Disclosure of HIV Status and Sexual Orientation Independently Predicts Increased Absolute CD4 Cell Counts Over Time for Psychiatric Patients ERIC D. STRACHAN,PHD, W. R. MURRAY BENNETT, MD, FRCPC, JOAN RUSSO,PHD, AND PETER P. ROY-BYRNE, MD Objective: The objective of this study was to replicate the relationship between disclosure of sexual orientation and immune functioning in HIV-positive persons and to extend those findings to a different type of disclosure (HIV status) and a different population (psychiatric outpatients in a publicly funded HIV/AIDS clinic). Methods: A sample of psychiatric outpatients (N = 373) from a large, urban HIV clinic was assessed for level of sexual orientation and HIV status disclosure as well as absolute CD4 cell counts over time. Mixed-effects random regression analysis was used to build a predictor model that included biobehavioral covariates. Results: Consistent disclosure of both sexual orientation and HIV status independently predicted increased CD4 cell counts over time controlling for important biobehavioral covariates. The only other significant effects in the model were baseline CD4 cell count and number of days between assessment of disclosure and assessment of CD4 cell count. Conclusions: Relieving potential psychological distress by disclosing sexual orientation and HIV status has a positive impact on CD4 cell counts over time even among outpatients stressed by psychiatric illness and economic disadvantage. Additional research is needed to understand whether and under what conditions disclosure should be part of HIV disease management. Key words: psychological inhibition, CD4 cell counts, mixed-effects random regression, HIV, sexual orientation. AIDS = acquired immune deficiency syndrome; BASIS-32 = Be- havior and Symptom Identification Scale; HAART = highly active antiretroviral therapy; HIV = human immunodeficiency virus; MCS = Mental Component Summary; PCS = Physical Component Summary; RSO = Relationship to Self and Others; SO = sexual orientation. INTRODUCTION F or more than 10 years, health psychology researchers have been working to establish and understand the connection between psychosocial variables and progression of human im- munodeficiency virus (HIV) disease. Several studies have shown that inadequate social support, fear of social rejection, and psy- chological inhibition, depression, and anxiety are associated with negative HIV outcomes such as more rapid decrease in CD4 cell counts, diagnosis with an acquired immune deficiency syndrome (AIDS) -defining illness, and AIDS-related mortality ((1–7), but see (8) for a discussion of the controversy regarding depression and anxiety as mediators of HIV disease progression). Other studies have shown that HIV-positive adults with relatively high levels of positive emotion have lower risk of AIDS mortality (9) and that the act of expressing emotions (both positive and neg- ative) through writing can improve CD4 counts over time (10). All of these studies have attempted in various ways to control for important biobehavioral confounds and some similar results have been obtained for women (e.g., (3,11)) and Latino men (12). The construct of psychological inhibition has been especially useful in demonstrating the impact of psychosocial variables on HIV disease progression (e.g., (1–2,7)). Defined as the “failure to publicly express any subjectively significant private experience, including, but not limited to, emotional, social, and behavioral impulses” ((13), p. 243), psychological inhibition appears to be a discrete stressor that affects immune function and other markers of mental and physical health (e.g., (14,15)). For example, Pen- nebaker and colleagues (16) found that writing about significant thoughts and feelings related to a past trauma for 4 consecutive days led to fewer visits to the doctor over the next 6 months compared with writing about a trivial topic. Although the mech- anism is not fully understood, Cole and colleagues (2) note that psychological inhibition (e.g., inhibiting the expression of certain thoughts and emotions) can increase activity in the sympathetic division of the autonomic nervous system. Such increased auto- nomic activity, in turn, appears to be associated with suppressing some aspects of immune function. It is important to note, how- ever, that the research done to support the former point (i.e., about the relationship between psychological inhibition and sympathetic autonomic nervous system [ANS] activity) and that done to support the latter point (i.e., immunosuppression) were not the same. In other words, there is an untested inference in making the full psychological inhibition–ANS activity–immunosuppression claim. In the realm of HIV, psychological inhibition has been largely operationalized as concealment of sexual orientation (SO). In other words, gay men who do not disclose their SO to others are considered to be psychologically inhibited. Such inhibition, in turn, appears to be associated not only with the HIV-related outcomes outlined previously (2,7), but also with significantly higher incidence of cancer and infectious disease (e.g., pneumo- nia, bronchitis) among HIV-negative gay men (1). SO, however, is not the only potential source of concealment among persons with HIV/AIDS. HIV infection itself is something that different people choose to conceal or disclose at different points in the course of disease progression for different reasons (17,18). Like sexual orientation, HIV status is a potentially complex stressor. As mentioned previously, the general theory of psy- chological inhibition as a mediator of physical health suggests that concealing personally important thoughts, behaviors, and emotions is a stressor that may produce negative immune function effects. However, disclosing HIV status can be an acute and recurring stressor because of stigma, prejudice, and loss of important interpersonal relationships (17,18). Even so, psychological inhibition researchers would hypothesize that concealment is a chronic stressor (as opposed to acute but recurring) and that disclosure should relieve some, if not all, From the University of Washington School of Medicine, Department of Psychiatry and Behavioral Sciences, Seattle, WA. Address correspondence and reprint requests to Eric D. Strachan, PhD, University of Washington School of Medicine, Department of Psychiatry and Behavioral Sciences, Harborview Medical Center, Box 359911, Seattle, WA 98104. E-mail: erstrach@u.washington.edu Received for publication December 8, 2005; revision received July 28, 2006. DOI: 10.1097/01.psy.0000249900.34885.46 74 Psychosomatic Medicine 69:74 – 80 (2007) 0033-3174/07/6901-0074 Copyright © 2007 by the American Psychosomatic Society