Stress management techniques such as relaxation training, cognitive restructuring, and coping skills training may reduce negative mood states in HIV-positive persons by lowering physical tension and increasing self-efficacy (Antoni, 2003a). These affective changes are thought to be accompanied by an improved ability to regulate peripheral catecholamines and cortisol via decreases in ANS activation and improved regulation of the HPA axis, respectively. Neuroendocrine regulation may be associated with a partial "normalization" of immune system functions, providing more efficient surveillance of pathogens such as latent viruses that may increase HIV replication and enhance vulnerability to opportunistic infections or neoplasias. This normalization of stress-associated immune system decrements may ultimately forestall increases in viral load and the manifestation of clinical symptoms over extended periods. A relatively small number of controlled trials have examined the effects of group-based stress management interventions on psychosocial and immune parameters in HIV-positive populations. There is mounting evidence that interventions employing stress management techniques enhance psychological adjustment, improve neuroendocrine regulation, and bolster immune status (Antoni, 2003a).
If stress management can modify negative mood by changing cognitive appraisals, coping responses and social support resources, then neuroendocrine changes and normalization of immune status may follow.
The modal stress management intervention tested in this regard is a 10-week cognitive behavioral stress management (CBSM) intervention for HIV-positive persons. Throughout previous trials, CBSM was tailored to psychosocial sequelae that may follow critical challenges for HIV-positive persons at various disease stages. In the initial trial, a cohort of 65 MSM awaiting HIV serostatus notification were randomly assigned to a 10-week CBSM intervention, a 10-week group-based aerobic exercise intervention, or a no-treatment control group. After 5 weeks of participating in one of these conditions, blood was drawn for antibody testing and the men received news of their HIV serostatus 72 hours later. Among the approximately one-third of men diagnosed as HIV positive (n = 23), those in the control condition reported significant increases in anxiety and depression. In contrast, men in the CBSM and aerobic exercise conditions showed no significant changes in anxiety or depression scores (LaPerriere et al., 1990; Antoni et al., 1991). Whereas HIV-positive men in the control condition showed declines in CD4+ and NK cell counts during this notification period, the HIV-positive men in CBSM displayed significant concurrent increases in CD4+ and NK cell counts as well as small increases in lymphocyte proliferative responses to mitogenic challenge and NK cell cyto-toxicity. Thus, CBSM appears to have to "buffered" the notification-associated affective and immunologic changes (Antoni et al., 1991).
There were also changes in indicators of antiviral immunity over the 10-week intervention period. Men assigned to either CBSM or exercise interventions showed significant decreases in IgG antibody titers (reflecting better immunologic control) to EBV and HHV-6, which moved into the normal range for age-matched healthy men. This was in contrast to IgG antibody titer values for assessment-only controls, which remained elevated (Esterling et al., 1992). The reductions in EBV IgG antibody titers in the CBSM group appeared to be mediated by the greater social support levels maintained in this condition (Antoni et al., 1996). Finally, a 2-year follow-up of the HIVpositive men in this trial found that less distress at diagnosis, decreased HIV-specific denial coping after diagnosis, and better participant adherence to CBSM treatment protocol all predicted slower disease progression to symptoms and AIDS (Ironson et al., 1994).
Another 10-week, group-based intervention designed to provide emotional support and coping skills after bereavement was tested in a cohort of 97 HIVpositive asymptomatic MSM dealing with loss. Results of this trial indicated that the bereavement intervention decreased grief and buffered CD4+ decline, and reduced plasma cortisol as well as the number of health care visits over a 6-month period, compared to a no-treatment control condition (Goodkin et al., 1998). In a subset of 36 men, the bereavement intervention also buffered against increases in HIV viral load (Goodkin et al., 2001). Therefore, group-based psychosocial interventions may be adaptable and successful in helping HIV-positive persons deal with different emotional challenges during the early asymptomatic stage of the infection.
In a subsequent trial of CBSM, this intervention was tailored to assist HIV-positive persons in managing the emergence of symptoms. HIV-positive MSM who had mild symptoms (category B of the 1993 CDC definition) were randomly assigned to either a 10-week group-based CBSM intervention or a modified wait-list control group. Men in the wait-list control group completed a 10-week waiting period before they were reassessed and invited to participate in a 1-day CBSM seminar. Results indicated that CBSM decreased depressive symptoms, anxiety, and mood disturbance over the 10-week intervention period (Lut-gendorf et al., 1997, 1998). Decreases in depressive symptoms and enhanced social support over the 10-week intervention period partially explained concurrent reductions in HSV-2 IgG antibody titers (Lut-gendorf et al., 1997; Cruess et al., 2000c). Subsequently, a buffering effect of CBSM on EBV IgG antibody titers was observed up to 1 year following CBSM (Carrico et al., 2005a). Similar to previous investigations with asymptomatic HIV-positive MSM (Antoni et al., 1996), intervention effects of EBV IgG antibody titers paralleled sustained increases in social support for men randomized to CBSM (Carrico et al., 2005a).
According to a theoretical model (Antoni et al, 1990; Antoni, 2003b) we reasoned that CBSM-related reductions in multiple indices of negative mood should be accompanied by concurrent changes in neuroendocrine regulation that could influence immune system status in this population. CBSM effects on neuroendocrine regulation have been observed in a number of studies, and these effects have been associated with changes in both affective and cellular-immune parameters (Antoni, 2003b). Specifically, CBSM effects on distress have been observed to co-vary with decreases in 24-hour urinary-free cortisol (Antoni et al., 2000b). Lending further support to the PNI model underlying this work, subsequent investigations have determined that reductions in depressed mood and 24-hour urinary-free cortisol during the 10-week intervention period mediate CBSM effects on recovery of transitional naïve T-cell counts over a 6- to 12-month follow-up period (Antoni et al., 2005).
Similarly, reductions in anxiety during the 10-week intervention period have been observed to co-vary with decreases in 24-hour norepinepherine. These intervention-related reductions in norepinepherine mediated the effect of CBSM on maintaining CD8+ T-cell counts through a 6- to 12-month follow-up (Antoni et al., 2000a). This buffering effect was such that men in the control condition had significant declines, while those in the CBSM group maintained CD8+ counts at the same level. CBSM has also been associated with plasma cortisol/DHEA-S decreases (Cruess et al., 1999) and testosterone increases in HIV+ MSM (Cruess et al., 2000d), which paralleled decreases in depressed mood over the 10-week intervention period. Taken together, this series of studies suggests that CBSM may affect hormonal regulation to promote herpesvirus surveillance and immune system reconstitution among HIV-positive MSM. By examining relations among PNI variables changing during the course of these interventions and at follow-up, we have found evidence that meaningful psychological and biological changes may be attributed to the stress management skills learned and the social support increases experienced as a result of participating in these groups (Lutgendorf et al., 1997; Cruess et al., 2000c).
In the HAART era, a variety of behavioral interventions for HIV-positive persons have been developed specifically to support medication adherence. Although psychological adjustment has not been uniformly conceptualized as a mechanism of enhanced adherence, research has supported the efficacy of pharmacist-led, individualized medication adherence training (MAT) interventions and those that employ cognitive-behavioral principles based on self-efficacy theory (Simoni et al., 2003). Consequently, we theorized that a modified form of CBSM may offer benefits in improving mood, health behaviors, and im mune status in the era of HAART. In order to test the added value associated with providing stress management training, 130 HIV-positive MSM were recruited for a trial in which the combination of CBSM and MAT (i.e., CBSM+MAT) was compared to MAT alone. In an intent-to-treat analysis, we observed no intervention-related changes in immune status. However, in a secondary analysis with 101 men who had a detectable HIV viral load at baseline, we observed a .56 lo gio reduction in HIV viral load over the 15-month investigation period, after controlling for anti-retroviral medication adherence. This clinically interesting effect of CBSM+MAT on HIV viral load was mediated by reductions in depressed mood during the 10-week intervention period. Importantly, these findings held even after controlling for adherence training exposure (each group received MAT) and statistically controlling for individual differences in reported adherence at each time point (Antoni et al., 2006). Thus, there appears to be some added value of reducing depressed mood in persons dealing with the complexities of HAART treatment. It is plausible that reducing depressed mood confers beneficial effects on viral load management by way of health behavior pathways (reduced substance use, improved sleep, and less exposure to sexually transmitted infections) and/or PNI pathways (better antiviral immunity against coinfections or less neuroendocrine-mediated HIV replication). It remains for future research to incorporate measures of PNI variables as well as indicators of HIV viral load and genetic resistance over extended periods as individuals on multidrug regimens participate in well-controlled psychosocial intervention trials.
It is plausible that an equally efficient strategy for conducting PNI research in HIV-positive individuals is to examine concurrent changes in mood, neuroendocrine, immune, and viral processes in the context of randomized trials of mood-modulating pharmaco-logic treatments. The work outlined in Chapters 11 and 32 elaborates on some of the contemporary pharmacological strategies available for addressing depressed mood and anxiety symptoms in HIV-positive persons. This seems like a logical starting point for designing future PNI studies that capitalize on the power of a randomized trial. This research approach offers the additional benefit of using a blinded-placebo design, a feature that has been elusive in psychosocial intervention trials.
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