Race and health
There is a growing debate in the literature concerning whether race and the emphasis on different racial ethnic groups should continue to play a prominent role in health research. The argument against it is premised upon the facts that race is essentially an ideological construction, that race is not the basis upon which differential health outcomes can be explained, and that racial identification is not necessarily stable over time (Nazroo 1998, Smaje 1995). However, from an epidemiological perspective, race remains a significant predictor of health outcomes and, therefore, is arguably a matter worthy of continued empirical attention. This perspective is consistent with the historical inclination of sociological research concerning matters of race on a wide variety of substantive topics (e.g. Emerson et al. 2001, Hughes and Thomas 1998, Hunt et al. 2000). Moreover, Byrd and Clayton (2002: 564) argue against the reinforcement of ‘the general perception in the scientific community that race and ethnicity research lacks rigor in conceptualization, terminology, and analysis’, as it obscures the need to study, understand, and rectify continuing disparities in health outcomes among a health underclass defined, in part, along racial lines. Thus, it would be reasonable to conclude that, so long as multiple social inequalities intersect in categories of a variable labelled ‘race’, sociological inquiry into matters of race will remain important.
Nevertheless, race is a social construction, not a biological fact (Smaje 2000), and explanations for racial differences in health premised upon genetic dissimilarity for the most part have been dismissed (Hayward et al. 2000, Kong et al. 1994). In fact, fewer than one per cent of excess deaths among Blacks can be attributed to differential propensity for hereditary conditions (Leigh 1995). Thus, observed racial patterns of health outcomes are primarily consequences of social forces, rather than genetic history. As Smaje (2000: 114) explains, ‘race in itself can never be invoked as a self-adequate explanation for patterns of health experience’. Nevertheless, as Schulz et al. (2000: 315) argue, ‘[r]ace, as a social construct, remains a powerful organizing feature of American social life, and racial categories both reflect and reinforce group differentials in power and access to social resources’. It follows that race is still a useful organising tool in efforts to understand and rectify inequity on many fronts, not the least of which is health (Gillum 2004).
Socioeconomic status and the racial gap in health
Historically, efforts to explain racial disparities in health in Western societies have focused on socioeconomic inequality and related correlates. In research dating back seventy years, Tibbits (1937) argued:
[i]t is well known that the Negro population is less fortunately situated than the white in terms of income, education, opportunities for obtaining medical care, etc. Hence it seems relatively safe to assume that where there is variation in the degree of health among different economic and social groups of the white population and where Negroes show a higher rate of ill health than the whites, the explanation lies partly, at least, in the low-income status of the Negro (1937: 417–18).
Much of the subsequent research on the topic has adhered to this theory, attempting to explain observed racial differences in chronic disease and premature morbidity through mechanisms rooted in socioeconomic inequality. This theory invariably leads to the hypothesis that, once inequality and related variables are controlled, racial differences in the incidence and prevalence of chronic disease and premature morbidity will disappear. A number of recent studies have continued the longstanding investigation of this hypothesis (e.g. Lantz et al. 1998, Mutchler and Burr 1991, Potter 1991, Rogers 1992), and the findings of these studies support the argument that SES is an important explanatory variable in Black-White differences in a variety of health outcomes.
Much attention also has been given to the proximal causes of this health differential as distinct from the distal cause (i.e. socioeconomic inequality). The objective underlying this class of papers is the enumeration of the mechanisms connecting SES to health. Generally speaking, these proximal causes can be divided into two broad categories: (1) health risk behaviours that are correlated with SES, such as smoking, excessive alcohol consumption, and physical inactivity (e.g. Wickrama et al. 1999, Williams and Collins 1995), and (2) mechanisms arising directly from unequal distribution and access to resources, such as inadequate medical care, dangerous working conditions, and exposure to environmental toxins (e.g. Smith and Kington 1997a, Williams and Collins 1995). While this distinction is important, an extensive review of this topic is outside the scope of this paper.3
The residual racial gap in health
While research on the relationship between socioeconomic inequality and health has explained a substantial segment of the racial disparities in health outcomes, most research still documents an unexplained racial gap in health after adjustment for socioeconomic differences. For example, Rogers (1992) found that adjusting for income and a set of demographic variables narrowed the health gap between Blacks and Whites, but did not fully eliminate it. Christenson and Johnson (1995) found that the protective effect of education on mortality benefited Blacks less than Whites. Huie et al. (2003) found a residual Black disadvantage in mortality net of racial differences in educational attainment, income, net worth, and demographic variables. Mutchler and Burr (1991), adjusting for four indicators of SES as well as various demographic measures, found significant differences between older Blacks and Whites remaining on one of six self-reported health measures and an increase in the Black-White differential on another of the six measures. Ferraro and Farmer (1996) found significant disadvantages for Blacks relative to Whites in the incidence of serious illness, in the declination of self-assessed health over time, and in survival rates, despite numerous controls, including education, income, access to medical care, and prominent health risk behaviours. Ferraro et al. (1997) found greater erosion of self-assessed health and greater increases in the incidence of chronic illness and disability among Blacks compared with Whites, net of prior health conditions, SES, and other relevant controls. Schnittker (2004) found poorer self-assessed health and lower scores on an index of physical health among Blacks relative to Whites after controlling for education, income, and the income-health gradient as it varied by level of educational attainment. In a particularly comprehensive study, Hayward et al. (2000) found a significant Black-White health gap remaining on seven health outcomes after controlling for educational attainment, household income, wealth, availability of health insurance, numerous health risk behaviours, a number of psychosocial characteristics, and other variables.
While just a few of the recent analyses of racial differences in health are documented here, the findings of numerous similar studies agree that SES and its correlates can explain much, but not all, of the differences in health outcomes between Blacks and Whites (Crimmins et al. 2004, Livingston et al. 2004, Smith and Kington 1997a). Authors’ conclusions often agree with the explanation offered by Williams and Collins (1995) in their review of the research addressing the White/Black health differential: ‘within each level of SES, blacks generally have worse health than whites’ (1995: 364). For example, Mutchler and Burr (1991) note that, ‘in terms of self-rated health and some associated health-related behaviours, older Blacks appear to have poorer health than Whites regardless of socioeconomic status’ (1991: 353). Likewise, Ferraro and Farmer (1996) observe that, even after accounting for the SES differential between Blacks and Whites, ‘there are important differences between the health status and health assessments of Black and White Americans’ (1996: 37). Thus, prior research repeatedly demonstrates a stubborn racial gap in health outcomes that persists despite adjustment for socioeconomic inequality and related mechanisms.
Consequently, we must ask, what are the missing factors that will explain the residual racial differences in health outcomes? Socioeconomic status and related mechanisms have been controlled statistically, yet health differences between Whites and Blacks remain. Why?
Explaining the unexplained racial gap in health
One possible explanation for the residual racial gap in health lies in the nature of socioeconomic controls. Measures of SES can only approximate the complex and multifaceted construct, leaving open the possibility of unmeasured covariation between SES and health outcomes (Krieger 2000, Williams and Collins 1995). In other words, the inability of SES to explain fully the race-health relationship may be a methodological artifact (Kaufman et al. 1997). However, the persistence of the residual race-health relationship in numerous studies, using a variety of data, and despite increasingly comprehensive measures of SES, suggests at least the possibility of an excluded explanatory variable operating independently of SES.
Among the potential excluded explanatory variables, chronic stress caused by experiences of racial discrimination is receiving increased attention in the literature (e.g. Brondolo et al. 2003, Clark 2003, Clark and Adams 2004, Karlsen and Nazroo 2002, Krieger 2000, Krieger et al. 1993, Leigh 1995, Livingston 1994, Myers et al. 2004). This line of research argues that the excess of stressors experienced by Blacks as a result of both intergroup and intragroup racism contribute to a chronic elevated physiological stress response (Clark et al. 1999). This elevated stress response is associated with a range of health problems (Berkman and Kawachi 2000, Fremont and Bird 2000, Krieger 2000), including at least two chronic diseases for which Blacks are severely disadvantaged: coronary heart disease and diabetes (Livingston and Carter 2004).
Another potential explanatory variable that is sometimes mentioned, but which has received comparatively little empirical attention, is nutritional healthfulness. Interestingly, the health-related consequences of stress are intertwined closely with nutritional deficiencies. Prolonged stress tends to deplete physiological stores of, and increase physiological demand for, essential nutrients (Semmes 1996). In addition, healthy nutritional behaviours serve as a barrier against the damaging effects of prolonged stress, and poor nutrition itself can induce a physiological stress response (Semmes 1996). Lastly, chronic stress contributes to feelings of helplessness, hopelessness, and loss of control, which, in turn, are associated with a greater propensity for unhealthy lifestyle behaviours, such as poor nutritional choices (Kristenson et al. 2004). Thus, as they pertain to health outcomes, nutritional quality and stress are interrelated.
In addition to the interrelationship between nutrition and stress, nutritional quality has a well-established, strong, and direct relationship to health outcomes.4 As Blocker (1994) observes, ‘[g]ood nutrition is crucial to the maintenance of health, and dietary factors contribute substantially to preventable chronic illness and premature death’ (2004: 267). The relationships between nutrition and cardiovascular disease, cancer, stroke, and diabetes − the first, second, third, and seventh leading causes of death in the United States − are particularly strong (Blocker 1994). An estimated 30 per cent of all deaths due to cancer in the United States can be attributed to diet (Harvard School of Public Health 1996), and dietary and physical inactivity patterns collectively cause 14 per cent of all deaths in the United States, second only to tobacco as the leading cause of death (McGinnis and Foege 1993). In addition to cancer prevention, it is estimated that dietary changes could reduce the risk of heart attack and stroke by 20 per cent to 30 per cent and the risk of preventable diabetes by 50 per cent to 75 per cent (Foerster et al. 1999).
The specific dietary practices associated with reduced risk of chronic diseases have been demonstrated repeatedly and, due in part to expanding public health campaigns, are rapidly becoming topics of common knowledge (although not necessarily common practice). Weisburger (2000) details a number of nutritional factors associated with lowered risk of chronic disease, including: reduced consumption of dietary fat, increased consumption of cereal bran fibre (e.g. wholegrains), increased consumption of fruits and vegetables, reduced consumption of fried and broiled foods, and increased consumption of dairy products. The consumption of saturated fats is correlated positively with the incidence of cancer, while the consumption of fruits, vegetables, and fibre is associated negatively with the incidence of cancer (Bal et al. 2001, Colditz et al. 2000, Willett 1994). The incidence of diabetes has been connected to dietary fat consumption (Blair et al. 1996). Consumption of fruits, vegetables, and whole grains is associated with reduced risk of stroke (Joshipura et al. 1999, Liu et al. 2000a). The incidence of cardiovascular disease (the broader category of chronic disease within which belong strokes) varies negatively with fruit, vegetable, and dietary fibre consumption, and varies positively with fat consumption and dietary cholesterol (Blair et al. 1996, Foerster et al. 1999, Liu et al. 2000b, Stampfer et al. 2000, Willett 1994). Moreover, these findings of specific associations between particular nutritional behaviours and the incidence of chronic disease are buttressed by research linking reduced risk of several major chronic diseases to comprehensive patterns of healthful eating (Hu et al. 2000, McCullough et al. 2000a, 2000b, Willett 1994). Also of note, foods that are high in fat have an interesting dual role in the development of chronic disease in that, in addition to being associated with increased incidence of chronic disease, they also tend to supplant healthier nutritional choices that have protective effects (Kant 2000). In sum, there is general agreement between medical and health researchers that increased consumption of fruits, vegetables, grains, fibre-rich foods, beans, and dairy products, and decreased consumption of dietary fat, substantially reduce the risk of many of the most common chronic diseases, including cardiovascular disease, cancer, stroke, and diabetes (Eyre et al. 2004, Foerster et al. 1999, Willett 1994).
Racial differences in nutritional behaviour
The omission of nutritional behaviour from prior analyses of the race-health relationship introduces one of two assumptions. The analyses must assume either that nutritional healthfulness does not differ meaningfully between racial groups or, alternatively, that nutritional healthfulness, as one expression of the general class of personal health behaviours, is perfectly correlated with (accounted for by) measures of SES. In point of fact, when variation in nutritional quality is mentioned as a potential mediating variable underlying Black-White differences in health outcomes, it is most often attributed to disparities in SES (e.g. Siewe 1999, Wickrama et al. 1999) or, more specifically, to the high rate of poverty among Blacks (e.g. Blocker 1994, Kittler and Sucher 1989, Leigh 1995). In other words, nutritional quality is theorised to mediate the SES-health relationship, to the exclusion of any mediating role it may play in the residual race-health relationship existing independently of the SES-health relationship.
Given, however, that controlling for SES has not eliminated the Black-White health disparities, and given the well-established relationship between nutrition and health, it is reasonable to conclude that other causal channels linking race to nutritional quality are worthy of exploration. In support of this argument, there is limited evidence that suggests that health-related nutritional behaviours do vary between Blacks and Whites independent of SES (Airhihenbuwa et al. 1996, Lindquist et al. 2000, Popkin et al. 1996). But each of the several previous studies that address the race-nutrition relationship, independent of SES, evidence significant weaknesses. For example, the Popkin et al. (1996) study was weakened by an oversimplified operationalisation of SES as a trichotomous indicator and the absence of controls for important demographic variables. The Lindquist et al. (2000) study was limited to a small convenience sample of young children. The Airhihenbuwa et al. (1996) qualitative study relied upon respondents’ own assessment of the effect of income on nutritional behaviour.
In addition to the limited empirical evidence, racial differences in health-related nutritional behaviours, independent of SES, would be expected for a number of reasons. Among these, Semmes (1996: 128) argues that nutritional deficiencies among Blacks are, in part, a result of ‘maladaptive dietary practices rooted in slave culture’, which is a perspective echoed in the interviews of Blacks conducted by Airhihenbuwa et al. (1996). Semmes (1996) argues that many present nutritional practices among Blacks are derived from ‘slave culture’, leading to an over-reliance on processed sugars and fatty meats and an underutilisation of fruits and vegetables. Kiple and King (1981) offer a contrasting, and much more detailed, assessment of Black nutrition under slavery, but the conclusion of significant nutritional deficiencies is the same. Other researchers have documented support for the influence of racial subcultures on dietary practices (e.g. Witt 1999) and, following from this, differences in nutritional quality (Kittler and Sucher 1989). In other words, cultural differences in preferred foods and cooking methods may contribute to differences in nutritional quality between Blacks and Whites, independent of SES. This causal explanation points to the importance of dietary patterns as components of social history and cultural memory, whereby knowledge and practice of nutritional behaviours are passed from generation to generation within families (Airhihenbuwa et al. 1996, Birch 1999).
One should note that, although this argument may be interpreted as ‘blaming the victim’, such an interpretation would be inaccurate. In particular, Semmes’ (1996) use of the word ‘maladaptive’ appears, on the surface, to imply that Black slaves had some degree of choice in the nutritional content of their diets. Of course, this was not the case. Instead, this argument points to the opposite situation: a people group who, by enslavement, were deprived of their culture, including their food culture, and forced to adapt to a severe state of scarcity, dislocation, and dispossession.
Racial differences in nutritional quality also may be rooted in residential segregation, which is, itself, another expression of racial discrimination (Krieger 2000). Blacks are subjected to the highest rate of residential segregation of any minority group in the US (Steinmetz and Iceland 2003), and Blacks in the US are 144 per cent more likely to live in ‘urban cores’ than are Whites (McKinnon 2003). The overrepresentation of Blacks in urban cores holds even for affluent Blacks (Bullard 1994), indicating that poverty is not the only contributing factor to racial residential segregation (Emerson et al. 2001, Erbe 1975, Farley 1977, Farley and Frey 1994, Iceland and Wilkes 2006, Massey et al. 1987). In fact, the evidence suggests that improvements in SES among Blacks generally contribute little to rectifying rates of residential segregation (Hwang et al. 1985, Villemez 1980).
Urban neighbourhoods, poor neighbourhoods, and neighbourhoods in which the residents are predominantly Black are characterised disproportionately by the notable absence of major supermarkets and specialty food stores, requiring residents to rely on the similarly notable excess of small convenience stores, which generally have higher prices and limited nutritional options (Cheadle et al. 1991, Emmons 2000, Krebs-Smith and Kantor 2001, Leigh 1995, Macintyre and Ellaway 2000, Morland et al. 2002, Williams and Collins 2001). A similar problem, termed ‘food deserts’ to refer to urban environments that lack adequate nutritional infrastructure, has been identified in the UK (Wrigley 2002), and improvements in nutritional infrastructure have been found to be associated with improvements in dietary quality (Wrigley et al. 2002). Furthermore, the problem of limited nutritional infrastructure is exacerbated by the high rate of poverty among Blacks, which tends to limit transportation alternatives, placing access to supermarkets in suburban and predominantly White neighbourhoods out of reach (Krebs-Smith and Kantor 2001, Leigh 1995, Morland et al. 2002).
Interestingly, several recent studies have found that Black-White differences on certain health outcomes shrink substantially, or even to statistical insignificance, once variables that address overarching aspects of community context (e.g. neighbourhood affluence or poverty, neighbourhood population, residential stability, racial segregation) are controlled (e.g. Browning and Cagney 2003, Huie et al. 2002, Robert 1998, Robert and Lee 2002, Subramanian et al. 2005). While the mechanisms that mediate the relationship between community context and health outcomes are still unclear, and while these prior studies do not address nutritional infrastructure specifically, these findings represent an intriguing parallel to the literature that addresses racial segregation, nutritional infrastructure, and nutritional quality. In particular, the contextual variables found to be significant in prior studies would be expected (either intuitively or based on prior research) to be correlated with nutritional infrastructure. Thus, nutritional infrastructure may constitute a key mediating variable in the relationship between community context and racial health disparities.
Another potential explanation for racial differences in nutritional quality is disparities in the nutritional information provided to Blacks via race-targeted product advertising. Semmes (1996) notes that advertisers of alcohol and tobacco have a long history of targeting the Black segment of the market, which, as one would expect, is correlated with residential segregation (Williams and Collins 2001). Research has identified differences in nutritional advertising as well. For example, Pratt and Pratt (1996) found evidence of significant disparities in the healthfulness of nutritional product advertising in popular print media targeted at Blacks versus that targeted at Whites. Specifically, in a longitudinal content analysis, Pratt and Pratt found that one widely circulated magazine targeted at Whites (Ladies’ Home Journal) carried significantly more nutritional advertising in support of dairy products, breads, cereals, vegetables, and fruits, than did two widely circulated magazines targeted at Blacks (Ebony and Essence). It follows that, to the extent that consumers depend upon nutritional advertising for making healthy nutritional choices, the gap in healthful nutritional information provided to Blacks may contribute to racial disparities in nutritional practice. In this regard, there is limited evidence that Blacks depend more heavily on advertising in making decisions about food choices than do Whites (Bock et al. 1998), potentially amplifying the effects of any differences in racially-targeted product advertising.
Finally, differences in the household compositions of Blacks and Whites may contribute to average differences in nutritional quality. Fully 58 per cent of all Black family households with children in the US are single-parent households, compared to 23 per cent of White family households with children (Fields 2004). While the effect of single-parent versus dual-parent living arrangements on adult nutritional quality is unknown, one might reason that single-parent living arrangements allow less time for grocery shopping and meal preparation, on average, than do dual-parent living arrangements. Thus, the excess of single-parent families among Blacks may contribute to a depression in average nutritional quality among Black adults.