Dispositional depression and hostility are associated with inflammatory markers of cardiovascular disease in African Americans
Highlight
► Our findings highlight the importance of examining dispositional characteristics when assessing cardiovascular disease risk in African Americans.
Introduction
Cardiovascular disease (CVD) is the number one cause of morbidity and mortality in the United States and disproportionately burdens African Americans (Yancy, 2005, Nabel, 2003). In comparison to Caucasians, African Americans have higher rates of diabetes mellitus (DM), obesity, and hypertension, which are associated with increased susceptibility to atherosclerosis, myocardial infarction (MI), coronary heart disease (CHD), and stroke (Berenson et al., 1998, Yusuf et al., 2004, Blankstein et al., 2011, Sacco et al., 2001, Carter et al., 1996, Flegal et al., 2010, Borrell, 2009). Although biological risk factors contribute to disparities between African Americans and other ethnic groups, psychological risk factors, such as depression and hostility, also contribute to the pathogenesis and expression of CVD and poorer cardiovascular health (Ariyo et al., 2000, Musselman et al., 1998, Kop, 1999).
The association between depressive symptoms, hostility, and CVD risk is greater among African Americans, when compared to Caucasians (Lewis et al., 2009, Jonas and Lando, 2000, Jonas and Mossolino, 2000, Davidson et al., 2000). Depressive symptoms have been associated with CVD risk factors, such as hypertension, obesity, DM, and stroke (Wuslin & Singal, 2003; Davidson et al., 2000, Dixon et al., 2003, Palinkas et al., 2004, Everson et al., 1998). Hostility has also been recognized as an independent predictor of CVD, CHD, low-density lipoproteins (LDL), cardiac death, MI, and hypertension (Graham et al., 2006, Miller et al., 1996, Brindley et al., 1993, Shekelle et al., 1983, Yan et al., 2003).
Psychological stressors can activate the hypothalamic-pituitary-adrenocortical (HPA) axis and the sympathetic nervous system to influence the onset and development of CVD. HPA activity can increase cortisol, which is implicated in the development of atherosclerosis and hypertension (Ghiadoni et al., 2000, Hajat et al., 2010, Whitworth et al., 2005). Moreover, the HPA axis can bi-directionally regulate the proinflammatory cytokine interleukin-6 (IL-6) and the hepatocyte produced C-reactive protein (CRP). Chronic IL-6 production can lead to the destruction of the cardiovasculature (Hou et al., 2008, Lagathu et al., 2003, Memoli et al., 2007, Singh et al., 2005, Fredj et al., 2005). Interleukin-6 is involved in the initiation and progression of atherosclerotic cardiovascular disease and can precede the onset of DM (Andersen and Pedersen, 2008, Memoli et al., 2007). Furthermore, CRP is a hallmark of acute and chronic inflammation. High levels of CRP are associated with risk of stroke, MI, and poor cardiovascular events, even among healthy individuals (Ridker et al., 1997). Both IL-6 and CRP are associated with sub-clinical and clinical CVD (Cesari et al., 2003, Ridker, 2007, Willerson and Ridker, 2004, Ridker et al., 2000, Ridker et al., 2002). Thus, examination of these markers concurrently may be a better predictor of CVD risk than when examined independently.
Studies show that greater depressive symptomatology and hostility are associated with increased concentrations of IL-6 and CRP in the blood (Suarez, 2004, Suarez, 2003a, Suarez, 2003b). A meta-analysis of studies conducted between 1967 and 2008 demonstrated a consistent association between depression, IL-6 and CRP, in both clinical and population-based studies, and suggested that depressive symptoms increased CVD risk even among non-patient samples (Howren et al., 2009). Of note, these studies have primarily examined the relation between acute depressive symptoms and inflammation to explain CVD risk. There is recent evidence to suggest that sustained long-term personality dispositions promote a more detrimental cardiovascular profile, particularly in African–American men (Sims et al., 2010).
Previous research has examined the joint effects of hostility and severity of depressive symptoms on inflammation (Suarez, 2003a, Miller et al., 2003, Stewart et al., 2008, Brummett et al., 2010). Consistently across these studies, an interactive relationship between depressive symptoms, hostility, and inflammatory marker levels was found. Suarez (2003a) categorized a sample of 90 relatively healthy men into groups based on depressive symptom and hostility scores. Results indicated that the group with higher depressive symptoms and higher hostility had greater levels of IL-6 compared to the remaining groups. Similarly, depressive symptoms moderated the relationship between hostility and IL-6 and CRP in a sample of 316 older individuals aged 50–70 years (Stewart et al., 2008). In these studies, positive associations between hostility and inflammatory markers were observed in participants that endorsed higher depressive symptoms, but not lower. However, Miller et al. (2003) found, in a sample of 100 ethnically diverse individuals, higher hostility was associated with greater IL-6 among participants with lower depressive symptoms scores. Sample differences among the studies may account for discrepant findings, although this is unclear. For example, gender composition may impact findings. Studies examining the moderating effects of gender on relations among depressive symptoms, hostility and inflammatory markers have yielded mixed findings. Brummett et al. (2010) found depressive symptoms were related to inflammatory markers more strongly in hostile women, while other studies did not find significant interactions between depressive symptoms, hostility, gender, and inflammatory markers (Stewart et al., 2008, Miller et al., 2003). Further, few studies have examined the combined effects of more longstanding personality styles. In one study, Boyle and colleagues (2007) found that a composite of depressive, angry and hostile personality styles predicted 10-year increases in complement component 3, an important marker of inflammation that is activated by CRP.
To our knowledge, there are no studies that have explored the temporal distinction in depression and further examined whether they work in tandem with hostility to influence inflammatory marker levels in African Americans. The current study investigated the independent and synergistic influences of state depression, dispositional depression and hostility on IL-6 and CRP. We posited that each of these psychological constructs would be independently associated with higher levels of inflammatory markers IL-6 and CRP. We further hypothesized that state and dispositional depression would be more strongly associated with markers of inflammation in the presence of higher levels of hostility, suggesting that greater cardiovascular risk is associated with the interaction of both negative affective and dispositional attributes. Moreover, we aimed to examine within-group differences to determine whether gender and socio-economic status (SES) influence CVD risk, as found in prior research (Lewis et al., 2011, Winston et al., 2009, Winkleby et al., 1998).
Section snippets
Methods
The current study was conducted as part of the National Minority Organ Tissue Transplant Education Program (MOTTEP) at Howard University entitled Psychoneuroimmunological Risk Factors in Renal Health and Disease and was approved by the Howard University (HU) Institutional Review Board. The study examined stress and psychoneuroimmunological factors in renal health and disease in African Americans. It was conducted from 2004 to 2007 at the General Clinical Research Center (GCRC) at HU Hospital.
Participant characteristics
The mean age of participants was 45.56 (SD = 11.60). The mean educational attainment of participants was 13.83 years (SD = 2.42). Women had more educational attainment than men t(195) = 2.58, p = .011. In contrast, more men earned greater than $50,000/year as compared to women (p < .05). Mean SBP fell in the pre-hypertensive range for the total sample, as well as for both men and women. Mean DBP was in the normal range. On average, women were obese, while men fell within the overweight range for BMI.
Discussion
African Americans have higher rates of CVD and associated morbidity and mortality compared to other racial/ethnic groups. Although higher rates of hypertension, DM, and obesity have prevailed in this population, biological risk factors alone have not fully explained the disparities that exist. Psychological factors have contributed to elevated inflammatory responses and are associated with increases in CVD risk. The current study sought to examine the influence of state depression,
Acknowledgments
This paper was made possible by Howard University’s General Clinical Research Center Grant #2MO1-RR010284 from the National Center for Research Resources (NCRR) a component of the National Institutes of Health (NIH) and its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH.
Health Promotion and Risk Reduction Research Center (HealthPARC).
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