Overview and Specific Aims

Reducing racial and socioeconomic position (SEP) health disparities in the United States are among the highest priorities of the National Institute of Health. Yet, the causes of disparities and the ways they might be eliminated remain poorly understood. We argue here that progress has been impeded by several problems, the two most important of which are the problem of health outcome misclassification and the failure to adequately assess differences in stress exposure. In our view, information on the origins of health disparities can most effectively be pursued by an approach that avoids the typical classification error of counting disordered individuals as non-disordered because they do not exhibit the particular disease or disorder under investigation or have a nascent disorder that has not progressed enough to be clinically detectable. Such misclassification is likely to have obscured potentially modifiable factors that are centrally implicated in the documented elevation in health risk among African Americans and persons of low SEP.  We argue that it can be avoided by a joining of biomarker methodologies for estimating physical health status and reliable estimates of the presence of psychiatric and substance use disorders/problems within a community-based population study.

In addition, there are good grounds for contending that the failure of prior research to take account of a range of social stressors has significantly biased estimates of racial and SEP differences in exposure to stress and resulted in the systematic underestimation of the contributions of stress exposure to the occurrence of racial and SEP disparities in health. This failure has left open the question of the relative contributions to health disparities of differences in exposure to stress and differences in vulnerability to stress. This is so because unmeasured differences in stress exposure across race or SEP will masquerade within research findings as difference in adaptational ability. Accordingly, poor measurement of exposure differences tends, incorrectly we believe, to foster conclusions that locate the source of health disparities largely within the skins of African Americans and persons of low SEP, which risks misplacing the blame for the disparities on the victims themselves.

Among the unique aspects of the proposed research are: 1) Avoiding epidemiologic misclassification by combining clinical and subclinical assessments of psychiatric and substance use disorders and problems with one or more measures of allostatic load and telomere-based cell aging assays; 2) Expanding the measurement of stress exposure to include, in addition to recent life events, lifetime exposure to major and potentially traumatic events, chronic stressors, discrimination stress, and, among African Americans, colorism, and stress arising from uncertainty and/or ambiguity associated with covert discrimination; and 3) Within the context provided by 1 and 2 above, to assess an exceptionally comprehensive array of risk/protective factors including environment-environment interactions and, through a subsequent grant application, gene-environment interactions.

Evidence revealing racial and socio-economic disparities in health has long been available and continues to accumulate.  Among those that are now well documented are Black-white inequities in overall health, all-cause mortality and life expectancy, low birth weight, infant mortality, cerebrovascular disease, cancer, hypertension, and stroke, as well as various psychiatric and substance use disorders. Similar disparities are found across SEP. Although race and SEP are associated, prior research has documented substantial health disparities across SEP within race and across race within SEP (Geronimus et al. 1996; Williams 1996).

These disparities imply massive impact in terms of unequal suffering and dramatic social and economic costs. It is thus no surprise that substantial research has focused on efforts to identify the origins of such disparities. It is clear that racial and SEP differences in the availability, use, and effectiveness of medical care (e.g. Escarce et al. 1993; Ferguson et al. 1997; Fincher et al. 2004; Johnson et al. 1993; Peterson et al. 1997; Klabunde et al. 1998), and in level of trust in health care institutions and physicians, are implicated (Doescher et al. 2000; Kao et al. 1998a, 1998b; Saha et al. 2003; Thom and Campbell 1997), as are differences in a variety of health behaviors (Healthy People 2000; McGinnis and Foege 1993; Fraser et al. 1997). However, it is also clear that adjustments for these collective differences leave the majority of racial and SEP health disparities unexplained (e.g. Lynch et al. 1996; Marmot et al 1997; Lantz et al. 1998, 2001). Available evidence points to the conclusion that potentially modifiable social factors play a fundamental role in racial and SEP health disparities-a role that includes but goes substantially beyond their significance for such well-established risk factors as poor nutrition, smoking, sedentary life style, and obesity. As the Director of the NIH Office of Behavioral and Social Sciences Research has recently noted “a general consensus has not emerged regarding the causes of disparities or regarding the best ways to eliminate disparities.”  The research proposed here addresses this gap in our knowledge by taking a transdisciplinary approach that will address some key contributing deficiencies of prior studies.

Multiple strands of evidence have accumulated in support of the role of differential stress exposure in the etiology of health disparities (e.g. Adler et al. 1993; Lantz et al. 1998; Wilkinson 1996), and stress “has emerged as a leading contender for translating low social status into poor health” (Dowd and Goldman 2006:633). Despite this, we contend that the explanatory significance of social stress with respect to health disparities has never been effectively tested because of misclassification in the distinction of the disordered from the well and the inadequate estimation of differences in exposure to stressors (additional limitations to previous research are described below). This study will address the social origins of race and SEP disparities, seeking to overcome these limitations and to identify potentially modifiable factors associated with increased or decreased health risk—within as well as across race and SEP.

 

Specific Aims

1.   To evaluate the stress hypothesis and assess the utility of an elaborated “stress process” model for explaining race and socioeconomic position (SEP) differences in health and changes in health over time, where:

a)   health status is estimated in multiple ways that address the problem of misclassification.

b)   variations in stress exposure are estimated more comprehensively than in prior research.

c)   the direct, mediating and moderation effects of an extended array of social and personal coping resources and of contextual and cultural factors are examined in the context of a) and b) above.

2.   To confirm and extend epidemiological estimates of race and SEP differences in the prevalence of health problems, variously and collectively defined, while addressing the misclassification problem.

3.   To evaluate the interrelationships of differing dimensions of health, variously estimated, and their risk significance for one another, in cross section and over time.

4.   To describe the distribution of each risk factor identified across race, SEP, age and gender while examining antecedent factors that put individuals and groups at differential risk for acquiring such risk factors.

5.   To obtain and preserve samples to support subsequent studies (not here proposed) on gene-environment interactions relating to factors identified to be, or hypothesized to be, of risk or protective significance.

 

 

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