Examining “race” in physiology

Abstract

Racial disparities in cardiovascular and cerebrovascular health outcomes are well described, and recent research has shed light on the mechanistic underpinnings of those disparities. However, “race” is a social construct that is poorly defined and continually evolving and is historically based on faulty premises. The continued categorization by race in physiological research suggests that there are inherent differences between races, rather than addressing the specific underlying factors that result in health disparities between groups. The purpose of this Perspectives article is to provide a brief history of the genesis of categorization by race, why such categorization should be reconsidered in physiology research, and offer recommendations to more directly investigate the underlying factors that result in group disparities in cardiovascular and cerebrovascular health.

INTRODUCTION

Differential risks of developing cardiovascular and/or cerebrovascular disease are often ascribed, at least in part, to membership in a particular race (43, 62). The underlying causative factors for ascribing such differences to “race,” however, are not clear and the assumption that the race membership is itself a risk factor for disease has been uncritically retained and insufficiently examined. Although important strides have been made toward understanding the underlying physiological mechanisms of racial disparities, there is a critical need for research to better understand the physiological and sociocultural underpinnings of apparent racial differences in cardiovascular and cerebrovascular health. To that end, consideration of the imprecise nature of “race” is warranted. This Perspective briefly 1) addresses the origins of categorizing humans by race and why such categorization is problematic in modern physiology research and 2) makes recommendations for moving away from categorization by race to more directly address underlying social determinants of health [i.e., conditions in the places where people live, learn, work, etc. that affect a wide range of health and quality-of-life risks and outcomes (42)] and environmental and biological factors that result in disparate cardiovascular and cerebrovascular health outcomes.

HISTORICAL PERSPECTIVES IN RACIAL THEORY

The origins of racial categorization began with the Swedish taxonomist Carl Linnaeus, who first categorized humans into four main groups—Homo Europaeus albescens, Homo Americanus rubescens, Homo Asiaticus fuscus, and Homo Africanus niger—according to skin color and geography (63). By 1758, Linnaeus had introduced the binomial nomenclature of Homo sapiens, and his original four classifications were retained as subspecies, with additional details of physical traits and mental and cultural characteristics (48). In 1777, the natural philosopher Immanuel Kant was the first to describe race as an immutable characteristic (40). In contrast to a “variety,” an organism that could revert to a common stock over generations, a “race” was fixed (33). Kant postulated that the four races—“first race,” very blonde/northern European; “second race,” copper red/American; “third race,” black/Senegambia; and “fourth race,” olive-yellow/Indian—stemmed from the genus “white brunette,” which represented the ideal human (20). Any variation away from this ideal was considered a degeneration from the original genus, resulting from less equable climates. Importantly, Kant suggested that such degradation was reflected not only in skin coloration but also in character or “talent” (20, 33). This served as the basis from which dark skin became associated with inferiority, and practices such as segregation and slave trade were justified (33). Race as a source of differences in humanity, morality, and physical well-being became a deeply ingrained construct that has served social purposes for centuries and continues to persist.

Use of the term race has become ubiquitous in physiological research and medicine, although it is a continuously evolving and ill-defined concept. The five racial categories used in the current US Census—white, black or African American, American Indian or Alaska Native, Asian, and Native Hawaiian or Other Pacific Islander—reflect social definitions of race that are “recognized in this country and not an attempt to define race biologically, anthropologically, or genetically” (7). The National Institutes of Health use six “racial and ethnic” categories, adding Hispanic or Latino to the five categories included in the Census, that are based primarily upon geographical origins (28). Further complicating matters is confounding the term race with ethnicity, which is defined by shared factors such as nationality, language, religion, values, and norms, and is considered voluntaristic (12, 46).

The ill-defined nature of race and ethnicity is particularly problematic in physiological research, given that most studies rely on participant self-identification. Racial self-identification embodies a myriad of social, biological, and morphological factors, including observed race (the race others believe you to be), reflected race (your perception of what race others believe you to be), skin color, ancestry, and hair texture (56). Some of the constructs encompassed under the term race may indirectly influence health status; for example, discrimination and perceived discrimination related to a socially assigned and reflected race are associated with poorer health outcomes (22, 49, 54, 65). By categorizing groups based on racial self-identification, we gain insight into how the intersection of the various dimensions of “race” influences health outcomes. However, although research aimed at understanding differences in disease processes between self-identified groups does provide important information, it also falls short by not considering the specific biological, social, and/or environmental foundations from which these differences arise.

“RACE” IN CARDIOVASCULAR RESEARCH

There is an expanding body of research investigating racial differences in cardiovascular and cerebrovascular health. In particular, there is substantial focus on characterizing the mechanisms of vascular dysfunction in the African American, or non-Hispanic black, population—important given that the African American population experiences greater rates of cardiovascular and cerebrovascular diseases compared with all other groups (26, 62). Dysfunction in this context is generally defined as divergent responses relative to a non-Hispanic white cohort, with the assumption that responses in non-Hispanic white participants represent “normal” function. Extensive reviews on this topic have recently been published (6, 17); therefore, this article will provide only a brief synopsis of the currently available literature.

Dysfunction of the peripheral macrovasculature and microvasculature, secondary to increased oxidative stress and reduced nitric oxide (NO) bioavailability, has been documented in otherwise healthy African Americans (9, 10, 18, 29, 31, 41). Similar dysfunction has been documented in the cerebral vasculature when examining cerebral vasomotor reactivity in response to hypercapnia (30). Furthermore, exaggerated vasoconstrictor responsiveness to phenylephrine infusion (59) and muscle sympathetic nervous system activity at rest (64) and during static exercise (19) has been observed in young, normotensive black adults compared with their white counterparts. Together, these studies have provided substantial and important insights into the mechanisms underlying the development of cardiovascular and cerebrovascular disease in the African American population. Although important strides have been made to elucidate the mechanisms of cardiovascular and cerebrovascular dysfunction in the African American population, less is known about other minority populations, including Hispanic, Asian, or Native Americans. However, some evidence exists for an increased prevalence of type 2 diabetes and associated cardiovascular dysfunction in the Hispanic and Asian American populations (2, 58). Additionally, there is some evidence of increasing prevalence of cardiovascular disease in the Native American and Alaska Native populations (13, 47, 53). Although relatively limited, these findings underscore the need for future research aimed toward better understanding the factors lending to the development of cardiovascular disease across diverse populations in the United States.

An important limitation to consider in much of the currently available literature regarding race differences in cardiovascular and cerebrovascular dysfunction is how participant groups are categorized. For example, there is an abundance of research that identifies participants as black, African American, or non-Hispanic black. Herein lies a significant problem; some individuals may identify as black or non-Hispanic black, but not as African American. An individual who identifies as black may be a first-generation immigrant from Africa, or from other regions such as the Caribbean or Melanesia. Importantly, differential rates of morbidity have been demonstrated in black adults born in majority white regions, such as the United States or Europe, compared with those who are first-generation immigrants to those regions (14, 27, 55). Past research has provided crucial information regarding the physiological mechanisms mediating racial disparities in cardiovascular and cerebrovascular function. However, the development of vascular dysfunction is multifactorial and most likely includes biological, social, and environmental underpinnings (discussed in more detail in correcting perceptions of race and improving study design in physiology). As such, future research in this area should attempt to specifically address the roles of these factors, rather than race per se, in the development of cardiovascular and cerebrovascular diseases.

CORRECTING PERCEPTIONS OF RACE AND IMPROVING STUDY DESIGN IN PHYSIOLOGY

Despite there being no direct biological distinction between one race and another (44, 67), the uncritical categorization of research subjects by race persists. Continued examination of mechanistic differences in cardiovascular and cerebrovascular function between racial groups, rather than addressing the underlying social and environmental factors that engender population health disparities, serves to promulgate the false narrative that there are inherent “racial” differences. Furthermore, the persistent use of race categories may, in and of itself, result in a widening of health disparities by promoting stereotype threat, whereby the perception of worse health in an individual’s own racial group triggers physiological and psychological processes that propagate the development of morbidity (1, 8). Accordingly, attempts should be made to directly assess the cardiovascular and cerebrovascular health effects of sociocultural, environmental, and biological factors that are encompassed under, and obscured by, the term “race.”

Chronic cardiovascular and cerebrovascular dysfunction may arise from societal conditions that result in increased exposure to daily stressors. Recent research has demonstrated that greater exposure to daily psychosocial stress in healthy adults is associated with cutaneous microvascular dysfunction, characterized by impaired vasodilator and exaggerated vasoconstrictor responsiveness (23, 24). Those who identify as belonging to a minority group are more likely to experience daily psychosocial stress (16, 36, 60). Personal experiences of discrimination result in more frequently experienced daily stressors that can, in turn, impact cardiovascular health (3, 57, 66). Furthermore, unhealthy behaviors adopted to cope with stress may exacerbate the development of physiological dysfunction (36). In the African American community, particularly in men, John Henryism coping [high-effort coping in the face of adversity, despite limited resources and higher psychosocial stress (37)] in those from low socioeconomic status backgrounds has been associated with worse cardiometabolic outcomes (5, 15, 38). However, mechanistic studies investigating the role of daily psychosocial stress in explaining population differences in the development of vascular dysfunction are still needed.

Differences in socioeconomic status can result in impaired cardiovascular and cerebrovascular health via less access to quality nutrition, health care, availability of recreational resources, and quality sleeping conditions. Higher socioeconomic status and availability of favorable food stores and physical activity resources are associated with better cardiovascular health (61). Minority and low-income neighborhoods are less likely to have recreational facilities (51), and concerns about safety and lack of organized, supervised activities may curtail the use of available park space for outdoor recreation (11, 25). Lower socioeconomic status and associated neighborhood disadvantage are associated with poorer sleep quality and may contribute to disparities in cardiovascular and cerebrovascular health outcomes (50, 52, 70). Unequal health outcomes also reflect inequalities in health care between populations, representing a significant barrier to bridging the gap in cardiovascular and cerebrovascular health. Future research considering the role of socioeconomic status in mediating the development of vascular dysfunction in at-risk populations is warranted.

Apart from psychosocial determinants of health, skin pigmentation represents a potential source of biological variation that may contribute to disparities in endothelial function by influencing bioavailability of nutrients that are metabolized via sun exposure. The vitamin D-folate hypothesis is the prevailing theory regarding the evolution of human skin pigmentation (34, 35, 39). The potential implications of skin pigmentation in the context of vascular health have recently been reviewed in-depth (69). Briefly, those with darkened skin pigmentation are at increased risk of vitamin D deficiency in relatively low ultraviolet radiation (UVR) environments. Vitamin D may have important roles in endothelial function and health by signaling for the transcription of endothelial nitric oxide synthase and/or by ameliorating inflammation- and oxidative stress-induced endothelial dysfunction (4, 21, 32, 45), suggesting a potential avenue for the development of endothelial dysfunction in darkly pigmented populations living in relatively low-UVR regions (68). The interaction between skin pigmentation, environmental UVR, and vascular health presents an additional avenue by which disparities in vascular health may arise.

CONCLUSIONS

The purpose of this brief Perspectives article is to encourage researchers of cardiovascular and cerebrovascular physiology to reconsider the practice of investigating health disparities based on race alone. We assert that the term “race” is ill defined and built on faulty scientific foundations. We do not mean to imply that race is inconsequential; perceptions of race and/or racial discrimination are factors that have significant health impacts. However, we propose that physiology researchers should directly acknowledge that physiological differences between populations are not due to inherent “racial” differences—rather, they are primarily functions of disparate social and environmental conditions—and design studies to specifically identify the conditions that result in differential health outcomes.

GRANTS

This work was supported by a Penn State Center for Human Evolution and Diversity Research Endowment Grant and National Institutes of Health Grant T-32-5T32AG049676-03.

DISCLOSURES

No conflicts of interest, financial or otherwise, are declared by the authors.

AUTHOR CONTRIBUTIONS

S.T.W., N.G.J., and W.L.K. conceived and designed research; S.T.W. drafted manuscript; S.T.W., N.G.J., and W.L.K. edited and revised manuscript; S.T.W., N.G.J., and W.L.K. approved final version of manuscript.