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Cognition and PsychoneuroimmunologyThe first PNI milestone is generally considered to be classical conditioning experiments conducted in the 1920’s by Metal’nikov at the Pasteur Institute in Paris. Although they were controversial at the time, they were repeated and enlarged upon by others in the 1950’s and 1960’s when immunoenhancive and immunosuppressive conditioning were demonstrated in man and other animals. In the USA, this conditioning work was largely ignored for several decades until 1975 when Ader and Cohen performed their first fascinating classical conditioning experiments to investigate immune modulation (, , , , 2). Since that time, several groups and a number of individuals have conducted excellent PNI research. A focus of much of the work has been on natural killer cells (NK cells). NK cells are powerful members of the immune system and are important in tumor control (). Pioneering work by Spector et al. in mice revealed conditioned NK cell activity increases of up to 39 fold (, ); conditioning reversal of an otherwise fatal cancer (, , ); and that very old animals can be taught to behaviorally increase their NK activity (). In a classical example of conditioning in humans, a conditioned stimulus of sherbet was repeatedly paired with the unconditioned stimulus of a subcutaneous injection of epinephrine (). Epinephrine injections tend to increase the number of NK cells in the blood. So, in this experiment, a post-injection increase in NK cells was seen (the unconditioned response). On the test day, although the sherbet was paired with a saline injection, increase in the number of NK cells was still seen. No increase in NK numbers was seen in the control groups that had previously received sherbet with saline, or epinephrine without sherbet. It would seem that the stimulus of sherbet was enough to increase NK cell numbers. Real world stress can be a combination of physical, chemical and psychological stresses. The result of these stressors combined with gene variances may result in initiation of disease or exacerbation of an already existing illness. Several studies have shown that certain types of chronic stress may increase the risk of some infections and even some cancers (1). The psychobiology of stress and psychological status on immunity and neuroendocrine modulation of the immune system have been studied in relationship to disease onset and progression (, , ). Acute stress and chronic stress seem to depress some measures of immune response (). In one study of gay men waiting for their HIV test results to determine if they were infected, the men had an almost 2-fold increase in the lymphocyte phytohemagglutinin response (PHA) (a commonly used measure of immune system function) one week after learning that they were HIV negative (). Elevated cortisol levels and lower denial coping scores were positively correlated with lower PHA scores (). People living in the region around the Three-Mile Island nuclear disaster and caretakers of family members with Alzheimer’s have decreased lymphocyte reactivity (, , ). West Point cadets who were struggling with schoolwork, having a high-level of motivation, or having fathers who were overachievers had more risk of infectious mononucleosis and indicated immunosuppresion by having higher levels of antibodies to Epstein-Barr virus upon seroconversion and greater pathology from infectious mononucleosis (). Reduction in NK cell activity (, ) and decreased immune system communication and activation molecules (such as IL-2, IL-4 (), and IFN-ã ()) production were seen in medical students while studying for exams. Classical conditioning of immune suppression has been induced in several animal models (, ). Stress and classical conditioning can cause immune suppression in overcrowded animals (, ). PNI studies have revealed that stress acting through the hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) axes can dysregulate the immune system (). The most labile systems to stress seem to be the HPA system that uses the hormones of the neuroendocrine stress response; and SAM that regulates immunity primarily by adrenergic neurotransmitters released by neuronal routes. Glucocorticoids such as cortisol are the main terminal endpoint effectors of the neuroendocrine part of the neuroendocrine immune system response network. Substantial advancements have taken place in understanding the immunomodulating roles of neuroendocrine mediators such as catecholamines, cortisol, estrogen, testosterone, and adenosine. Abnormalities in these modulators have been linked to autoimmune rheumatic diseases such as systemic lupus erythematosis (SLE) and rheumatoid arthritis (). As in any new branch of science, there are many questions that need to be answered. One of the more salient yet one of the more difficult questions to answer is, “What is the influence of individual genetics on susceptibility to stress?” Gender, age, and reproductive status mediated in part by hormonal effects on disease susceptibility genes may modify inhibitory stress responses of the immune system (). In SLE, recent evidence shows that estrogen enhances and testosterone suppresses autoantibody production, which may help to explain the female gender prevalence in SLE (). Animal models also indicate that many autoimmune disease regulatory genes are gender influenced (, 1). Applying principles of PNI to clinical interventions has been slow. Several possibilities for this exist. One possibility is contradictory information that sometimes exists between human and other animal studies (). One of the excellent expeditions probing into molecular mechanisms of stress has been guided by Glaser and Kiecolt-Glaser at Ohio State University College of Medicine. They have delved into emotions and morbidity () and shown that a variety of human negative emotions can increase disease susceptibility and intensity. Of equal importance, Kemeny at UC San Francisco () and Taylor’s group at UCLA have shown that positive close personal relationships and positive beliefs can have a beneficial impact on health partly through their influence on the endocrine and immune systems (). The rason d’tre of PNI studies is the hypothesis that regulatory pathways of the central nervous system may modify susceptibility to various morbid states such as infectious diseases, cancer, and autoimmunity. The tempting corollary is that we may willfully tap into and change for the better the outcome of this neural regulation. Norman Cousins attributed his remission of anklyosing spondylitis to the effect of humor and laughter on immune function and resilience to stress (, 3). He believed that some part of our coping mechanisms, personality, emotional state, or other behavior influences the outcome and progression of disease. Many health practitioners hold to the belief that attitude can affect our ability to ward off cancer (4, 5). Simonton has hypothesized that maybe immune surveillance mechanisms or responses to incipient tumors may be suppressed by stressors acting through the neuroendocrine immune system. And, if so, we might be able to modulate that influence through the use of cognitive PNI processes. He suggests visual imagery of our immune system fighting off the cancer (5). Counseling, psychotherapy and support groups have been shown to improve the quality of life in cancer patients, and in some studies, but not all, to prolong survival in people with breast cancer or melanoma (, , , ). On the other hand, other studies have not shown that depression or personality types influence the incidence or progression of cancer (, , ). Reviews have occasionally summarized the literature on psychological interventions in cancer care and their possible psychological and physical health benefits (, ). A recent review (2006) integrates clinical, cellular, and molecular research on stress, lack of social support, and chronic depression on cancer incidence and progression, and the reviewers describe novel psychological or pharmacological interventions that might help improve cancer prognosis (). Correlation studies between lymphocyte levels and coping styles in folks with AIDS are sometimes contradictory and often revealing (, , , ). Cognitive behavioral stress management (CBSM) interventions, as propounded by Antoni et al. at the University of Miami, shows great promise in enhancing quality of life and boosting the immune response in those folks with HIV-1 infections (, ). For more information, the book Psychoneuroimmunology for the Health Sciences has several chapters that review studies examining various affective states in healthy and unhealthy folks.
References (Not PubMed Indexed)
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