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Positive Affect Predicts Lower Risk of AIDS Mortality

From the Osher Center for Integrative Medicine at the University of California San Francisco, San Francisco, California.

Address reprint requests to: Judith Tedlie Moskowitz, PhD, Osher Center for Integrative Medicine at the University of California San Francisco, 1701 Divisadero, Suite 150, San Francisco, CA 94115. Email: moskj{at}ocim ucsf.edu

Received for publication June 18, 2002; revision received October 1, 2002.

	ABSTRACT

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 
OBJECTIVE: The objective of this study was to test the association of positive affect as measured by the Center for Epidemiologic Studies Depression Scale (CES-D) with risk of AIDS mortality, controlling for the other CES-D subscales and laboratory measures of disease progression.

METHODS: Data come from the San Francisco Men’s Health Study, a prospective study of a household probability sample of single men in San Francisco. The subjects were 407 men who were HIV+ at study baseline.

RESULTS: In time-dependent Cox proportional hazards models, the positive affect subscale of the CES-D was significantly associated with lower risk of AIDS mortality (RR = 0.89, CI = 0.84–0.95). When risk estimates were adjusted for time-dependent covariates of CD4, serum ß₂-microglobulin, P24 antigen, antiretroviral use, and the other subscales of the CES-D, positive affect remained significantly predictive of lower risk of AIDS mortality (RR = 0.90, CI = 0.85–0.97). When the CES-D subscale predictors were lagged by 12, 24, and 36 months in order to address the possibility that positive affect was simply a marker for better health, positive affect remained significantly predictive lagged by 12 months and marginally predictive lagged by 24 months.

CONCLUSIONS: Positive affect seems to be the "active ingredient" in the association of scores on the CES-D depressive mood scale and mortality in this sample of HIV+ men. Future work should expand the traditional negative-affect-only focus to encompass the significant role that positive affect plays in living with HIV.

Key Words: positive affect, • CES-D, • HIV/AIDS, • mortality.

Abbreviations: AIDS = acquired immunodeficiency syndrome;; AZT = zidovudine;; CES-D = Center for Epidemiologic Studies Depression Scale;; CI = confidence interval;; ddI = dideoxyinosine;; ddC = dideoxycytidine;; HAART = Highly Active Antiretroviral Therapy;; HIV = human immunodeficiency virus;; RR = relative risk;; SD = standard deviation.

	INTRODUCTION

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Although depression has been linked to morbidity and mortality in coronary artery disease (1), cancer (2–4), as well as all-cause mortality (5, 6), the evidence for a link between depressive symptoms and progression of HIV/AIDS is mixed (7–14). In an 8-year longitudinal study of gay men in San Francisco, Burack et al. (8) found that baseline depressive mood scores on the Center for Epidemiologic Studies Depression Scales (CES-D) (15) were associated with a more rapid decline in CD4 count but were not associated with mortality. Similarly, in an analyses of these same data, Page-Shafer et al. (13) found CES-D scores at baseline were associated with a more rapid progression to AIDS but were not significantly associated with mortality. In contrast, in a larger sample of HIV+ gay men, Lyketsos et al. (11) found no association of CES-D scores at baseline with CD4 decline, time to AIDS, or mortality.

Depressive mood, however, can be quite labile and it may be unreasonable to expect depressive mood scores at a single measurement point to be strongly predictive of outcomes several years later. Chronic depressive mood, rather than a single depressive mood score at baseline, may be more likely to be associated with illness progression (12). In a 9-year study of 96 HIV+ gay men, Leserman et al. (10) found that, although a greater number of cumulative average depressive symptoms was not significantly predictive of mortality, it was associated with faster progression to an AIDS clinical condition. In a reanalysis of the same data used by Burack et al. (8), Mayne and colleagues (11) demonstrated that men who were 1 standard deviation above the mean on the affective subscale of the CES-D at all waves of data collection had a 1.67 (95% CI = 1.01–2.78) times greater risk of mortality than men whose CES-D scores were never above the mean. Taking a similar approach to the analysis of data from HIV+ women, Ickovics et al. (9) found that women who had an elevated CES-D score at 75% or more of their study visits were at twice the risk of mortality than women with limited or no elevation in depressive symptoms (RR = 2.0, 95% CI = 1.0–3.8). Taken together, these studies indicate that although elevated depressive symptoms at a single time point may not be predictive of long-term risk of HIV progression or AIDS mortality, chronically elevated depressive symptoms pose an increased risk of progression and mortality in both men and women with HIV.

Depressive mood, however, is only part of the overall picture of emotional well-being. Measures of depressive mood such as the CES-D (15) used in the majority of the research cited above include items that reflect negative affect (eg, "I felt sad") as well as items that reflect positive affect (eg, "I enjoyed life") that are then reverse coded and added to negative affect, interpersonal, and somatic items to make the full depressive mood scale. A large body of psychological literature demonstrates that positive and negative affect are not simply bipolar opposites on a single continuum (16–18) and suggests that positive and negative affect should be measured and analyzed as relatively independent constructs. On a physiological level, there is abundant evidence that positive and negative affect are associated with separate neurophysiological systems (19–22) and different levels and patterns of autonomic activation (23). The evolution of separate underlying physiologies suggests that positive and negative affect may, at least in some contexts, serve different functions and have different consequences.

Emerging evidence indicates that positive affect has a stronger association with health outcomes than negative affect. Ostir and colleagues (24) demonstrated that the positive affect items from the CES-D ("I felt I was just as good as other people," "I felt hopeful about the future," "I was happy," and "I enjoyed life"), but not the negative affect items, were predictive of risk of stroke over a 6-year follow-up in a sample of over 2400 community-dwelling adults, controlling for other known risk factors such as age, education, body mass index, smoking, diabetes, and blood pressure. The effect was the same across gender and racial groups. Ostir and colleagues (25) examined the association of the positive affect items from the CES-D with subsequent mobility, functional status, and mortality in a sample of elderly Mexican Americans. Controlling for baseline functional status, sociodemographic variables, major chronic conditions, body mass index, smoking status, drinking status, and negative affect at baseline, positive affect was associated with better mobility and functional status and lower risk of mortality over the 2-year course of the study. These findings suggest that positive affect may have a unique impact on risk of mortality, independent of the effect of negative affect.

The purpose of the present study was to test the association of positive affect and mortality in a sample of HIV+ men. To this end, we reanalyzed the data set used by Burack et al. (8), Page-Shafer (13), and Mayne et al. (12) in their tests of the association of depressive mood and HIV progression. To our knowledge, only one published study has examined the effect of positive affect on morbidity and mortality in an HIV+ sample and the results indicated that positive affect at baseline was not associated with time to AIDS, time to death, or CD4 decline (11). The lack of a significant impact of the positive affect subscale may be because a single instance of elevated positive affect at baseline is not sufficient to influence clinical outcomes. Based on the findings of Mayne et al. (12), Ickovics et al. (9), and Leserman et al. (10), we tested average positive affect over the course of the study as the primary predictor of risk of AIDS mortality.

	METHODS

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Sample Design and Subject Criteria
The San Francisco Men’s Health Study (SFMHS) was a prospective cohort study conducted from 1984 to 1993 of 1043 single men aged 25 to 53 years. The sample was drawn from 19 census tracts in San Francisco with the highest AIDS case rates in 1983. Participants were interviewed and had blood drawn for serological and cellular studies every 6 months for up to 16 waves of data collection (a maximum of 7.5 years). Details of sampling, recruitment, and data collection are reported elsewhere (26–29).

Participants for the present analyses were HIV+ at baseline. Four hundred seven men met these criteria. HIV antibody status was determined retrospectively through analysis of frozen serum as the HIV antibody test was not yet available at the first wave of data collection in 1984.

Measures
The CES-D (Center for Epidemiologic Studies Depression Scale) (15) is a 20-item self-report scale that assesses aspects of depressive mood that occurred during the previous week. Responses are on a scale from 0 = "rarely or none of the time" to 3 = "most or all of the time." Factor analyses of the scale in both HIV and non-HIV populations suggest four subscales: positive affect, negative affect, somatic, and interpersonal (30–32). The items that comprise each subscale, along with the scores on internal reliability (Cronbach’s alpha) at baseline, in this sample appear in Table 1. The average scores on the subscales across all waves of data collection were 9.5 for positive affect (range = 0–12, SD = 2.12); 3.49 for negative affect (range = 0–18, SD = 3.25); 4.28 for somatic (range = 0–18, SD = 3.15); and 0.41 for interpersonal (range = 0–4, SD = 0.66). Note that the number of items differs by subscale. There were seven items each for the negative affect and somatic subscales, four items for the positive affect subscale, and two items for the interpersonal subscale.

Dependent Measure
The dependent measure was the date of death from AIDS. Dates of death were determined every 6 months throughout the study period through information from friends, relatives, and published obituaries. In addition, once per year, the California Automated Mortality Listing and the National Death Index were searched, even after the conclusion of data collection. Details are described in Royce et al. (28).

Statistical Analyses
We conducted a series of time-dependent Cox proportional hazards models to test the association of the CES-D subscales with risk of death from AIDS (33). We used the SAS PHREG procedure (34) which selectively retains subjects at any time point for which their covariates can be evaluated. Subjects were excluded from the analysis only if they were missing one or more covariates for all time points. The cumulative averages were based on nonmissing points with no data imputation. All subjects were coded Alive, Died from AIDS (the predicted event), Died from Other Causes, or Died from Unknown Causes. All categories except Died from AIDS were considered censored.

As a first step, univariate Cox proportional hazards models were used to test the association of average scores on each CES-D subscale individually with risk of mortality from AIDS. In the time-dependent Cox proportional hazards model, time-dependent covariates are repeatedly defined in terms of the participant’s history up to the failure time defining each risk set. Overall risk ratios associated with the variables of interests are then calculated over the entire period of data collection.

We then adjusted the risk estimates for time-dependent CD4, serum ß₂-microglobulin, and P24 antigen in four separate analyses – one for each subscale of the CES-D. Next, we calculated time-dependent CD4, ß₂-microglobulin, P24, and antiretroviral use and tested the association of positive affect and risk of mortality, adjusting for these time-dependent covariates as well as the other subscales of the CES-D. In a final set of analyses, we lagged the CES-D subscale average scores by 12, 24, and 36 months in an attempt to further address the question of whether affect is simply tracking the downturn of physical health (ie, one has higher levels of positive affect because death is not imminent) rather than preceding it. For all analyses, we rescaled CD4 counts and P24 antigen measurements to make parameter estimates more interpretable. CD4 counts were divided by 1000, P24 measurements, originally in pg/ml, were divided by 100.

Mayne et al. (12) used, as a time-dependent covariate, the proportion of measurement occasions on which scores on the affective subscales of the CES-D were greater than 1 standard deviation above the mean. This measure appropriately reflects the fact that survival depends more on chronic than on episodic depression. The selection of cutoffs for the various subscales is somewhat arbitrary, however; and the use of time-dependent proportions also require that the first three death times in the sample be dropped to stabilize the proportions. Mayne et al. (12) reported that the analysis of time-dependent averages yielded similar results and, because averages obviate the concerns of cutoffs and unstable values, they are what we used here.¹

	RESULTS

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The average number of waves completed per participant was 9.5 (SD = 5.1). Of the 407 men who met the inclusion criteria, 222 died of AIDS over the course of the study. Among those who died of AIDS, the average time to death was 6.2 years (SD = 2.6, range = 1.3–10.8 years).² The means on the CES-D subscales were similar to means for HIV+ gay men reported elsewhere (31) and appear in Table 2 along with the intercorrelations among the subscales, averaged across all waves of data collection. With the exception of the correlation between the negative affect and somatic subscales, which approaches the reliability of the scales, the other correlations are moderate and indicate that it is reasonable to examine the subscales as individual predictors of mortality.

When we tested the subscales of the CES-D individually, controlling for other time-dependent predictors of mortality (CD4, ß₂-microglobulin, P24 antigen, and antiretroviral use) but excluding the other CES-D subscales, higher average positive affect remained significantly associated with lower risk of mortality (RR = 0.90, CI = 0.85–0.97, p = .002). For every 1-point increase in positive affect, the risk of death decreased by 10%. Controlling for time-dependent CD4, ß₂-microglobulin, P24, and antiretroviral use, the time-dependent negative affect score became nonsignificant (RR = 1.03, CI = 0.99–1.07, p = .13) as did the time-dependent somatic subscale score (RR = 1.04, CI = 0.99–1.08, p = .13). The association of the interpersonal subscale with risk of death remained nonsignificant when the markers of illness progression were included in the model (RR = 1.03, CI = 0.83–1.28, p = .79). When all CES-D subscales as well as markers of illness progression and antiretroviral use were included in a single model, average positive affect remained significantly predictive of lower risk of death (RR = 0.86, CI = 0.77–0.96, p = .009). The effect of the other CES-D subscales remained nonsignificant. Thus when all variables were included in the model, with every 1-point increase in positive affect, the risk of death dropped by 14%. Stated in terms of standard deviations, for every 1 standard deviation increase in positive affect, the risk of death dropped by 28%. As a comparison, note that, for every 1000 cells/µL increase in CD4, the risk of death dropped by 76%. In terms of standard deviations, for every 1 standard deviation increase in CD4, the risk of death dropped by 68%. The results of the full model are in Table 3.

	DISCUSSION

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Participants who had higher cumulative average positive affect scores as measured by the CES-D (15) had a significantly lower risk of death from AIDS than participants who had lower average positive affect scores, even when markers of illness progression (CD4, ß₂-microglobulin, P24 antigen) and antiretroviral use were included in the model. This effect is particularly striking given that elevated average scores on the other subscales of the CES-D – negative affect, somatic, and interpersonal – were not associated with risk of mortality when the effect of illness progression was statistically controlled. By separating the CES-D into its component subscales, these data demonstrate that not only does positive affect have unique associations with risk of mortality but that the other subscales are not significantly associated with mortality. These findings strongly suggest that positive affect is the "active ingredient" in the association of scores on the CES-D depressive mood scale and mortality in this sample of HIV+ gay men. Positive affect was operationalized in the present study as the frequency of a psychological state consisting of feeling just as good as other people, feeling hopeful, feeling happy, and enjoying life in the week before the data were collected. Although a number of investigators have examined the association of potentially related constructs such as spirituality (35), finding meaning (36), and AIDS-specific optimism (37) with AIDS-related morbidity and mortality, the link between these constructs and positive affect has not been firmly established and no one has examined the association of positive affect per se with AIDS mortality.

Even in longitudinal data such as these, issues of causality cannot be answered definitively. Affect is obviously closely responsive to illness progression – the sicker one is, the lower positive affect is likely to be. Although the analyses presented here demonstrated that elevated levels of positive affect preceding death by as much as 12 months were strongly associated with lower risk of mortality, we cannot conclude that high levels of positive affect cause one to live longer with HIV. By controlling for the illness progression markers available at the time of the data collection and by separating in time the measurement of positive affect from the outcome in the lagged analyses, we were able to demonstrate that higher levels of positive affect are protective well in advance of death and that positive affect is not simply an indicator of better health. However, short of conducting a clinical trial in which participants are randomized to a positive affect enhancement condition, the question of whether positive affect is causally associated with lower risk of mortality remains unanswered.

These findings highlight several important measurement issues. First, in the study of the association between affective states and health outcomes, these findings suggest that multiple assessments are important because it is the chronic levels of affect that have an impact rather than the affect levels at a single point in time. The ability to consistently maintain positive affect, regardless of levels of negative affect seems to be key in living longer with HIV, at least in the days before the widespread use of highly active antiretroviral therapies (HAART). Second, the differential impact of positive and negative affect on mortality is further evidence that positive and negative affect are not simply opposite extremes on a single continuum. It is important for researchers and clinicians to recognize that positive affect can occur, even in the presence of elevated levels of negative affect (38, 39), and that positive and negative affect should, therefore, be studied as separate constructs. Although most studies to date that examine the association of positive affect and mortality used the positive affect items from the CES-D, the effect is not exclusive to measurement with the CES-D. Danner et al. (40) analyzed handwritten autobiographies written by 180 Catholic nuns just before entering the convent. Positive emotional content in the autobiographies was strongly inversely correlated with risk of mortality 60 years later controlling for age, education, and measures of linguistic ability. Future studies on the influence of positive affect on longevity should explore a variety of measurement options for positive affect in order to test the generality of the effect.

What are the possible mechanisms through which a psychological state such as positive affect might have an impact on a clinical outcome such as mortality? One logical possibility is that the experience of positive affect bolsters the immune system directly. Various immune parameters have been shown to be susceptible to influence by experimentally induced as well as naturally occurring affective states (41, 42). It isn’t clear, however, the extent to which these studies of changes in various immune parameters in response to positive affect in healthy individuals translate to individuals with HIV. Work by Antoni and colleagues (43–46) demonstrates that stress management interventions designed to reduce distress in HIV+ samples improve immune function (eg, increased CD4/CD8 ratio, increased NK cytotoxicity). Although it can be assumed that stress management interventions increase positive affect as well as decrease negative affect, positive affect has not been explicitly assessed as a mediator of the association of stress reduction interventions and improvement in immune parameters. Finally, it should be noted that even when CD4 was statistically controlled in the present analyses, positive affect remained a significant predictor of mortality. Thus these data suggest that mediation by immune parameters, at least as measured by CD4, is not the key mechanism in this case.

A second possible mechanism for the influence of positive affect on AIDS mortality is improved health behaviors. Depressive mood is associated with substance abuse (47–49), poorer adherence (50–52), and increased sexual risk behavior (48) but few studies have tested the unique association of positive affect with health behaviors. Recent experimental work in HIV-negative samples indicates that positive emotions may facilitate attention to and processing of health-relevant information, which is a crucial step in the process of health promotion (53). Further evidence for an association between positive affective states and attention to health relevant information comes from studies of dispositional optimism (generalized positive expectancies about future outcomes). Optimism is associated with greater attention to, processing of, and recollection of health-relevant information (54, 55) and has, ultimately, been linked to higher risk of death (56). Optimism and positive affective states are positively correlated (57, 58), therefore it is possible that the association between optimism and attention to relevant health information is mediated by positive affect.

It may be that there are many intermediary steps between increased positive affect and improved health outcomes. Positive affect is hypothesized to have a number of adaptive effects, including facilitation of social support and enhancement in other coping resources (59, 60), and both social support and some forms of coping have been shown to be associated with longer survival or slower progression of HIV (10, 14, 46, 61). These suggested pathways for the influence of positive affect on clinical outcomes are not mutually exclusive and may, in fact, all operate to some extent.

The results reported here suggest that, rather than focusing exclusively on reducing negative affect, interventions should also focus on increasing opportunities to experience positive affect. Positive emotions can occur with relatively high frequency, even in the most dire stressful circumstances, and they can occur at the same time that depression and distress are significantly elevated (38, 62). Future work should explore whether interventions to increase positive affect are as effective (or perhaps more effective) than interventions to decrease negative affect in terms of impact on physical health.

This is the first demonstration of a link between positive affect and mortality in an HIV+ sample. Replication of this finding in other HIV samples (eg, women, people on HAART) is necessary. In addition, the finding should be replicated with other measures of positive affect in order to demonstrate the generalizability of the effect. Future work should address the questions regarding predictors of positive affect under conditions of chronic stress and explore the potential mechanisms through which positive affect impacts physical health.

The risk of proclaiming that positive affect influences progression of HIV is that it may seem to minimize the pain and serious individual and societal consequences associated with living with HIV and AIDS. The goal is not to advocate a simplistic "don’t worry–be happy" approach. Such a Pollyanna-ish stance could easily degenerate into blaming the victims if they do not think the positive thoughts that maintain positive affect. Rather, the point is that the human response to stress is very complex and includes positive as well as negative affective responses. Therefore future research should expand the traditional negative-affect-only focus to encompass the significant role that positive emotions play in the context of living with HIV.

	ACKNOWLEDGMENTS

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Data analysis and writing were supported by Grant R01 MH58069 from the National Institute of Mental Health and the National Institute of Nursing Research. Data collection was supported by contracts N01-A1–32519 and N01-A1–82515 from the National Institute of Allergy and Infectious Disease.

The author thanks Michael Acree, PhD, for his statistical support and especially for his good-natured perseverance. The author also thanks Steve Bent, MD, Susan Folkman, PhD, Dennis Osmond, PhD, Eric Vittinghoff, PhD, and an anonymous reviewer for their very helpful comments on earlier drafts of this paper.

	NOTES

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¹However, it should be noted that, in an attempt to replicate the approach of Mayne et al. (12) and Ickovics et al. (9), we also conducted all analyses using proportion scores on the four CES-D subscales. We used the mean scores on the subscales reported by Ostrow et al. (31) as the cutoffs and used the time-dependent proportion of times the participant’s scores were above the mean as time-dependent predictors of hazard of death. The results of the Cox regression analyses and the associated conclusions did not differ substantively from those reported here in which we used averages on the CES-D subscales instead of cutoffs.

²Although participants participated in data collection in the study for a maximum of 7.5 years, dates of death were tracked a number of years after the conclusion of the study. This accounts for the maximum of 10.8 years from entry into study until time of death.

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TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION NOTES ACKNOWLEDGMENTS REFERENCES

 

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