Biomedical subjects

T B Herbert

Publications and source records attributed to T B Herbert.

10 recordsLinked to original sources

PubMed1997

Lymphocyte subset redistribution during acute laboratory stress in young adults: mediating effects of hemoconcentration.

Acute psychological stress is known to alter the distribution of circulating lymphocyte subsets and also to cause a reduction of plasma volume. Data were reanalyzed from 4 previously reported studies (E. A. Bachen et al., 1995; T. B. Herbert et al., 1994; A. L. Marsland, S. B. Manuck, T. V. Fazzari, C. J. Stewart, & B. S. Rabin, 1995; A. L. Marsland, S. B. Manuck, P. Wood, et al., 1995) to determine the extent to which changes in the concentration of lymphocyte subsets are attributable to such hemoconcentration. Meta-analytic procedures showed circulating concentrations of T-suppressor/cytotoxic (CD8) and natural killer (NK) cells to increase following acute laboratory challenge, whereas T-helper (CD4) and B- (CD19) cell populations did not change. Adjustments for concomitant hemoconcentration reduced the magnitude of stress-related increases in CD8 and NK cells significantly and revealed a decrease in CD4 and CD19 cell concentrations from baseline to stress measurements. These data provide evidence (a) that increases in circulating numbers of CD8 and NK cells following acute stress are partially attributable to hemoconcentration and (b) that CD4 and CD19 cell concentrations decrease during acute stress when hemoconcentration is taken into account.

Adult↗

PubMed1996

Health psychology: psychological factors and physical disease from the perspective of human psychoneuroimmunology.

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.

Acquired Immunodeficiency Syndrome↗

PubMed1995

Effects of acute psychological stress on serum lipid levels, hemoconcentration, and blood viscosity.

BACKGROUND: While there is substantial evidence that psychological stress enhances risk for coronary artery disease, the mechanisms underlying such an influence remain unclear. We examined the effects of short-term psychological stress on serum lipid levels, hemoconcentration, fibrinogen level, and plasma viscosity. METHODS: Forty-four healthy young adults were randomly assigned to perform a distinctly frustrating cognitive task for 20 minutes (stress condition) or to rest quietly for the same period (control condition). RESULTS: Relative to controls, stressed subjects showed significant increases in blood pressure and heart rate; total, low-density, and high-density lipoprotein cholesterol levels; hematocrit; hemoglobin level; and total protein concentration. Stressed subjects also showed significant reductions in plasma volume and increased plasma viscosity and estimated whole-blood viscosity compared with controls. A similar trend in fibrinogen level was not statistically significant. Individual differences in blood pressure and heart rate response to stress correlated highly with changes in total cholesterol levels and hematocrit. CONCLUSIONS: Our investigation provides further evidence that exposure to short-term mental stress elicits hemoconcentration with associated increases in serum lipid concentrations, hemostatic factors, and blood viscosity.

Acute Disease↗

PubMed1994

Analysis of lymphocyte proliferation data: do different approaches yield the same results?

We addressed whether different approaches to the treatment of lymphocyte proliferation data influence the interpretation of results. We focused on two specific issues: (1) the impact of using optimal concentrations of mitogen versus a repeated measures approach using all concentrations and (2) the impact of correcting for unstimulated wells, and the method chosen for doing so. First, analysis of only the optimal concentration yields the same results as using a repeated measures approach. Second, uncorrected stimulated data, difference scores, and statistical control of unstimulated values all yield identical conclusions. The stimulation index, however, frequently yields different outcomes than the other approaches. We discuss reasons for these differences, note that the equivalence between repeated measures and optimal concentration techniques is limited to studies predicting suppression of proliferation irrespective of concentration, and suggest situations when the various approaches to analysis be used.

Adult↗

PubMed1993

Depression and immunity: a meta-analytic review.

A meta-analysis indicated that clinical depression was associated with several large alterations in cellular immunity. Analyzing only methodologically sound studies, reliable immune alterations included lowered proliferative response of lymphocytes to mitogens (effect size rs = .24-.45), lowered natural killer cell activity (r = .28), and alterations in numbers of several white blood cell populations (rs = .11-.77). Immune alterations were greater in both older and hospitalized samples. There was also evidence of a linear relation between intensity of depressive affect and indicators of cellular immunity. Estimates of sample sizes needed to detect reliable effects for each immune outcome are provided. How neuroendocrine mechanisms or health practices might link depression to immunity is discussed, and design features needed to better understand these pathways are specified.

Adult↗

PubMedDate not supplied

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

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.

Female↗

PubMedDate not supplied

Cardiovascular reactivity and the course of immune response to an acute psychological stressor.

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.

Adolescent↗

PubMedDate not supplied

Adrenergic blockade ameliorates cellular immune responses to mental stress in humans.

This study evaluated the sympathoadrenal modulation of behaviorally evoked immune responses by administration of a nonselective adrenoceptor antagonist (labetalol) to subjects exposed to mental stress. In a 2 x 2 factorial design, subjects were assigned to a labetalol or saline condition and, within each condition, were exposed either to acute laboratory stress or no stress (control). Lymphocyte subsets, natural killer (NK) cell cytotoxicity, and T cell proliferation to phytohemagglutinin and concanavalin A were assessed pre-experimentally, at baseline after infusion and after 18 minutes of mental stress (or rest). By comparison with the other three conditions, the saline-stress group showed a greater peripheral NK cell number and cytotoxicity, lower mitogenic response to phytohemagglutinin and concanavalin A, and diminished ratio of CD4:CD8 cells after the stressor. As predicted, immune responses did not differ among the remaining groups (labetalol-stress, saline-rest, labetalol-rest). Group differences in NK cell cytotoxicity were not significant after controlling for differences in NK cell numbers. These findings demonstrate that the occurrence of certain immunologic responses to acute psychological stress are dependent on concomitant activation of the sympathetic nervous system.

Adolescent↗

PubMedDate not supplied

Cardiovascular and immune responses to acute psychological stress in young and old women: a meta-analysis.

OBJECTIVE: To describe the relationships between cardiovascular and natural killer (NK) cell number changes on acute psychological stress in women. METHOD: Data from eight different studies were analyzed. A total of 128 healthy female subjects, 85 younger (18-45 years) and 43 older (49-87 years), had been subjected to a speech stressor (N = 80) or a mental effort stressor (N = 48), mental arithmetic, or the Stroop test. Correlations between changes in NK cell numbers, systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were computed. Meta-analysis programs were used to study correlations across studies and to examine whether correlations differed with stressors or age. RESULTS: In all studies, significant increases over baseline were observed for each variable. Across studies, the mean weighted r between changes in HR, DBP, and SBP was medium (rw = .25) to large (rw = .64). A medium to large average correlation between HR and NK changes (rw = .37) was observed, whereas average correlations of changes in NK cell numbers with blood pressure changes were small to medium (rw < or = .23). Correlations between changes in NK cell numbers and cardiovascular variables were homogeneous across studies, whereas mutual correlations between cardiovascular variables were heterogeneous. One moderator variable showed itself: correlations between HR and DBP reactions were larger in studies with older than younger subjects. CONCLUSION: NK cell changes and HR responses induced by acute stress in women are regulated, to some extent, by the same mechanisms. Neither the type of stressor nor age seem to be very important when considering correlations between NK cell and cardiovascular changes. This study integrates information about NK cell and cardiovascular responses in women that can be used as reference material in future studies.

Adolescent↗

PubMedDate not supplied

Pathways linking major depression and immunity in ambulatory female patients.

OBJECTIVES: The goals of this study were to investigate whether depression is associated with cellular immunity in ambulatory patients and to identify neuroendocrine and behavioral pathways that might account for this relationship. METHODS: We studied 32 women who met Diagnostic and Statistical Manual of Mental Disorder, fourth edition, criteria for major depressive disorder and 32 healthy female control subjects. The groups were matched for age and ethnicity. None were taking medication, and all were free of disease involving the immune system. RESULTS: Depressed subjects had reduced proliferative responses to the mitogens concanavalin A and phytohemagglutinin compared with control subjects. Natural killer cell activity was reduced among older depressed subjects but enhanced among younger depressed subjects. Although depression was associated with elevated circulating levels of norepinephrine and estradiol, these hormones could not account for the immunologic differences between depressed and control subjects. Depression was also associated with greater tobacco and caffeine consumption, less physical activity, and poorer sleep quality. Mediational analyses were consistent with physical activity acting as a pathway through which depression was associated with reduced lymphocyte proliferation. CONCLUSIONS: Ambulatory patients with mild to moderately severe depression exhibit reduced mitogen-stimulated lymphocyte proliferative responses and altered natural killer cell cytotoxicity. The relationship between depression and proliferative responses may be mediated by physical activity.

Adult↗