The present report meta-analyzes more than 300 empirical articles describing a relationship between psychological stress and parameters of the immune system in human participants. Acute stressors (lasting minutes) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity. Brief naturalistic stressors (such as exams) tended to suppress cellular immunity while preserving humoral immunity. Chronic stressors were associated with suppression of both cellular and humoral measures. Effects of event sequences varied according to the kind of event (trauma vs. loss). Subjective reports of stress generally did not associate with immune change. In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.

/pdf/psychological-stress-and-the-human-immune-system-a-meta-3lp53rp4yz.pdf

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry

The notion that chronic stress fosters disease by activating the hypothalamic-pituitary-adrenocortical (HPA) axis is featured prominently in many theories. The research linking chronic stress and HPA function is contradictory, however, with some studies reporting increased activation, and others reporting the opposite. This meta-analysis showed that much of the variability is attributable to stressor and person features. Timing is an especially critical element, as hormonal activity is elevated at stressor onset but reduces as time passes. Stressors that threaten physical integrity, involve trauma, and are uncontrollable elicit a high, flat diurnal profile of cortisol secretion. Finally, HPA activity is shaped by a person's response to the situation; it increases with subjective distress but is lower in persons with posttraumatic stress disorder.

If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans.

In considering new paradigms for the prevention and treatment of disease and disability, we need to incorporate ways to promote social support and develop family and community strengths and abilities into our interventions. There is now a substantial body of evidence that indicates that the extent to which social relationships are strong and supportive is related to the health of individuals who live within such social contexts. A review of population-based research on mortality risk over the last 20 years indicates that people who are isolated are at increased mortality risk from a number of causes. More recent studies indicate that social support is particularly related to survival postmyocardial infarction. The pathways that lead from such socioenvironmental exposures to poor health outcomes are likely to be multiple and include behavioral mechanisms and more direct physiologic pathways related to neuroendocrine or immunologic function. For social support to be health promoting, it must provide both a sense of belonging and intimacy and must help people to be more competent and self-efficacious. Acknowledging that health promotion rests on the shoulders not only of individuals but also of their families and communities means that we must commit resources over the next decade to designing, testing, and implementing interventions in this area.

/pdf/the-role-of-social-relations-in-health-promotion-32f4f5hqk8.pdf

The role of social relations in health promotion

This article presents a meta-analysis of the literature on stress and immunity in humans. The primary analyses include all relevant studies irrespective of the measure or manipulation of stress. The results of these analyses show substantial evidence for a relation between stress and decreases in functional immune measures (proliferative response to mitogens and natural killer cell activity). Stress is also related to numbers and percent of circulating white blood cells, immunoglobulin levels, and antibody titers to herpesviruses. Subsequent analyses suggest that objective stressful events are related to larger immune changes than subjective self-reports of stress, that immune response varies with stressor duration, and that interpersonal events are related to different immune outcomes than nonsocial events. We discuss the way neuroendocrine mechanisms and health practices might explain immune alteration following stress, and outline issues that need to be investigated in this area.

Stress and immunity in humans: a meta-analytic review.

The links between the psychological and physiological features of cancer risk and progression have been studied through psychoneuroimmunology. The persistent activation of the hypothalamic-pituitary-adrenal (HPA) axis in the chronic stress response and in depression probably impairs the immune response and contributes to the development and progression of some types of cancer. Here, we overview the evidence that various cellular and molecular immunological factors are compromised in chronic stress and depression and discuss the clinical implications of these factors in the initiation and progression of cancer. The consecutive stages of the multistep immune reactions are either inhibited or enhanced as a result of previous or parallel stress experiences, depending on the type and intensity of the stressor and on the animal species, strain, sex, or age. In general, both stressors and depression are associated with the decreased cytotoxic T-cell and natural-killer-cell activities that affect processes such as immune surveillance of tumours, and with the events that modulate development and accumulation of somatic mutations and genomic instability. A better understanding of the bidirectional communication between the neuroendocrine and immune systems could contribute to new clinical and treatment strategies.

https://www.thelancet.com/pdfs/journals/lanonc/PIIS1470-2045(04)01597-9.pdf

L.G. Kiloh

Papers

Depressed lymphocyte function after bereavement.