 |
|
|
| |
Childhood Trauma and Health Outcomes in HIV-Infected Patients: An Exploration of Causal Pathways
|
| |
| |
Download the PDF here
JAIDS Journal of Acquired Immune Deficiency Syndromes: 1 April 2012
This article draws on data from the Coping with HIV/AIDS in the Southeast (CHASE) Study, an observational cohort study designed to describe and explore the associations between psychological characteristics, health behaviors, and health outcomes in HIV-infected patients engaged in medical care.
"greater lifetime trauma exposure was associated with all outcomes considered (Table 3). Each additional type of lifetime trauma was associated with 18% increased odds of unprotected sex, 13% (3% to 24%) increased odds of ARV nonadherence, 12% (4% to 21%) increased odds of hospitalization, 14% (6% to 22%) increased odds of ED use, 13% (5% to 22%) increased odds of more than 4 days in bed, a 12% (0% to 24%) increased hazard of HIV disease progression, and a 0.8-unit (0.4-1.2) lower SF36 physical health score."
"Two primary observations emerge from these analyses. First, in models designed to estimate the total effect of trauma on HIV outcomes (ie, adjusting for sociodemographic confounders but excluding potential mediators), greater lifetime exposure to traumatic experiences is associated with a wide range of deleterious behavioral and health consequences in this sample of people living with HIV. It should be noted that we reported associations in terms of each 1-unit increase in the continuously measured trauma exposure variable. If 1 additional type of trauma is associated with a 13% increased odds of nonadherence, for example, an individual with the sample median of 3 lifetime traumatic experiences would be expected to have 44% increased odds of medication nonadherence (1.133 = 1.44) compared with someone with no trauma history. This finding is consistent with research that suggests a cumulative effect of lifetime traumatic experiences on health-related outcomes.1 It also supports findings that trauma may accelerate disease progression in individuals living with HIV.38,39
Second, trauma history demonstrated persistent associations with this wide range of behavioral and health outcomes even after adjustment for a detailed set of hypothesized psychosocial mediators. Although about half of the association of trauma with health care utilization outcomes appeared mediated by psychosocial variables (in particular, recent stressful events), there was no evidence of psychosocial mediation for the associations between trauma and behavioral (sexual risk behaviors and medication adherence) or health outcomes (physical symptoms and HIV disease progression).
The observation that none of the proposed psychosocial mediators fully explains the association between lifetime trauma and HIV-related outcome variables suggests the consideration of other causal pathways. Behavioral and lifestyle-related factors not measured in this study that may help explain the effect of early trauma on later health and behaviors include effects of trauma on low self-esteem, dissociative symptoms, worse self-care behaviors such as nutrition and exercise, and predisposition to experiencing other traumatic situations such as intimate partner violence.40-42 Some recent research also suggests that biological or neurological pathways may explain part of the effect of trauma on later health, for example, through dysregulation of the hypothalamic-pituitary-adrenal axis (eg, higher cortisol) and greater autonomic activation (eg, higher catecholamines).43-49 Recent neuroimaging studies have also begun to document lasting changes in areas of the brain, specifically the amygdala, hippocampus, and prefrontal cortex, associated with traumatic stress."
Pence, Brian Wells PhD, MPH*,; Mugavero, Michael J. MD, MHSc; Carter, Tandrea J. PhD; Leserman, Jane PhD; Thielman, Nathan M. MD, MPH,#; Raper, James L. JD; Proeschold-Bell, Rae Jean PhD,; Reif, Susan PhD, MSW,; Whetten, Kathryn PhD, MPH,,**
*Department of Community and Family Medicine, Duke University, Durham, NC Center for Health Policy and Inequalities Research, Duke University, Durham, NC Duke Global Health Institute, Duke University, Durham, NC Division of Infectious Diseases, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL Institute for Health and Human Services, Appalachian State University, Boone, NC Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC #Division of Infectious Diseases and International Health, Department of Medicine, Duke University, Durham, NC **Terry Sanford School of Public Policy, Duke University, Durham, NC.
Correspondence to: Brian W. Pence, PhD, Center for Health Policy and Inequalities Research, Box 90392, Durham, NC 27705 (e-mail: bpence@aya.yale.edu).
Presented at the 2010 American Psychosomatic Society Annual Meeting, March 10-12, 2010, Portland, OR; and at the 6th International Conference on HIV Treatment and Prevention Adherence, May 22-24, 2011, Miami, FL
Abstract
Objective: Traumatic life histories are highly prevalent in people living with HIV/AIDS and predict sexual risk behaviors, medication adherence, and all-cause mortality. Yet the causal pathways explaining these relationships remain poorly understood. We sought to quantify the association of trauma with negative behavioral and health outcomes and to assess whether those associations were explained by mediation through psychosocial characteristics.
Methods: In 611 outpatient people living with HIV/AIDS, we tested whether trauma's influence on later health and behaviors was mediated by coping styles, self-efficacy, social support, trust in the medical system, recent stressful life events, mental health, and substance abuse.
Results: In models adjusting only for sociodemographic and transmission category confounders (estimating total effects), pasttrauma exposure was associated with 7 behavioral and health outcomes including increased odds or hazard of recent unprotected sex [odds ratio (OR) = 1.17 per each additional type of trauma, 95% confidence interval = 1.07 to 1.29], medication nonadherence (OR = 1.13, 1.02 to 1.25), hospitalizations (hazard ratio = 1.12, 1.04 to 1.22), and HIV disease progression (hazard ratio = 1.10, 0.98 to 1.23). When all hypothesized mediators were included, the associations of trauma with health care utilization outcomes were reduced by about 50%, suggesting partial mediation (eg, OR for hospitalization changed from 1.12 to 1.07), whereas point estimates for behavioral and incident health outcomes remained largely unchanged, suggesting no mediation (eg, OR for unprotected sex changed from 1.17 to 1.18). Trauma remained associated with most outcomes even after adjusting for all hypothesized psychosocial mediators.
Conclusions: These data suggest that past trauma influences adult health and behaviors through pathways other than the psychosocial mediators considered in this model.
Traumatic life experiences such as childhood sexual and physical abuse are recognized as having profound and far-reaching implications for health and health-related behaviors.1 Early research on childhood trauma documented elevated rates of a range of psychological disorders in survivors of childhood sexual and physical abuse. Later studies have extended these findings, first by considering a wider range of lifetime traumatic experiences1 and second by demonstrating associations of traumatic exposure with harmful health behaviors (high-risk sexual behaviors, poor adherence to medical treatments) and increased somatization, poorer health outcomes, and higher mortality rates.2-4 These associations are particularly pronounced and consistent in medically ill populations, including people living with HIV/AIDS.5-7
Although this literature suggests far-reaching health consequences of childhood traumatic experiences, a theoretical understanding of the causal pathways through which pasttrauma influences later health behaviors and outcomes is incomplete. Proposed causal mediators include both psychosocial and physiologic responses to trauma.6 Briere et al suggest that childhood sexual and physical abuse can impact psychological symptoms into adulthood.2,3,8 Other research postulates that traumatization, especially early in life, can have a direct effect on physiologic processes including suppressing immune function.6 However, empirical tests of the causal models relating trauma to health outcomes are rare.
The purpose of the present article is 2-fold. First, drawing on data from a large cohort of patients receiving outpatient care for HIV infection with detailed information on traumatic exposure, psychosocial characteristics, health care utilization, health behaviors, and health outcomes, we document elevated rates of a range of deleterious outcomes associated with lifetime trauma exposure. Second, we empirically test the extent to which these observed associations between trauma and later outcomes can be explained by mediation through psychosocial pathways to extend our understanding of the causal mechanisms underlying these relationships.
DISCUSSION
Two primary observations emerge from these analyses. First, in models designed to estimate the total effect of trauma on HIV outcomes (ie, adjusting for sociodemographic confounders but excluding potential mediators), greater lifetime exposure to traumatic experiences is associated with a wide range of deleterious behavioral and health consequences in this sample of people living with HIV. It should be noted that we reported associations in terms of each 1-unit increase in the continuously measured trauma exposure variable. If 1 additional type of trauma is associated with a 13% increased odds of nonadherence, for example, an individual with the sample median of 3 lifetime traumatic experiences would be expected to have 44% increased odds of medication nonadherence (1.133 = 1.44) compared with someone with no trauma history. This finding is consistent with research that suggests a cumulative effect of lifetime traumatic experiences on health-related outcomes.1 It also supports findings that trauma may accelerate disease progression in individuals living with HIV.38,39
Second, trauma history demonstrated persistent associations with this wide range of behavioral and health outcomes even after adjustment for a detailed set of hypothesized psychosocial mediators. Although about half of the association of trauma with health care utilization outcomes appeared mediated by psychosocial variables (in particular, recent stressful events), there was no evidence of psychosocial mediation for the associations between trauma and behavioral (sexual risk behaviors and medication adherence) or health outcomes (physical symptoms and HIV disease progression).
The observation that none of the proposed psychosocial mediators fully explains the association between lifetime trauma and HIV-related outcome variables suggests the consideration of other causal pathways. Behavioral and lifestyle-related factors not measured in this study that may help explain the effect of early trauma on later health and behaviors include effects of trauma on low self-esteem, dissociative symptoms, worse self-care behaviors such as nutrition and exercise, and predisposition to experiencing other traumatic situations such as intimate partner violence.40-42 Some recent research also suggests that biological or neurological pathways may explain part of the effect of trauma on later health, for example, through dysregulation of the hypothalamic-pituitary-adrenal axis (eg, higher cortisol) and greater autonomic activation (eg, higher catecholamines).43-49 Recent neuroimaging studies have also begun to document lasting changes in areas of the brain, specifically the amygdala, hippocampus, and prefrontal cortex, associated with traumatic stress.50
Although this dataset was rich in psychosocial measures, it did not include markers of potential physiologic pathways such as cortisol38 and natural killer cells51,52 that would have allowed a direct comparison of the explanatory power of psychosocial versus physiologic mediators. However, our study does make a significant contribution to the growing body of research, which suggests that the cumulative burden of lifetime trauma affects a variety of outcomes for individuals living with HIV.6 By failing to fully explain our results based on a range of psychosocial mediators, it highlights the importance of further research to better understand the mechanisms through which trauma affects later health and health-related behaviors.
Strengths of this study include the large multisite sample, the consecutive sampling strategy, the longitudinal design, the detailed lifetime trauma history, and the wide range of psychosocial domains systematically assessed with validated measures. Although the sample is reflective of HIV patients in care in the southern United States, the results may not generalize to more urbanized parts of the country or to HIV-infected individuals not in medical care.
Psychosocial characteristics vary over time. The putative mediators may have had different values at the time they were measured for this study than at the time they would have exerted their mediating influence or may have been imprecisely measured by the scales selected. This measurement bias would tend to attenuate the associations of the mediators with the exposure and outcome variables, potentially underestimating the importance of the mediators' role. All mediators were measured at both baseline and 27 months, and the intraclass correlation coefficients for this set of variables between the 2 time points ranged between 0.41 and 0.59, suggesting moderate stability of the mediators over an extended time period. Measurement error may also have affected our self-reported measure of trauma history, most likely through omission of past events, although the severity of the experiences queried on the trauma assessment would tend to reduce such underreporting.
CIs around the mediation ratios were broad, reflecting the general low power of tests of mediation even in large samples such as this one. However, it is notable that even these broad CIs excluded complete mediation (mediation ratio of 100%) for medication adherence, unprotected sexual intercourse, and general health, suggesting that even if these psychosocial pathways explain part of the association of trauma with outcomes, at least part of the effect likely goes through other pathways.
In summary, the present study supports other research in documenting strong associations of past trauma with a wide range of negative health-related behaviors and health outcomes in HIV-infected patients. It additionally suggests that these associations are largely not mediated by a range of psychosocial characteristics including coping, self-efficacy, social support, trust, stressful events, and current mental health and substance abuse. Further research on the mechanisms through which trauma impacts later behaviors and health is essential to build effective interventions that will promote use of safer sexual practices, optimal antiretroviral medication adherence, and better health outcomes for HIV-infected patients.
RESULTS
Sample Description
Participants in the CHASE Study were primarily between 30 and 50 years of age; approximately one-third were female and 44% were men who reported having sex with other men (Table 1). Approximately two-thirds were of African American race and one-third were white non-Hispanic. Participants had been infected with HIV for a mean of 6.8 years (standard deviation: 4.4 years). Three-quarters were on antiretroviral therapy, and 46% had an HIV RNA viral load <400 copies per milliliter at baseline.
Distribution of Exposure and Outcomes
Participants reported a median of 3 types of lifetime traumatic experiences (range: 0-12; interquartile range: 1-4) (Table 2). Twelve percent reported having had unprotected sex in the past 9 months, and 24% of those on ARVs reported having missed a dose in the past week. Twenty-six percent had been hospitalized and 39% had visited the ED. Participants' overall physical health was slightly worse than the US population average (median SF36 score = 48; US population mean = 50), and 33% had spent >4 days in bed in the past 9 months. HIV disease progression (incident OI or AIDS-related death) was observed in 50 participants over a total of 1033 person-years of observation.
Unadjusted Associations
In bivariable models (model 1), greater lifetime trauma exposure was associated with all outcomes considered (Table 3). Each additional type of lifetime trauma was associated with 18% (95% CI: 9% to 28%) increased odds of unprotected sex, 13% (3% to 24%) increased odds of ARV nonadherence, 12% (4% to 21%) increased odds of hospitalization, 14% (6% to 22%) increased odds of ED use, 13% (5% to 22%) increased odds of more than 4 days in bed, a 12% (0% to 24%) increased hazard of HIV disease progression, and a 0.8-unit (0.4-1.2) lower SF36 physical health score. These estimates shifted only marginally after adjustment for the potential confounders of age, race, sex, education, and self-reported HIV transmission category (model 2).
Mediation Analysis
In comparing the model adjusted only for confounders (model 2, path c) to the model additionally adjusting for all potential mediators (model 5 or model 6, path c'), the odds ratio for each additional type of lifetime trauma shifted from 1.17 to 1.18 (95% CI: 1.06 to 1.32) for unprotected sex, from 1.13 to 1.15 (1.02 to 1.29) for medication nonadherence, from 1.12 to 1.07 (0.97 to 1.18) for hospitalization, from 1.12 to 1.07 (0.98 to 1.17) for ED use, and from 1.13 to 1.06 (0.97 to 1.17) for >4 days in bed (Table 3). The hazard ratio for HIV disease progression shifted from 1.10 to 1.12 (0.97 to 1.30). In modeling the SF36 physical health score, the coefficient for trauma shifted from -0.8 to -0.7 (-1.1 to -0.3).
The mediation ratio for the combined effects of all putative mediators was 39% for hospitalizations, 41% for ED use, 50% for >4 days in bed, 12% for SF36 physical health scores, and <0% for unprotected sex, medication nonadherence, and HIV disease progression. Bootstrapped 95% CIs around the mediation ratios were wide. Although point estimates for unprotected sex, medication nonadherence, and HIV disease progression shifted unexpectedly away from the null upon adjustment for mediators, these shifts were minor relative to the sampling uncertainty (CIs) around the estimates. For bed days, hospitalization, and ED use, the largest shift in point estimates was between models 3 and 4, with the addition to the model of the stage 2 mediator (recent stressful life events) (Fig. 2A). Point estimates for other outcomes changed little between models 2 and 5 (Fig. 2B).
|
| |
|
|
|
|
|
