Integrating multidimensional HIV prevention programs into healthcare settings.

Effective secondary prevention programs to reduce HIV transmission risk-relevant behaviors among HIV-infected individuals must go beyond the traditional, common sense prevention components to develop biomedically and epidemiologically informed behavioral interventions as part of comprehensive, integrated, multidisciplinary HIV care. Incorporating and expanding on the Serostatus Approach to Fighting the Epidemic, a five-pronged strategy set forth by the Centers for Disease Control and Prevention in 2001, we discuss recent findings from the biomedical sciences on viral and host factors that influence infectiousness to support the idea that the most proactive prevention programs will explicitly integrate biomedical interventions and approaches designed to reduce infectiousness, and thus the sexual transmission of HIV. Based on studies of emerging and spreading drug-resistant HIV variants, we have posited the potential development of biodisparity as the biological entrenchment of disparities in socioeconomic status, access to care, and HIV risk-relevant behaviors that differentially affect minorities living with HIV in the US. It is clear that creative approaches based on an expanded behavioral medicine interface with the latest HIV biomedical and epidemiological research are needed to enhance the efficacy of HIV secondary prevention.

Coping as a multisystem construct associated with pathways mediating HIV-relevant immune function and disease progression.

We review psychoneuroimmunological research linking coping with HIV disease progression and its indicators, as well as with viral and host factors that may mediate or contribute to HIV progression. Our perspective on coping broadly encompasses the attempts of multiple mental and biological systems to adapt to changing internal and environmental conditions and to reestablish homeostasis. Accordingly, we discuss studies within four dimensions of coping: cognitive (appraisals, expectancies, and explanatory style), emotional (the Type C coping pattern and related constructs), active-passive strategies and behavior patterns, and physiological (autonomic reactivity and recovery). Finally, we present a model that integrates key studies linking coping with HIV prognostic indicators and clinical disease progression. Based on empirical evidence, the model suggests plausible mechanisms by which coping may be connected to HIV progression/antiprogression factors and immunopathogenesis to affect HIV clinical progression.

Type C coping, alexithymia, and heart rate reactivity are associated independently and differentially with specific immune mechanisms linked to HIV progression.

The maladaptive Type C coping style has been linked to disease progression in HIV and other immunologically mediated disorders. We hypothesized that strong Type C coping, higher levels of alexithymia, and greater cardiovascular (particularly heart rate) responses to, and prolonged recovery from stress would be associated with poorer functioning of immune parameters previously linked to HIV pathogenesis and progression: (1) antigen-stimulated production of the beta (beta)-chemokines MIP-1 alpha and MIP-1 beta, which bind to the HIV co-receptor CCR5 and block HIV entry into CD4(+) lymphocytes; and (2) antigen-stimulated production of the proinflammatory cytokine interleukin-6 (IL-6), which synergizes immune activation associated with HIV replication. We examined relations among psychological, cardiovascular, and immune variables in a baseline sample of 200 HIV-infected, predominantly African American outpatients attending an HIV primary care clinic in inner-city Baltimore. In regression analyses adjusted for CD4(+) count and age, strong Type C coping was associated with significantly higher IL-6 production, as predicted. The theoretically related construct of alexithymia was correlated with significantly lower stimulated production of HIV-inhibiting MIP-1 alpha. Independent of alexithymia, greater heart rate reactivity, and poorer heart rate recovery in response to experimental stressors were also significantly associated with lower production of MIP-1 alpha, adjusted for cardiovascular medications, methadone use, CD4(+) count, and age. These findings support our primary set of hypotheses that maladaptive Type C coping, alexithymia, and heart rate reactivity/recovery are associated with disturbances in two key immune parameters implicated in HIV pathogenesis. Our secondary hypothesis, that dysregulated heart rate reactivity may mediate the connections between Type C coping and/or alexithymia and IL-6/ MIP-1 alpha was not confirmed. The finding that Type C coping, alexithymia, and heart rate reactivity/recovery are associated independently and differentially with specific aspects of relevant immune functioning may reflect distinct biobehavioral pathways that contribute to HIV progression.

Rethinking research on psychosocial interventions in biopsychosocial oncology: an essay written in honor of the scholarly contributions of Bernard H. Fox.

In his best known contribution to the field of psychooncology, the late Dr Bernard H. Fox applied his breadth of scholarship in biopsychosocial cancer epidemiology to address the question of whether and to what extent stress and other psychosocial factors may contribute to cancer risk. Less well known but equally important to the field is his incisive critique of the 1989 study by Spiegel et al. on survival time of patients with metastatic breast cancer following a psychosocial intervention. This essay represents an attempt to take Fox's line of thought to the next logical level of rethinking research on psychosocial interventions in biopsychosocial oncology. Following an analysis of the inadequacy of randomized clinical trials (RCT) to evaluate the causal effects of psychosocial interventions on cancer outcomes and distinguish these from mere prediction, an integrated RCT design is suggested to take into account the psychogenicity of a given intervention, potential mediating mechanisms, and individual differences that could help illuminate hypothesized causal processes linking an experimental intervention and cancer outcomes.

Change is complex: rethinking research on psychosocial interventions and cancer.

The widely discussed 1989 study by Spiegel and colleagues, which suggested that a psychosocial group intervention affected survival in metastatic breast cancer, was not replicated by Goodwin and colleagues in 2001. We analyze methodological issues in both studies, including issues of sampling, randomization, interpretation, and the adequacy and validity of psychosocial constructs and measures to assess hypothesized ingredients of change. The notion of psychogenicity is introduced, conceived as the ability of psychosocial interventions to elicit changes hypothesized to be linked to desired medical outcomes. These considerations lead to the conclusion that there is insufficient evidence to be able to generalize from either study for or against the notion that psychosocial interventions can affect survival in breast cancer. The failure to incorporate into research designs a comprehensive understanding of how coping patterns and related factors may interact with psychosocial interventions to influence cancer progression, and to address hypothesized mediating mechanisms is discussed. Finally, strategies are proposed for future biopsychosocial and intervention research in the field of biopsychooncology.