural responses (decreased psychomotor activity, anorexia, weight loss, decreased social exploration and sexual behaviour, impaired cognitive function and increased somnolence) that are common to both psychiatric syndromes, notably depression, and the illness behaviour of sick animals. In recent years, the possible role of cytokines, as mediators of not only the immunological and metabolic responses to infection and inflammation but also a co-ordinated behavioural response, has been described. Further, a range of possible mechanisms for these effects has been postulated, notably involving corticotropin releasing factor (CRF) and prostaglandins of the E series (PgE) with the central nervous system (CNS). Here we outline a series of human clinical conditions where neuropsychiatric syndromes co-occur with a host response to infection or inflammation. These may be characterized by cytokine production (e.g. acute, recurrent and chronic viral illness, systemic autoimmune diseases and chronic fatigue syndrome). Other clinical situations characterized by exposure to or in vivo production of cytokines (e.g. treatment of chronic infections and malignancies, progression and/or recurrence of malignancies) are also discussed. We postulate that the stereotyped behavioural repertoire observed is mediated by cytokine-dependent mechanisms within the CNS. Systematic studies of the behavioural responses of such patient groups are suggested, noting specifically correlations between the time course and severity of immune and neuroendocrine and behavioural responses and dose-response effects.

This study examined psychosocial correlates of immune function and illness in 89 male first-year US Air Force Academy cadets. A psychosocial questionnaire was administered to cadets prior to their arrival at the academy and was readministered during cadet orientation and during the stressful environment of Basic Cadet Training (BCT). Immune responsiveness was analyzed by PHA-, PMA-, or anti-CD3-stimulated thymidine uptake in mononuclear leucocytes. Illness episodes were assessed via medical chart review and self-reported symptoms. There were significant increases in distress levels as cadets entered BCT. No psychosocial measure assessed prior to arrival at the academy predicted level of PHA-, PMA-, and anti-CD3-stimulated thymidine uptake or risk of illness. However, hostility levels reported during BCT predicted risk of illness in the four weeks following psychosocial assessment (odds ratio = 7.1; 95% confidence interval: 1.4-36.1). Elevated response to environmental stressors and lower well-being levels also predicted impending illness, but only in the cohort of cadets who had not contracted food poisoning prior to assessment during BCT (OR = 9.3, CI = 1.9-46.7; OR = 0.09, CI = 0.02-0.53). These results suggest that self-report measures of hostility, response to environmental stressors and well-being may be useful predictors of impending illness episodes in males encountering high stress environments.

There is evidence linking psychosocially mediated immunological alterations with cancer, infectious illness, and HIV progression. The data reviewed suggest that immune modulation by psychosocial stressors and/or interventions may importantly influence health status. The research literature also suggests that the impact of chronic stressors and psychosocial factors on sympathetic nervous system and endocrine function influences the immune system, thereby providing shared mechanisms that may impact on disease susceptibility and progression across a broad spectrum of disorders. A better understanding of individual vulnerability, such as occurs with aging, may help to pinpoint those at greatest risk.

Psycho-neuroimmunology depicts a conceptual frame in which possible interactions between psychic and physical processes can be examined. It could be very significant in the field of psychosomatics when the courses of psychic and somatic processes are examined. However, the research results from this field of study are varied and only for a few parameters of immunity is it possible to prove correlations with psychic variables. Many of the studies that have been conducted up to date were construed as cross-section studies and possibly therefore are not very suitable for depicting the probably very complicated forms of interactions between psychic and somatic levels in an adequate manner. In the framework of stationary psychosomatic psychotherapy two single case studies were carried out in order to examine temporal connections between psychic and immunological course parameters. Both single case studies are to be viewed as explorative attempts of examining questions of examination design and organization which are highly resolved regarding time. Furthermore we report several interesting individual results which emphasize in general the correlation between psychic and somatic parameters also in the course of time. However the limits of such studies regarding the significance of the individual immunological parameters, using time serial analytical methods as well as constructing models in the field of psycho-neuroimmunology are discussed.

In recent years, several studies have been carried out concerning the effect of psychosocial factors on the course of infection due to the human immunodeficiency virus (HIV). After summarizing the current status of general knowledge in the field of psychoimmunology, this article reviews the results of studies conducted in regard to HIV. Two conclusions are reached. The first is that current research has not shown psychosocial factors to have any impact on either the immunity status of seropositive patients or the medical complications inherent to AIDS. The second conclusion is that several types of intervention, in particular psychoeducational approaches, stress management programs, and the strengthening of social and family support, give good results where the psychosocial well-being of patients is concerned and should motivate various health professionals to improve the focus of their interventions. Furthermore, significant methodological weaknesses in several indexed studies are noted, and these should be rectified to enable future studies to confirm or correct the present observations.

This empirical study investigates defined influences and central tendencies within the process of an inpatient treatment in a case of urticaria. The results demonstrate substantial correlations between the course of treatment and endocrinological as well as immunological data. Objective biological parameter and psychodynamic case description complement and enrich each other.

This study evaluated the temporal nature of cellular immune responses, as well as the effects of cardiovascular reactivity on immune responses after exposure to an acute psychological stressor. Lymphocyte subsets and lymphocyte proliferative response to phytohemagglutinin were assessed at baseline and at 5 and 21 minutes after stressor onset in the experimental group and at the same time points in a nonstressor control group. By 5 minutes after stressor onset, the number of CD8 suppressor/cytotoxic T and CD16/56 natural killer cells increased and proliferative response to phytohemagglutinin decreased. These changes were maintained at 21 minutes. Those subjects showing the greatest cardiovascular reactivity had the largest immune alterations. These data did not indicate that gender significantly moderated immune responses. Results are consistent with the hypothesis that sympathetic activation mediates stressor-induced quantitative alterations of peripheral blood lymphocyte subpopulations and nonspecific mitogen stimulated proliferation.