Immunity, emotions and stress with special reference to the mechanisms of stress effects on the immune system.
TL;DR: This paper found that stress and central nervous system lesions affect thymus-derived lymphocytes (T-cells) and play a role in cell-cell interaction or the release of mediators from reacting lymphocytes.
Abstract: Evidence from a variety of sources supports the notion that stress and emotional distress may relate to dysfunction and hypofunction of the immunologic system. We have experimental evidence that some forms of stress reduce primary and secondary antibody response to low dose antigen stimulation in rats and that adult immunologic responsivity may be altered by early infantile experience. Mixed-sex group housing at high male-female ratios increases severity of adjuvant-induced arthritis in the male rat. Graft-versus-host reactions are diminished by food-limitation stress to recipient animals. Sex segregated group-housed mice show larger murine virus-induced sarcomas when inoculated at 6 and 9 months of age than males housed individually with two or more females. Electric shock stress for 3 days prior to inoculation with virus reduces incidence and size of MSV tumors, while shock administered 3 days following inoculation increases tumor size. Female mice that develop spontaneous fighting behavior show significantly greater resistance to MSV tumors. Acutely ill schizophrenic patients with relatively high levels of IgA and IgG have a poorer short-term prognosis. Electrolytic lesions of the ventromedial and posterior nuclei of the hypothalamus of recipient and possibly also of donor animals impair the GVH reaction. Our experimental findings suggest that stress and central nervous system lesions affect thymus-derived lymphocytes (T-cells) and play a role in cell-cell interaction or the release of mediators from reacting lymphocytes. Ultimately, we may find that stress affects the macrophage, a hormone-sensitive cell that plays a role in afferent, central and efferent limbs of the immune system.
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TL;DR: An illness-induced taste aversion was conditioned in rats by pairing saccharin with cyclophosphamide, an immunosuppressive agent, and there was no attenuation of hemagglutinating antibody titers in response to injection with antigen.
Abstract: An illness-induced taste aversion was conditioned in rats by pairing saccharin with cyclophosphamide, an immunosuppressive agent. Three days after conditioning, all animals were injected with sheep erythrocytes. Hemagglutinating antibody titers measured 6 days after antigen administration were high in placebo-treated rats. High titers were also observed in nonconditioned animals and in conditioned animals that were not subsequently exposed to saccharin. No agglutinating antibody was detected in conditioned animals treated with cyclophosphamide at the time of antigen administration. Conditioned animals exposed to saccharin at the time of or following the injection of antigen were significantly immunosuppressed. An illness-induced taste aversion was also conditioned using LiCl, a nonimmunosuppressive agent. In this instance, however, there was no attenuation of hemagglutinating antibody titers in response to injection with antigen.
814 citations
TL;DR: The long-term survivors were more symptomatic overall, with particular elevations on measures of anxiety and alienation, and substantially higher levels of dysphoric mood (eg, depression, guilt) than the short- term survivors.
Abstract: Thirty-five women with metastatic breast cancer received a battery of baseline psychological tests; results were correlated with length of survival. Patients who died in less than one year from baseline were categorized as short-term survivors, while patients who lived for one year or longer were assigned to the long-term survivor group. The long-term survivors were more symptomatic overall, with particular elevations on measures of anxiety and alienation, and substantially higher levels of dysphoric mood (eg, depression, guilt) than the short-term survivors. Short-term survivors revealed significantly lower levels of hostility, with higher levels of positive mood. Treating oncologists perceived the long-term survivors to show significantly poorer adjustment to their illnesses than the short-term survivors, and an interviewer's ratings indicated that long-term survivors had significantly poorer attitudes toward their physicians. Measures of clinical status and demographic data revealed few differences between the two groups. (JAMA242:1504-1508, 1979)
509 citations
TL;DR: An in-depth knowledge of periodisation of training theory may be necessary to promote optimal performance improvements, prevent overtraining, and develop a system for incorporating a screening system into the training programme.
Abstract: Overtraining appears to be caused by too much high intensity training and/or too little regeneration (recovery) time often combined with other training and nontraining stressors. There are a multitude of symptoms of overtraining, the expression of which vary depending upon the athlete's physical and physiological makeup, type of exercise undertaken and other factors. The aetiology of overtraining may therefore be different in different people suggesting the need to be aware of a wide variety of parameters as markers of overtraining. At present there is no one single diagnostic test that can define overtraining. The recognition of overtraining requires the identification of stress indicators which do not return to baseline following a period of regeneration. Possible indicators include an imbalance of the neuroendocrine system, suppression of the immune system, indicators of muscle damage, depressed muscle glycogen reserves, deteriorating aerobic, ventilatory and cardiac efficiency, a depressed psychological profile, and poor performance in sport specific tests, e.g. time trials. Screening for changes in parameters indicative of overtraining needs to be a routine component of the training programme and must be incorporated into the programme in such a way that the short term fatigue associated with overload training is not confused with the chronic fatigue characteristic of overtraining. An in-depth knowledge of periodisation of training theory may be necessary to promote optimal performance improvements, prevent overtraining, and develop a system for incorporating a screening system into the training programme. Screening for overtraining and performance improvements must occur at the culmination of regeneration periods.
484 citations
TL;DR: It is assumed that different conditioning and stressful environmental circumstances induce different constellations of neuroendocrine responses that constitute the milieu within which ongoing immunologic reactions and the response to immunologic signals occur.
Abstract: The acquisition and extinction of the conditioned suppression or enhancement of one or another parameter of antigen-specific and nonspecific defense system responses have been documented in different species under a variety of experimental conditions. Similarly, stressful stimulation influences antigen-specific as well as nonspecific reactions. Moreover, both conditioning and stressful stimulation exert biologically meaningful effects in the sense that they can alter the development and/or progression of what are presumed to be immunologically mediated pathophysiologic processes. These are highly reproducible phenomena that illustrate a functional relationship between the brain and the immune system. However, the extent to which one can generalize from one stressor to another or from one parameter of immunologic reactivity to another is limited. Few generalizations are possible because the direction and/or magnitude of the effects of conditioning and "stress" in modulating immune responses clearly depend on the quality and quantity of the behavioral interventions, the quality and quantity of antigenic stimulation, the temporal relationship between behavioral and antigenic stimulation, the nature of the immune response and the immune compartment in which it is measured, the time of sampling, a variety of host factors (e.g. species, strain, age, sex), and interactions among these several variables. It seems reasonable to assume that the immunologic effects of behaviorally induced neural and endocrine responses depend on (interact with) the concurrent immunologic events upon which they are superimposed. Conversely, the efficacy of immunologic defense mechanisms seems to depend on the neuroendocrine environment on which they are superimposed. We seek to determine when and what immunologic (or neuroendocrine) responses could be affected by what neuroendocrine (or immunologic) circumstances. We therefore need studies that provide a parametric analysis of the stimulus conditions, the neuroendocrine and/or immunologic state upon which they are superimposed, and the responses that are being sampled. The neural or neuroendocrine pathways involved in the behavioral alteration of immune responses are not yet known. Both conditioning and stressor-induced effects have been hypothesized to result from the action of adrenocortical steroids, opioids, and catecholamines, among others. Indeed, all of these have been implicated in the mediation of some immunologic effects observed under some experimental conditions. We assume that different conditioning and stressful environmental circumstances induce different constellations of neuroendocrine responses that constitute the milieu within which ongoing immunologic reactions and the response to immunologic signals occur.(ABSTRACT TRUNCATED AT 400 WORDS)
329 citations
TL;DR: Patients who scored above the median on loneliness had significantly higher urinary cortisol levels and had significantly lower levels of natural killer cell activity, as well as a poorer T‐lymphocyte response to phytohemagglutinin.
Abstract: This study examined the associations among loneliness, stressful life events, urinary cortisol levels, and immunocompetency. Blood and urine were obtained from 33 psychiatric inpatients on the day after admission, at which time the patients completed the UCLA Loneliness Scale, the Psychiatric Epidemiology Research Interview Life Events Scale (PERI), and the MMPI. Patients who scored above the median on loneliness had significantly higher urinary cortisol levels. The high loneliness group also had significantly lower levels of natural killer cell activity, as well as a poorer T-lymphocyte response to phytohemagglutinin. The high loneliness subjects descibed themselves as more distressed than the low loneliness group on the MMPI. There were no consistent significant effects on either the immunologic measures or the MMPI associated with the PERI.
310 citations