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Promoting Health: Intervention Strategies from Social and Behavioral Research PAPER CONTRIBUTION L Behavioral and Psychosocial Intervention to Modify Pathophysiology and Disease Course Andrew Baum BEHAVIOR, STRESS, AND DISEASE Evidence of behavioral influences in disease outcomes is growing and comes from many diverse sources. This paper considers summaries of this rapidly growing literature focusing on studies of cardiovascular disease, cancer, and HIV disease/AIDS (Figure 1). Other diseases and serious medical conditions are also considered briefly. Stress and Cardiovascular Disease The effects of stress on the pathophysiology of heart disease, hypertension, stroke, and other cardiovascular disorders are broad and increasingly well documented. Stress appears to contribute directly to atherosclerotic processes by which blood vessels become increasingly narrow and unable to adapt to changing circulatory demands (e.g., Smith and Gallo, 1994; Kopp, 1999). Among the effects of stress on the circulatory system are increases in damage to vessel walls and lining, increases in fat deposits in injured intimal areas and lipid pro- Dr. Baum is director, Behavioral Medicine and Oncology and professor of psychiatry and psychology, University of Pittsburgh Cancer Institute, Pittsburgh Mind-Body Center, Departments of Psychiatry and Psychology, University of Pittsburgh. This paper was prepared for the symposium on “Capitalizing on Social Science and Behavioral Research to Improve the Public's Health,” the Institute of Medicine and the Commission on Behavioral and Social Sciences and Education of the National Research Council, Atlanta, GA, February 2–3, 2000.
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Promoting Health: Intervention Strategies from Social and Behavioral Research FIGURE 1 Schematic drawings of the basic relationships between stress or behaviors and diseases discussed in this chapter. The first describes simple relationships between behavioral variables and cardiovascular disease, the second considers behavioral influence and cancer, and the third depicts simple relationships between behavior and HIV disease.
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Promoting Health: Intervention Strategies from Social and Behavioral Research files in general, and increases in plaque associated with repair and overgrowth of these injury sites in blood vessels (Schneiderman, 1983; Foreyt and Poston, 1996). Though far more complex than can be portrayed here, atherosclerosis is a lifelong process of gradual narrowing of arteries and veins, in part because of this repeated pattern of vessel damage, repair, and growth of plaque. In coronary heart disease, factors such as diet, tobacco use, and stress modify the vessels that provide nutrients to the heart and periphery and demand for delivery of nutrients. Sharp increases in demand in an organism with occluded coronary arteries can precipitate cardiovascular events such as infarction, angina, or arrhythmias (e.g., Kamarck and Jennings, 1991). Stress also affects platelets and other clotting factors in the blood that can increase the likelihood of troublesome or dangerous clot formation, pulmonary embolism, or other untoward events (Markovitz and Matthews, 1991; Allen and Patterson, 1995). Finally, these factors can increase blood pressure in several different ways (e.g., Barnes et al., 1997). Some influences on blood pressure are directly related to stress, as is the case, for example, for beta-adrenergic receptor density (Dimsdale et al., 1994). Other effects are more broadly caused by a number of biobehavioral processes, and differences in the magnitude of acute blood pressure and heart rate changes associated with stress appear to be a risk factor for hypertension and coronary heart disease (e.g., Manuck and Krantz, 1984; Manuck et al., 1997). However, evidence is mixed, with some studies suggesting that acute stress-related effects on blood pressure are related to hypertension and some finding little or no evidence of such a relationship (Fredrikson and Matthews, 1990; Picketing and Gerin, 1990). Overall increases in blood pressure associated with chronic stress may also contribute to hypertension (Blumenthal et al., 1995). Direct evidence that stress and other behavioral factors cause cardiovascular dysfunction or disease is increasingly conclusive, but the data are not complete. This is due in part to the nature of these diseases and their development over one's lifetime. Because the development of disease is a very long term process, it is difficult if not impossible to monitor all potential contributors to pathophysiologic disease processes or to pinpoint specific instances of stress-related plaque formation or blood pressure adjustment. However, general patterns are very clear and intermediate events or changes in a bodily system that are highly correlated with disease outcomes (such as elevated blood pressure or intimal narrowing of coronary arteries) are reliably observed as a function of stress. Animal studies, in which investigators can observe or control major stressors and can exert greater experimental control (including the possibility of genetic comparability or manipulation), offer some of the best evidence of stress effects on cardiovascular diseases (e.g., Manuck et al., 1983). Animal studies clearly suggest that stress can accelerate pathogenesis of coronary heart disease and hypertension and can evoke cardiac events (Smith and Gallo, 1994). Although not all studies agree that stress
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Promoting Health: Intervention Strategies from Social and Behavioral Research can cause cardiovascular problems, there is certainly enough evidence to warrant further study and intervention (e.g., Elliott, 1995). As an example, consider a series of experimental and observational studies of cynomolgous monkeys by Manuck and colleagues. This species shares many characteristic cardiovascular properties with humans, and many aspects of their behavior also resemble or parallel human social activity (e.g., Kaplan et al., 1982). When these animals have been exposed repeatedly to disruption of their social environments, they have exhibited greater evidence of coronary heart disease (Manuck et al., 1986). When unfamiliar animals are introduced into a stable group of monkeys, the result is a destabilization of the social hierarchy that had been established. This destabilizing influence is a powerful social stressor for the monkeys, and they respond to it by becoming more aggressive and more prone to cardiovascular disease (Manuck et al., 1986). Periodic reorganization of social groups has been used to generate chronic stress as animals repeatedly experience unstable social conditions, and this manipulation has permitted detailed observation of the impact of social dominance, diet, and stress on the development of cardiovascular disease (Kaplan et al., 1984). Dominant monkeys in unstable conditions exhibited the most extensive signs of heart disease, but these effects were dramatically increased by high-cholesterol diets (Manuck et al., 1986). Interestingly, when females were studied, dominant animals showed few signs of atherosclerosis but subordinate females showed more evidence of atherosclerosis and elevated cortisol as well as ovarian dysfunction (Kaplan et al., 1996). Further stress was associated with endothelial injury through sympathetic activation (the effect was reduced by beta-adrenergic blockage), suggesting that stress-related central nervous system arousal can initiate as well as exacerbate arterial damage (Skantze et al., 1998). Epidemiological studies of large samples of people who were thought to vary in level of chronic stress provide the most general evidence of stress effects on cardiovascular disease. For example, longitudinal studies of civil servants in the United Kingdom found that lower-status occupations thought to be more stressful were associated with higher rates of cardiovascular disease (Marmot, 1994). Several other explanations for such an effect are possible, but stress remains a viable explanation for many effects attributed to socioeconomic status (SES) (e.g., Baum et al., 1999). Other large-scale studies have found robust correlations between stress and cardiovascular outcomes, although these relationships are frequently complicated by moderating variables such as SES, social support or social integration, and personality variables (e.g., Mellors et al., 1994). For example, hostility and Type A behavior have been associated with cardiovascular disease or related intermediate outcomes in several studies (e.g., Suarez and Williams, 1990; Bennett and Carroll, 1990a; Rosenman, 1991; Houston et al., 1992), presumably because of the effects of these personality or behavioral styles on biological processes regulating atherosclerosis or other as-
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Promoting Health: Intervention Strategies from Social and Behavioral Research pects of cardiovascular pathophysiology. Depression also appears to be related to some cardiovascular outcomes (Freedland et al., 1992; Musselman et al., 1998), and several studies have related low social support or poor social integration to disease (e.g., Uchino et al., 1996; Knox and Uvnaes-Moberg, 1998). All of these studies suggest that stress, together with a number of other psychosocial or behavioral variables, affects cardiovascular disease enough to represent targetable variance in disease risk management (Niaura and Goldstein, 1992). Another complicating factor in studies of stress and cardiovascular risk is the fact that many other behavioral influences on cardiovascular disease, such as diet, active versus sedentary life-style, tobacco use, and coronary-proven behaviors are correlated with stress (e.g., Eysenk, 1990, 1991; Shekelle et al., 1991; Krantz et al., 1996). Smoking, consumption of high-fat diets, sedentary behavior, and hostile, competitive behaviors are independently correlated with cardiovascular outcomes but are also reliably influenced by stress. Smoking contributes to a range of outcomes and appears to be influenced by stress, as is exercise or other behavioral factors that may affect cardiovascular health (e.g. Krantz et al., 1996). Separating direct effects of stress on physiological activity from those effects of stress-induced smoking, sleep problems, or other potential behavioral pathogens is difficult but necessary if we are to most effectively target disease processes for intervention (Matarrazo, 1980). Most of these studies look at one or more conditions thought to be stressful and statistically isolate relationships between these conditions and cardiovascular disease. For example, among women, stress associated with having several roles (e.g., employment, educational attainment) appears to increase risk for cardiovascular disease (Baum and Grunberg, 1991; Brezinka and Kittel, 1996). Job stress, particularly when demand is high and control is low, has also been linked to cardiovascular disease (e.g., Johnson et al., 1996; Kasl, 1996; Theorell and Karasek 1996; Peter and Siegrist, 1997; Weidner et al., 1997). Several studies find associations between mood or distress and hypertension, coronary artery disease, or other disorders (e.g., Carney et al., 1995; Kubzansky et al., 1998; Everson et al., 1998; Barrick, 1999; Jacob et al., 1999). Personality variables related to hostility, optimism, and coping and social variables such as support that typically buffer the effects of stress are also associated with the development of disease, disease events, and recovery outcomes (e.g., Eaker, 1989; Fontana et al., 1989; Johnson et al., 1989; Orth-Gomer and Unden, 1990). In general, research shows a broadly characterized effect of life-style behaviors and stress on cardiovascular disease and health (Kringlen, 1986; Krantz et al., 1988). Stress and Cancer Like heart disease, cancer is a slowly developing disease that features gradual pathophysiological activity and disease events that may have specific triggers. Also like cardiovascular disease, cancer may be influenced by behavioral factors
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Promoting Health: Intervention Strategies from Social and Behavioral Research at several different stages. However, cancer is also different from cardiovascular disease in several ways. First, the underlying pathophysiology is difficult to identify or measure, so detection and intervention during this long recruitment stage are difficult or impossible. In addition, the immune system appears to have direct surveillance responsibilities in cancer defense and some of the most important medical advances in treatment are those that boost immunological defenses or help the immune system identify and target malignant or premalignant cells. Adding to this is the fact that cancer is not a single disease nor does it attack only one or a few systems. Cancer is best thought of as a group of more than 100 diseases that all feature dysfunctional controls on cell proliferation. Cancer begins with mutations that occur in a cell or small cluster of cells, and progresses and becomes malignant through several other mutations in these same cells. These mutations are a function of increasing genomic instability due to age, exposure to mutagenic agents, or other factors, and are reflected in greater and greater relaxation of inhibitions on cell proliferation. In other words, each mutation makes the likelihood of uncontrolled cell growth and proliferation more likely and affected cells begin to grow in uncontrolled fashion. This instability is also related to repair rates or capabilities of cells throughout the body to repair mutations or flush them out. Mutations or more basic damage to DNA that could contribute to further mutation or instability is ordinarily repaired through a variety of cellular repair processes or eliminated through apoptotic activity (which leads cells to destroy themselves). In some cases, repair mechanisms are inhibited, damage is increased, and/or apoptotic controls are reduced, allowing mutations to be reproduced and further increasing proliferation of abnormal cells. Recent theory in immunology posits several mechanisms for immune system surveillance and defense against developing tumors; natural killer (NK) cells, for example, can conjugate or bind with tumor cells, create pores in the tumor cell membrane, and inject substances that can initiate apoptosis in tumor cells. Immune defenses against tumor cells depend on accurate identification of tumor cells and rapid elimination of them. Anything that interferes with these processes may inhibit overall tumor rejection and enhance cancer development. There is some evidence that stress can contribute to the onset of cancer, including a considerable amount of circumstantial evidence of such links, mostly in the form of correlations between stressors and cancer diagnosis. Most studies that address stress or other behavioral factors in the etiology of cancer do not find large effects of these variables, for many reasons. The most important, perhaps, is the issue of timing and matching disease-related events to stressful episodes or other life experiences. If one is interested in the relationship between stress and cancer etiology, it is necessary to identify stressors characterizing a fairly long, extended period during which the disease develops. Unfortunately, we cannot detect early development of most cancers and cannot specify the length of the recruitment period. In some cases, a nascent breast cancer, for example, may be detectable after 5 years of development, in other cases, this developing tumor
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Promoting Health: Intervention Strategies from Social and Behavioral Research may grow for 10 years before it is detected. Correlating stressful life events or other stressors with possible disease processes that cannot be identified readily over such long periods of time is a difficult task and is likely to yield moderate to weak correlations due to “noise” or nuisance variance associated with other events or other illnesses generated during these extended periods. Large, long term prospective studies in high-risk populations involving collection of biomarkers of disease development are needed, to accomplish this in a meaningful and interpretable manner; such studies would be very expensive, and time consuming, and are presently not feasible given the state of biomarker research and scientific funding. As a result, we are left with suggestive studies indicating that psychosocial variables are related to cancer incidence and progression (Spiegel et al., 1996). For example, loss experienced within a 7-year period preceding diagnosis of cancer was associated with this diagnosis (e.g., Ramirez et al., 1989). Cancer is a stressful disease and treatments for it are stressful as well. Increasing stress, together with economic costs and loss of self-esteem, confer a substantial burden for many patients (Schulz et al., 1995). There are also many animal studies that suggest a link between stress and tumor growth or rejection of neoplasms (e.g., Sklar and Anisman, 1981; Kerr et al., 1999). A meta-analysis of 46 studies linking mood and anxiety disorders, childhood environment, personality, coping, and stress with the development of breast cancer yielded small but significant effects for denial or repressive coping, separation and loss experiences, and stressful life events (McKenna et al., 1999). The authors concluded that there was evidence of a moderate association between these psychological variables and breast cancer, but the size of these relationships was interpreted as equivocal support for the notion that stress contributes to development of the disease (McKenna et al., 1999). However, a more limited review and meta-analysis of research on breast cancer and stressful life events did not find evidence of an association between negative events and the onset of breast cancer (Pettigrew et al., 1999). Given the considerations discussed briefly above, however, it is possible or likely that methodological limitations made it unlikely that stronger effects could be found. The observed modest effect sizes provide some evidence of a connection between stress and coping on the one hand and cancer development on the other and may actually underestimate one's risk. There is some evidence that stress or other behaviors affect damage and repair processes in individual cells. As noted earlier, cells can experience damage from any number of sources, including radiation, some toxins, sun exposure, tobacco and tobacco smoke, and some chemicals. The extent to which damage is experienced and the rate at which damage is repaired are critical in early events characterizing the development of cancer and would appear to be a viable mechanism underlying the effects of behavioral processes on cancer pathophysiology. An early study (Kiecolt-Glaser et al., 1985) found that stress was associated with slower repair of x-ray-induced DNA damage, and subsequent
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Promoting Health: Intervention Strategies from Social and Behavioral Research studies found evidence of stress-related suppression of DNA repair enzymes in rats (Glaser et al., 1985). Studies of medical students comparing high-stress examination periods with lower-stress periods also yielded evidence of inhibited apoptotic activity following cell damage and decreased RNA expression of genetic tumor regulation in stressed medical students (Tomei et al., 1990; Glaser et al., 1993). Although not extensive, these data suggest that stress can interfere with basic cellular processes that could constitute a pathway to the development of new cancers or the enhancement of existing tumor growth. Investigators have reported considerably more evidence that stress, coping, and other behavioral or psychosocial variables affect the course of cancer. Stress has been associated with relapse and recurrence of cancer in several studies (e.g., Spiegel et al., 1998). The extent to which the original diagnosis of cancer was stressful did not predict recurrence of breast cancer in one study but chronic stress assessed before cancer diagnosis was made was a strong predictor of relapse (e.g., De Brabander and Gertis, 1999). Other studies have also shown associations between stress or other biobehavioral factors and cancer recurrence or progression (e.g., Levy et al., 1985, 1989, 1990; Ramirez et al., 1989). Animal studies show this relationship even more clearly and suggest immunological mediation of some of these effects (e.g., Ben-Eliyahu et al., 1991, 1999). Because of the central role of immune system activity in defense against tumors, studies showing relationships between stress and immune system activity among cancer patients are particularly important, suggesting that stress-related immune system changes and tumor growth or metastasis of tumor cells are related (Tejwani et al., 1991; Ishihara et al., 1999). Moreover, investigation of immune system variables that might be modifiable should have an important impact on the course of cancer. There is growing evidence of stress effects on immune system activity mediated principally by central and sympathetic nervous system activity and neuroendocrine systems (e.g., O'Leary, 1990; Felten and Felten, 1991). As noted, the immune system plays several roles in cancer defense, including immunosurveillance functions that involve immune system activity directed at locating and eliminating new or developing tumors and controlling metastases (e.g., Herberman, 1991). Natural killer cells, cytotoxic T lymphocytes, and other effectors in the system can detect tumor cells and in most cases conjugate or adhere to them to produce killing. These processes are mediated by a number of other activities, factors, and cells, suggesting that a broad look at immune system mediation of stress effects on cancer course is necessary. Evidence suggests that behavioral intervention in healthy populations or in groups with other immune system-related diseases are useful in supporting or boosting a number of aspects of immune function (e.g., Hall and O'Grady, 1991; McGrady et al., 1992). There is also evidence that these relationships hold in studies of people who have cancer. For example, anticipating surgery shortly after the diagnosis of cancer or other stressors associated with cancer or cancer treatment may sup-
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Promoting Health: Intervention Strategies from Social and Behavioral Research press natural killer cell activity and thereby inhibit defense against micrometastases or spread of cancer cells (e.g., Van der Pompe et al., 1998). A good deal of evidence of stress-related effects on NK cells has been reported (e.g., McKinnon et al., 1989; Kiecolt-Glaser and Glaser, 1992; Cohen et al., 1993; Schedlowski et al., 1993; Delahanty et al., 1996; Ironson et al., 1997;) and many of these effects are also apparent in cancer patient populations (e.g., Levy et al., 1985; Van der Pompe et al., 1998; Gerits and De Brabander, 1999). Cancer surgery has also been associated with suppressed NK cell lysis of tumor cells, interferon production, and lymphocyte proliferation to mitogen challenge (Andersen et al., 1998). Studies have found endocrine sequelae of stress in cancer patients that are associated with immune system regulation in healthy populations, including elevated resting levels of cortisol and attenuated hypothalamic-pituitary-adrenal reactivity to acute stressors (e.g., Van der Pompe et al., 1996). To make a long and growing story short, evidence strongly suggests that stress and other behaviors or biobehavioral processes can affect cancer course and likely do so through effects on cellular repair mechanisms and on immune system surveillance. Stress and HIV Disease HIV disease and AIDS are also different from cardiovascular disease in many ways. They refer to the chronic disease established by infection with the human immunodeficiency virus, a relatively new retrovirus that lives in and destroys components of the immune system. Earlier we noted that advances in sanitation, public health, and drug development had greatly limited the dangers of infectious illnesses and had eradicated most of them as major sources of disease and disability. HIV disease and AIDS are an exception to this trend, having emerged in the past 25 years as a major threat to life and well being. The virus is resistant to traditional antiviral therapies. It is spread through intimate sexual contact or in blood or blood products and is therefore commonly contracted as a result of sexual activity or intravenous drug use. It is lymphotropic, being drawn to and living in lymphocytes that are integral components of the immune system. Once established, it replicates itself many times over and destroys its host cell, releasing new viral particles to search for additional host cells. Historically, we have gauged the disease's progress by monitoring helper T lymphocytes, which appear to be a preferred and/or primary host for the HIV. Advancing disease ordinarily causes a precipitous decline in the numbers of helper cells and a corresponding inhibition of immunocompetence. While HIV disease is initiated when the virus is introduced into the body and infection established, it can pass through many stages before reaching its end stage, AIDS. Often it passes through a period of latency or greatly reduced activity. Several viruses similarly become latent once establishing infection, and herpes viruses are reactivated periodically when immune or neural control of them is reduced or eliminated. Unlike these viruses, however, latency and
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Promoting Health: Intervention Strategies from Social and Behavioral Research reactivation of HIV do not appear to be recurrent, episodic phenomena. Once the HIV is activated or is able to overcome immune system defenses that hold it in check, it systematically compromises the immune system and affects a range of other functions. Criteria for AIDS have varied as classification schemes for the disease have been proposed and revised, but generally AIDS refers to the point at which the immune system has been so compromised that the patient becomes susceptible to opportunistic infections—diseases or disorders that are not as prevalent or dangerous when the immune system is intact. Behavioral issues have been particularly important in studying and dealing with the HIV/AIDS epidemic. First, HIV infection is associated with behaviors such as sexual activity and drug use, and infection can generally be prevented through a combination of abstinence, monogamy, contraception, and use of clean, uninfected needles. Most attention from the behavioral science community has been in this area of prevention, with program development in teaching people to use “safer sex,” distribution of bleach and/or clean needles to intravenous (IV) drug users, and so on. Less attention has been paid to whether behavioral factors affect the HIV and progression of disease once infection has been established. However, there are now sufficient data to establish a plausible case for such influences. Like cardiovascular disease and cancer, HIV disease has a variable course and progresses through latency or as it overwhelms immune defenses at widely variable rates. Some people who have been infected with HIV may remain healthy and free from opportunistic infection for many years, but others decline more rapidly and become symptomatic soon after infection (e.g., Munoz et al., 1989; Phair et al., 1992). This variable course has been attributed to differences in viral strains, host immune resistance, and psychosocial variables such as stress (e.g., Levy, 1991; Kemeny, 1994; Cole et al., 1996). Early in the study of HIV disease and AIDS, scientists interested in the effects of stress or behavior on immune status and function began to theorize about application of this work to HIV progression (Soloman, 1987; Solomon et al., 1991). Noting that HIV disease could be discussed in the context of interactions between the central nervous system and the immune system, these theorists argued that anything that perturbed or altered the ability of the immune system to defend the organism could affect the speed of spread of HIV and hasten the development of AIDS. Early data suggested that several variables might be involved, most notably stress, coping, social support, and emotional or autonomic reactivity (Solomon et al., 1991). Since then data have accumulated suggesting that stress and coping are significant predictors of progression of HIV disease (e.g., Goodkind et al., 1992; Remiea et al., 1992; Reed, 1994; Schlebush and Cassidy, 1995; Mulder et al., 1999). Coping and self-efficacy appear to mediate stressful effects of being HIV seropositive, reducing distress and stress-related immune system fluctuations (e.g., Antoni et al., 1995; Benight et al., 1997). Major stressors may cause exacerbations or intensification of disease processes or symptoms in several
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Promoting Health: Intervention Strategies from Social and Behavioral Research diseases (e.g., Lutgendorf et al., 1995), and variation in stress hormones appears to be related to differences in rates of HIV infection (e.g., Antoni et al., 1991). Depression is also known to affect immune status and function but is not necessarily associated with progression of HIV disease (Lyketsos et al., 1996; Miller et al., 1997). Finally, there is some evidence that psychological inhibition confers negative effects on several basic bodily processes and that gay man with HIV infection appear to progress more rapidly when they report concealing their sexual orientation (Cole et al., 1996). Interpretation of these studies is complicated by their correlational nature and the complexities of the disease and its social context. For example, social or stress-related changes associated with HIV disease may be both a cause and an effect of disease progression. In a study of 925 Australians living with HIV disease or AIDS, disease progression predicted employment status (Ezzy et al., 1999). Half of those leaving work reported that declining health was the reason, and since unemployment appears to be stressful one could expect that losing work might further contribute to disease progression. This same reasoning complicates the appropriate interpretation of studies of depression and HIV/AIDS. For example, Siegel and her colleagues found that gay and bisexual men with HIV or AIDS were at greater risk for psychological distress than would be expected if they did not have the disease and that risk increased as their disease progressed (Siegel et al., 1996). The results of this clearly indicated that adjustment problems associated with HIV disease were an important source of distress but could not specify whether these adjustment problems were a product of disease progression or fed back to affect disease course. An interesting avenue of investigation has been studies of inhibition and stress as predictors of disease course. As noted earlier, psychological inhibition, defined as either voluntary or involuntary constraint of discussion or disclosure about a stressful or important event or fact, can also affect well being (e.g., Pennebaker et al., 1987). Many people living with HIV are gay or bisexual, and some of these people may be reluctant to disclose their sexual identities or lifestyles. It is possible, then, that the concealment of one's sexual preferences is stressful and that men who do not disclose such information are at risk for more serious disease. This is similar to the findings of a study by Cole and his associates (Cole et al., 1996) that followed HIV-seropositive but asymptomatic men for 9 years. Time to critical levels of helper lymphocytes, AIDS, and AIDS-related mortality were related to the degree to which homosexual activities were concealed (Cole et al., 1996). These effects may have been due to coping style differences associated with disclosure rather than to the effects of psychological inhibition (e.g., Ostrow, 1996), but the importance of these findings is broader than the specific mechanisms involved. There are not many studies that specifically measure the mediating effects of immune system activity when evaluating effects of stress on HIV disease progression. There is evidence that changes in several immune parameters that
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Representative terms from entire chapter: