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Transgenerational Consequences of Racial Discrimination for African American Health

Bridget J. Goosby* and Chelsea Heidbrink Bridget J. Goosby: [email protected] *Department of Sociology, University of Nebraska Lincoln, 742 Oldfather Hall, Lincoln, NE 68588, United States

Abstract

Disparities in African American health remain pervasive and persist transgenerationally. There is a

growing consensus that both structural and interpersonal racial discrimination are key mechanisms

affecting African American health. The Biopsychosocial Model of Racism as a Stressor posits that

the persistent stress of experiencing discrimination take a physical toll on the health of African

Americans and is ultimately manifested in the onset of illness. However, the degree to which the

health consequences of racism and discrimination can be passed down from one generation to the

next is an important avenue of exploration. In this review, we discuss and link literature across

disciplines demonstrating the harmful impact of racism on African American physical health and

the health of their offspring.

Racial differences in health outcomes in the United States are widespread and stark. Though

there have been important technological advances contributing to the increase in population

life expectancy in the past fifty years (Gortmaker and Wise 1997), the gap in health

outcomes between whites and certain minority groups remains substantial. According to the

Center for the Disease Control’s most recent report, rates of morbidity and mortality over

the life course remain higher for African Americans than for most other race/ethnic groups

(CDC/NCHS 2011). Moreover, African Americans have the highest rates of low birth

weight births and substantially higher rates of infant mortality than other racial groups

(Williams 2002). African American children also experience higher rates of chronic health

conditions such as asthma and obesity across socioeconomic status (CDC/NCHS 2011), and

during adulthood, African Americans exhibit the highest rates of hypertension and cancer

mortality (Williams 2002). Though life expectancy has risen for all populations in the U.S.,

both African American men and women still exhibit the lowest life expectancy across race

ethnic groups with men’s average life expectancy at 70 years old and women’s at 77

compared to 76 for White men and 81 for White women (CDC/NCHS 2011).

Sociologists systematically demonstrate the pervasive, harmful nature of social inequality

for minority disparities across a range of outcomes including health, education, income, and

family processes (Reskin 2012). There is an increasing awareness that racial discrimination

is a salient mechanism perpetuating racial gaps in health with African Americans showing

some of the most substantial differences in prevalence and severity of certain health

conditions across the life course (Williams 2012). The Biopsychosocial Model of Racism as

a Stressor (BMRS) elucidates the psychosocial and biological pathways through which

NIH Public Access Author Manuscript Sociol Compass. Author manuscript; available in PMC 2014 May 19.

Published in final edited form as: Sociol Compass. 2013 August 1; 7(8): 630–643. doi:10.1111/soc4.12054.

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racism functions as a mechanism for perpetuating declines in health, particularly among

African Americans (Clark et al. 1999). Though there have been important strides in

uncovering the life course pathways through which racial inequality perpetuates health

outcomes across the life course of racial minorities, the sociological literature has yet to

effectively examine the degree to which the health consequences of racial discrimination are

transmitted transgenerationally.

The health consequences of racism and discrimination can be persistent and passed from one

generation to the next through the body’s ‘biological memory’ of harmful experiences

(Thayer and Kuzawa 2011). Specifically, the psychosocial and biological pathways through

which racism affects racial minority health can also have consequences for their offspring,

potentially perpetuating the existing disparities in the next generation, in part, by the

embodiment of inequality transmitted through epigenetic influences (Kuzawa and Sweet

2009). In other words, stressful conditions and poor health experienced by mothers can lead

to alterations in her offspring’s gene expression without changing his or her genotype. These

changes in gene expression can have important implications for the healthy functioning of

bodily systems in mothers and their offspring.

The goal of this paper is to elaborate on the contribution of the complex, interactive

dynamics of racism and racial discrimination for driving persistent racial disparities in

health across generations. In this review we draw upon an interdisciplinary literature to

inform our sociological understanding of the persistence of health disparities across

generations. We use African American women’s health as a descriptive example illustrating

the importance of eradicating racial inequality as a key solution to improving health

outcomes of marginalized groups. Specifically, we argue that discrimination is a socially

generated but physiologically disruptive force that influences health across generations.

The Biopsychosocial Consequences of Racial Discrimination as a Stressor

Racism refers to the beliefs, attitudes, institutional arrangements, and interpersonal acts that

malign a person or group people based on their racial or ethnic affiliation (Clark et al. 1999).

Racist ideology and beliefs have been historically used as justification for discrimination

both at the individual and institutional levels in the Unites States and remain ubiquitous

(Reskin 2012; Williams 2012). The consequences of this racially discriminatory structure

have given rise to system wide inequities and disparate racial differences in health

outcomes. Structurally, discrimination was instrumental in creating the most harmful

conditions for minority health- economic marginalization and segregation, which have been

examined at length in the sociological literature (Williams and Sternthal 2010). While

structural inequality is instrumental in creating unequal access to goods and resources

including quality education and health care, safe communities, and economic mobility

(Geronimus and Thompson 2004), racial discrimination also takes a toll on the physiological

and psychological health of minority group members who may internalize racial

discrimination (Clark et al. 1999).

The Biopsychosocial Model of Racism as a Stressor (BMRS) posits that the stress of racial

discrimination is instrumental in African American health disparities due to the

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physiological responses to chronic and acute stress brought on by racist experiences (Clark

et al. 1999). Specifically, the exposure to environments perceived as racist can result in an

overactive physiological stress response. In other words, normal bodily systems responsible

for adjusting to stressful conditions remain perpetually activated in the presence of chronic

stress, leaving individuals vulnerable to illness due to elevated wear and tear on the body

(McKewen 1998; McKewen and Seeman 1999)- conditions which we will elaborate in more

detail in the following section. We expand the original BMRS model to suggest that not only

is the perception of racial discrimination important for African American health, but also

just as important, is the disproportionate exposure to social stressors brought on by being

part of a racial group that is systematically discriminated against and marginalized

(Geronimus 2001).

Recent findings indicate that African Americans are disproportionately exposed to social

stressors of higher frequency and severity (Sternthal et al. 2011). The high prevalence of

African Americans living in racially segregated conditions is a key structural mechanism

through which they are exposed to elevated numbers of stressors (Williams and Sternthal

2010). African Americans, even in the middle class, are more likely to live in conditions

where they are exposed to, or in close proximity, to concentrated disadvantage, high

unemployment rates, pollution, violent crime, and poor housing conditions (Reskin 2012;

Geronimus and Thompson 2004; Sternthal et al. 2011). Subjection to such stressful, noxious

conditions can play a harmful role in overall well-being and illness onset and progression.

Although disproportionately represented in poverty, African Americans across

socioeconomic strata exhibit poorer health on average relative to Caucasians. Middle class

African Americans are more likely to be exposed to discrimination at the individual or

interpersonal levels, with more frequency because they are more likely to work in

predominantly white environments, elevating the risk of discriminatory experiences and

racist microaggressions (Colen 2011). Furthermore, socioeconomic status does not share

equivalent meanings across race/ethnic groups with middle class African Americans having

less overall wealth than their Caucasian counterparts thereby living in more economically

tenuous conditions (Williams and Sternthal 2010). Consequently, middle class African

Americans are more vulnerable to descending into poverty during economic downturns and

are at an elevated risk for experiencing perpetual stress (Sternthal et al. 2011).

The Physiologic Consequences of Stress

The Biopsychosocial Model (BMRS) asserts that African Americans who perceive certain

circumstances as racist experience physiological stress responses that can be exacerbated by

sociodemographic (e.g.- socioeconomic status) and psychological characteristics (e.g.-

depression) along with behavioral factors (e.g.- smoking, alcohol use), and coping responses

(e.g.- ability to mobilize social support) to such experiences (Clark et al. 1999).

Consequently, perpetual stress responses to acute and chronically stressful conditions

elevate one’s vulnerability to disease. Both human and animal model studies of health and

disease progression demonstrate that individuals lower in the social hierarchy have poorer

health and higher disease risk than those who occupy higher social strata (Sapolsky 2006;

McKewen and Seeman 1999). Although among humans, health risk behaviors such as

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smoking, drinking, and unhealthy eating habits are more likely to happen among socially

marginalized groups, these behaviors do not completely account for health differences

across social strata (Williams 2008). The psychosocial stress and burden of coping with

limited access to resources and the harmful challenges associated with social

marginalization can place substantial wear and tear on bodily systems important for

managing stress and coping (allostatic load), thus leaving individuals vulnerable to disease

(McEwen and Seeman 1999).

The human body’s physiologic response to stressful conditions can elevate vulnerability to

disease through metabolic, cardiovascular, and immune function (McEwen and Gianaros

2010). Moreover, the body’s stress response is also tied to accelerated aging and cellular

degradation (Epel et al. 2004). The body is made up complimentary systems that work

synergistically to maintain normal functioning or homeostasis. In order to enable stability,

the body works to create allostasis by adjusting bodily systems according to changes in the

environment. In the event of abnormal functioning in the body, for instance when the body

experiences chronic stressors, wear and tear may occur as a consequence of the of the body

attempting to turn on or shut down certain systems to maintain allostasis - this condition is

called allostatic load (McEwen and Seeman 1999). [Table 1 here]

Cardiovascular and Metabolic Function

The cardiovascular and metabolic systems are linked to diseases including atherosclerosis,

insulin resistance, and cardiovascular disease. In the presence of negative stressors, the

body’s cardiovascular system can respond by increasing blood circulation through elevated

heart rate, a protective measure in the presence of acute stress, but if left unchecked can lead

to the thickening and rigidity of the arterial walls (Sapolsky 2006). This process happens in

concert with the mobilization of metabolic hormones such as cortisol, which are controlled

by the hypothalamic-pituitary-adrencortal (HPA) axis (McEwen 2000). Cortisol is a

glucocorticoid hormone that is, in large part, responsible for managing energy storage and

expenditures, immune function, mood, and the processing of fat, protein, and carbohydrates

in the body. Cortisol also regulates the release of glucose (i.e.- blood sugar) into the blood

stream in order to provide energy during times of stress (Sapolsky 2006).

Chronically high levels of glucose in the blood stream can escalate arterial thickening due to

inflammation and scarring from the viscous blood containing high levels of glucose and

cholesterol that damage the arterial walls. The consequences are twofold - first, the

combinations of elevated blood pressure with high levels of glucose and cholesterol particles

circulating in the blood exacerbates the risk of cardiovascular conditions including

hypertension and atherosclerosis (Brindly and Rolland 1989). Second, high levels of

unregulated glucose circulation elevate the risk of other conditions associated with

cardiovascular disease including insulin resistance, abdominal obesity, and Type 2 diabetes,

which when present together are defined as metabolic syndrome (Seeman et al. 2010; Black

2003).

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Immune function

Adrenal steroids including the hormone cortisol also help regulate immune function by

controlling movement of immune cells to organs or tissues that require protection from

infections or other noxious conditions (McEwen and Seeman 1999). In the same way that

stress responses can lead to dysregulation among the metabolic and cardiovascular systems,

unchecked immune dysregulation can elevate disease risk through immune suppression or

immune overactivity by way of a complex feedback loop. Specifically, in response to stress,

the body prepares for infection by increasing immune function for wound healing by

mobilizing energy (i.e.- releasing glucose into the blood stream) and increasing levels of

hormone secretion related to immune function including cortisol (Sapolsky 2006). When

there is chronic overactivity of these processes, perpetually high levels of cortisol secretion

actually suppresses the immune system thus leading to elevated risk of infections (McEwen

1998). In certain cases, however, exposure to stress can lead to overactivity of immune

function where the immune system begins to attack the body in the absence of infections

causing inflammation and autoimmune disorders such as rheumatoid arthritis, multiple

sclerosis, and lupus (Segerstrom et al. 2004).

Accelerated Aging or Cell Degradation

Recently, emerging evidence points to the consequences of both perceived stress and the

presence of chronic stressors for the rate at which cells age and degrade (Epel et al. 2004).

Telemores are stabilizing caps at the ends of chromosomes that shorten through cell division

until a cell destabilizes or begins to deteriorate with age (senescence) (Allsopp 1992; see

Geronimus et al. 2010). Oxidative stress is a key biological process through which people

experience accelerated aging or cell senescence. There is evidence that the presence of

social stressors and psychological distress are linked to elevated levels of oxidative stress,

consequently leading to shortened telomeres (Eppel et al. 2004). Furthermore, overactivity

of the HPA axis, discussed in prior sections, has been linked to oxidative stress as a

consequence of excessive secretion of glucocorticoids such as cortisol (McIntosh et al.

1998). Shortened telomeres are particularly important for health outcomes because as

telomere lengths shorten, risk of mortality increases. Moreover, there is clinical evidence

that heart attack patients have similar telomere lengths to healthy individuals who are

approximately 11 years older. Strikingly, in a study assessing telomere lengths in

premenopausal women who experience chronic stress, the researchers found that women

who experienced chronic stressors had telomere lengths that resembled those of people who

had experienced heart attacks in early middle age (Epel et al. 2004).

Racial Discrimination and African American Health

The health consequences of racial discrimination are produced through structural (e.g. -

chronic poverty, poor infrastructure in non-white communities), institutional (e.g. -

educational institutions and employment discrimination), and individual processes (e.g. -

interpersonal discriminatory acts; Harrell et al. 2011; Clark et al. 1999). Stress related

chronic illness is a leading reason for the high rates of morbidity and mortality among

African Americans, particularly in urban areas (Geronimus and Thompson 2004). African

American women are especially vulnerable to the harsh conditions brought about by the

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combination of racial inequality and poor socioeconomic conditions as evidenced by

markedly higher rates of chronic illness and earlier onset of functional impairment across

socioeconomic strata (Gorman and Read 2006). In this section, we discuss the processes

through which racial discrimination contributes to stress-related illness and accelerated

aging among African Americans in general and African American women specifically.

Structural Discrimination and Health

For African Americans living in a race conscious society, persistently experiencing

stigmatization and disadvantage leaves them susceptible to physiological deterioration,

subsequent illness and early mortality (Geronimus et al. 2006). African Americans have

disproportionately higher numbers of co-occuring stressors such as job discrimination,

relationship stress, and financial hardship, that when experienced, are of greater intensity in

their lives relative to Caucasians even after accounting for socioeconomic status (Sternthal

et al. 2011). A key suggested structural mechanism for such differences in stress exposure

and African American health is racial segregation and the risks associated with it. African

Americans, particularly African American women, are more likely to live in racially

segregated conditions with high rates of poverty regardless of their socioeconomic status

(Williams 2012). Those living in such segregated conditions are more likely to be exposed

to stressors such as concentrated poverty, exposure to violent crime, limited access to

institutional resources, poorer schools, and fewer safe outdoor spaces (Williams 2008).

Consequently these conditions are associated with elevated levels of stress and hardship.

African American Women’s Health Profiles

African American women’s health profiles show marked differences in the prevalence,

onset, and severity of certain health conditions. Though African American men have lower

life expectancy relative to African American women, women suffer from higher rates of

chronic illness and experience functional impairment with earlier onset (Gorman and Read

2006). Furthermore, comorbid chronic illnesses are more prevalent in African American

women relative to white women (Williams 2002). African American women also show

different health profiles in cancer risk; African American women have a lower incidence of

breast cancer than white women, but are more likely to experience a more aggressive form

that is associated with substantially higher rates of cancer mortality relative to Caucasian

women (Williams 2002).

African Americans, in general, have higher rates of cardiovascular and diabetes related

mortality relative to their Caucasian counterparts (Mensah et al. 2005) and are more likely to

experience blindness, amputations, and end stage kidney failure from diabetes (Williams

2002). There are gender differences in morbidity and mortality, however, with women being

more likely to live with heart disease and other chronic conditions such as arthritis over

time, while men are more likely to experience cardiovascular disease related mortality

(Crimmins et al. 2002). Among African Americans, there is variation in health conditions by

socioeconomic strata as well. Low-income African American women are more likely to

exhibit symptoms of accelerated aging manifested in higher allostatic load (Geronimus et al.

2006) compared to their Caucasian counterparts. In higher socioeconomic strata, however,

African American women show stark health differences relative to Caucasian women, with

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evidence that in addition to structural racial inequality, perceptions of racism and

discrimination also take a toll on their health.

Discrimination and African American Women’s Health

There are important social pathways that contribute to African American female health

outcomes. African American women even at higher levels of SES are more likely to live in

highly racially segregated areas (Williams 2002). Low-income African American women

experience alarming rates of early onset chronic illness and related mortality such as

cardiovascular disease (Geronimus 2001), however, there are also marked black-white

health differences among African American women occupying the upper socioeconomic

echelons. Such differences are suggested to be related not only to their high risk of living in

residentially segregated environments, but also due their likelihood of exposure to both

structural and interpersonal discrimination. Middle class African American women,

specifically, are more likely to be exposed to discrimination in the form of structural (i.e.

encountering the ‘glass’ ceiling effect in employment mobility) and interpersonal

discrimination due to their presence in predominantly white environments (Colen 2011;

Thomas et al. 2008). The perpetual stress of being in a predominantly white work place may

contribute to feelings of social isolation due to their ‘token’ status as an African American

female (Jackson 1995; Colen 2011).

Across socioeconomic status obesity rates among African American women are higher than

that of Caucasian women, which may in part be due to structural differences in their

proximity to racially segregated communities which limit opportunities for physical activity

(Geronimus 2001). However, the stress of experiencing racial discrimination is also linked

to cardiovascular and metabolic conditions along with immune function in African

American women. Specifically, African Americans who reported higher levels of racism in

their lives report poorer self-rated health, higher rates of diseases including immunological,

infectious, or endocrine conditions and more frequent common colds (Kwate et al. 2003).

The stress of experiencing high levels of both lifetime and everyday discrimination is

positively associated with weight gain and abdominal obesity in African American women

(Cozier et al. 2009). Experiencing racial discrimination is also associated with coronary

artery calcification (Lewis et al. 2006), glucose intolerance, and diabetes (Tull and

Chambers 2001; Tull et al. ł999), suggesting long-term impacts on health.

Although not directly linked to the stressor of discrimination specifically, but to stress more

generally, African American women are more vulnerable to experiencing accelerated aging.

Specifically, Geronimus and colleagues found that middle age African American women

had markedly higher rates of aging, with telomere lengths by age 49–55 that signified being

approximately 7.5 years biologically older than white women. The authors note that these

findings persisted even after accounting for perceived stress, poverty, and waist to hip ratio

(WHR). They posited that increased waist to hip ratio (an indicator of abdominal fat) may be

a key pathway through which race and also poverty impact telomere length and overall

health (Geronimus et al 2010). Such conditions are also linked African American women’s

birth outcomes.

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Biological Memory of Racism and the Role of Epigenetics

Racial discrimination is linked to birth outcomes among African American women even

after accounting for psychological well-being, educational attainment, and risk behaviors

such as alcohol use and smoking. African American women who are exposed to and

internalize racial discrimination over their lifetime and during pregnancy are more likely to

have preterm and/or low birth weight births (Mustillo et al. 2004; Collins et al. 2004; Collins

et al. 2000; Rosenberg et al. 2002). Kuzawa and Sweet (2009) argue that the process through

which African Americans experience elevated risks of lower birth weight and subsequent

chronic health conditions such as cardiovascular disease in adulthood are the result of a

complex biosocial process where fetal exposure to maternal stress is manifested through

biological modifications during fetal development (Kuzawa and Sweet 2009; Thayer and

Kuzawa 2011).

As mentioned in the previous section, chronic and acute stressors can initiate and perpetuate

heightened activity in various bodily systems that impact metabolic and immune function.

These processes, however, are not only harmful for mothers experiencing such conditions,

but for their offspring as well. Figure 1 illustrates the pathways through which maternal

stress experiences can influence health across generations through the interactions of

biological and social contexts. In their discussion of the epigenetic consequences of racial

inequalities for African American cardiovascular disease risk, Kuzawa and Sweet (2009)

outline the pathways through which the health consequences of racial inequality can persist

across generations. The authors argue that the human body has a ‘biological memory’ of

early life exposure to harmful conditions that can impact gene expression without changing

the underlying nucleotide sequences-, which in the case of African Americans includes the

deleterious impact of discrimination.

Much dialogue regarding genetic predispositions and phenotypic characteristics imply that

genes are static; however, the epigenetic research indicates that social and physical

environments can influence specific gene expression (i.e. epigenesis). For example, fetal

undernourishment and other environmental conditions associated with low birth weight can

lead to epigenetic alterations of genes in offspring, elevating their risk of hypertension,

insulin resistance, and changing the composition of body fat cells contained in adipose tissue

(i.e. body fat; Lampl et al. 2002; Jensen 2007; Zhang 2005). These epigenetic changes,

however, do not alter the underlying DNA sequence, but instead ‘turn on’ or ‘off’ certain

sets of genes associated with specific physiologic functions.

There is evidence that chronically stressful social conditions that impact African American

women’s health in adulthood can be transferred as health risk to her children due to the fetal

environment in which their offspring develop (i.e. prenatal stress), thus altering their

metabolic and physiological development, demonstrated through the first and second arrows

in Figure 1. Specifically, women who experience severe stress during pregnancy are at

elevated risk for passing the stress hormone cortisol (third arrow) through their placenta

which can restrict fetal growth and increase risk for preterm and low birth weight births

(Phillips et al. 1998). Consequently, such exposure alters fetal HPA axis development and

subsequent offspring biological stress reactivity.

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In addition, women experiencing hypertension, insulin resistance, and diabetes during

pregnancy are also at risk for low birth weight offspring (see Kuzawa and Sweet 2009).

Because African American mothers are more likely themselves be low birth weight, her own

prenatal experience may influence the in utero environment of her offspring through the

above health conditions. In addition to low birth weight risk, insulin resistance and diabetes

in pregnant mothers elevate the likelihood of similar weight gain patterns and metabolic

dysregulation in their offspring into adulthood through the transmission of high levels of

glucose (e.g. blood sugar) via the placenta to the fetus (Dabelea et al. 2000; Lampl and

Jeanty 2004; Silverman et al. 1995). Likewise, it is also important to note that in addition to

fetal exposure to maternal stress and health conditions, transgenerational transmission of

health is also passed through the ‘the continuity of [sic] environment’ (Kuzawa and Sweet

2009, p9). In other words, offspring are born into the stressful environments in which their

mothers lived and are also likely to experience similar risk factors including racial

discrimination, that their mothers did, thus perpetuating a cycle of health risks across

generations.

Racial inequalities in birth outcomes remain a persistent deleterious condition that

disproportionately impacts African American’s long-term health prospects. A key social

force driving such marked differences is African Americans’ disproportionate experiences

with poverty and economic hardship, demonstrated by the similarity in birth outcomes

between low-income African American and Caucasian mothers. Specifically, among this

particular population, both groups of women have similar rates of low birth weight births,

however, once health risk behaviors such as smoking and drinking are accounted for, the

birth weight disparity between black and white women widens (Reichman et al. 2008)

suggesting that additional factors beyond poverty and risk behavior may contribute to

disparities in birth outcomes. Furthermore, more marked black-white differences in birth

outcomes emerge more starkly among middle class women.

Economic mobility among African American women who were poor in childhood does not

provide the same protections from low-birth weight risk that it does for white women.

Specifically, for white women who spent their childhoods in poverty, their risk of having a

low birth weight child was reduced by 48% for every unit increase in family income while

for African American women who experience income increases, there was not a statistically

significant effect (Colen et al. 2006). Moreover, African American females with a college

degree have higher infant mortality rates than Hispanic and white women with a high school

degree (Williams 2012). These findings compliment prior literature showing that middle

class, college educated African American women are at a substantially higher risk of having

low birth weight children compared to their comparable Caucasian counterparts (Foster et al.

2000; McGrady et al. 1992; Schoendorf et al. 1992).

Birth weight is a particularly salient outcome to consider for later African American health

over the life course because birth weight is associated with a wide array of outcomes

correlated with overall life chances. Being born low birth weight is associated with a variety

of health conditions such as obesity, diabetes mellitus, hypertension, and cardiovascular

disease (Phillips et al. 1998). Moreover, low birth weight status elevates the risk of poor

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cognitive development, lower academic achievement (Goosby and Cheadle 2009), and

reduced chances of high school completion (Cheadle and Goosby 2010).

The ‘Long Arm’ of Discrimination

Assumptions of inherent immutable biological (i.e. genetic) differences between racial

ethnic groups can lead health care providers specifically and the medical establishment in

general to ignore the clear structural and social processes that perpetuate racial and ethnic

differences in health outcomes. Several months ago, the popular press reported on a study

released that suggested African American girls who engaged in comparable levels of

exercise relative to their Caucasian counter parts did not exhibit the same levels of weight

loss. The headline of the article was ‘Exercise Not As Beneficial For Black Girls As Whites,

Study Says’ (Huffington Post 6/5/12) and the authors of the article suggested that different

strategies are needed such as reducing energy (i.e. caloric) intake for African American girls

(White and Jago 2012) to address this disparity.

The popular press article went on to discuss the markedly high rates of obesity among

African Americans and then cited an editorial in the New York Times where writer Alice

Randall argued that African American women ‘want to be fat’ in response to the article and

the study it was based on (New York Times 5/5/2012). This study and the perception that

African American women want to be fat is a gross oversimplification of the complex

challenges that lead to persistent issues with obesity and related health conditions. An

important omission left from this dialogue was the uniqueness of environmental factors

facing African American children generally and girls specifically that may predispose them

to risk for obesity and chronic illness.

As discussed in previous section, African American health trajectories are shaped in part by

maternal life conditions including the experiences of racism and discrimination that can

shape later outcomes of their offspring through potential changes in the child’s metabolic

functioning subsequently elevating the risk of experiencing obesity and other chronic

illnesses. So, in fact, the metabolic differences exhibited in the medical literature suggesting

that African Americans have phenotypes predisposed to obesity and other risk factors for

cardiovascular disease (White and Jago 2012; Lee Arslanian 2008) makes a remarkable

omission by not accounting for or even mentioning the harmful nature of structural

inequality and discrimination for the differences among youth obesity rates. Indeed, there is

evidence that among adolescents of African descent experiencing racism is associated with

body fat distribution and insulin resistance (Chambers et al. 2004), two conditions strongly

associated with the body’s physiological response to chronic stress (Sapolsky 2006). Taken

together with early risk consequences minority youth may experience as early as in utero,

the ‘long arm’ of discrimination becomes increasingly more evident.

While there is growing acceptance that racial inequality does play a role in differential

minority health outcomes, the example above demonstrates that the assumption of inherent

genetic differences between racial groups still exists. These arguments do not account for

deep systemic inequalities established based on racist ideology and the fact that much of the

socioeconomic disadvantages and stressful conditions brought about by social

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marginalization can have lasting impacts on the overall health of people in marginalized

groups. It has been established and accepted in the field of sociology, that racial categories

in the U.S. are socially constructed and have been used as a tool to maintain power and

oppress disenfranchised groups. Interestingly, however, there is more genetic variation

within racial groups than across groups (Krieger 2005) indicating flawed assumptions in

how racial differences in health occur.

Racial discrimination is persistent, systemic, and pervasive- emerging in multiple social

contexts over life course for African American youth. For those already susceptible to stress

related conditions, additional noxious experiences related to racial inequality can exacerbate

health risks. There is an expanding literature demonstrating that interpersonal interactions as

well as larger structural environments such as neighborhoods and schools can also play a

salient role for shaping African American life course health. There is evidence regarding the

youth physiological stress responses to racism and discrimination, where particularly

African American girls who experience racism have higher waist circumference (Chambers

et al. 2004). Moreover economic and neighborhood disadvantage are linked to gender

differences in physiological stress responses among African American youth (Hackman et

al. 2012) both conditions in which African American youth are disproportionately

represented.

Interestingly, there is also evidence that school context is a key factor during childhood and

adolescence that can exacerbate existing health risks among African American youth by

perpetuating exposure to racism and discrimination as well as social alienation (Goosby and

Walsemann 2012; Juvonen et al. 2006). Specifically, African American adolescents

attending predominantly white schools report more depressive symptoms and somatic

complaints (stomach aches, nausea, headaches, etc.) and poorer self-rated health in early

adulthood relative to youth in more integrated schools (Walsemann et al. 2011a,b; Goosby

and Walsemann 2011). Such studies illustrate the emerging cycle of racial discrimination

across generations and can exacerbate already existing health risk brought about by their

parents’ experiences with discrimination.

Conclusion

While protective social conditions such as family support and higher income may offset

some of these risks for African Americans, the added stress of being part of a marginalized

group and experiencing discrimination may curtail potential gains made by economic

mobility, thus leading to continued health risks associated poor birth outcomes in the next

generation. Increasingly, policy makers are escalating strategies to address health disparities

through eliminating differential treatment among health care providers, increasing access to

care, and altering health risk behaviors. While these are important systemic changes, more

attention is required to target the underlying social mechanism of racial discrimination at the

structural and interpersonal levels that contribute to these disparities. The physiological

consequences created by racial and economic inequality are not inalterable, however. But

without addressing the harmful consequences of racial discrimination, improving the health

of African Americans as well as other marginalized groups, will remain inadequately

addressed.

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Biographies

Dr. Bridget Goosby is interested in the consequences of social inequality generally and

racial discrimination specifically for African American health over the life course. She is

currently funded by a National Institute of Child Health and Human Development Mentored

Research Award (NICHD K01), where she is studying and identifying the biological stress

processes that interact with social contexts to create health disparities that persist across

generations. Her work has recently appeared in Journal of Health and Social Behavior,

Society and Mental Health, Health and Place, Social Science Research, and Journal of

African American Studies. Before becoming an assistant professor of Sociology at the

University of Nebraska-Lincoln, she was a National Institute of Mental Health Racial,

Ethnic, and Cultural Disparities in Mental Health Postdoctoral fellow at the University of

Michigan Institute of Social Research Program for Research on Black Americans. She

received her PhD in Sociology and Demography from the Pennsylvania State University and

her BA in Sociology from Southwestern University in Georgetown, Texas.

Chelsea Heidbrink is currently working towards a Masters of Education in Educational

Administration and a post-baccalaureate degree in pre-medicine at the University of

Nebraska-Lincoln, where she also received her B.A. in History. Her current research

examines how social stress in underrepresented populations triggers epigenetic

modifications that lead to elevated risks for chronic disease. She also works as a Nebraska

Legends Coordinator in the University of Nebraska Undergraduate Admissions office.

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Figure 1. Transgenerational Pathways of Health through Prenatal Stress

Note: From Kuzawa, C.W. and E. Sweet. 2009. “Epigenetics and the embodiment of race:

Developmental origins of U.S. racial disparities in cardiovascular health.” American Journal

of Human Biology 21: 2–15. (figure requires publisher’s permission)

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Table 1

Key Physiology Terms

Stress reactivity Environmental or social conditions that affect mental and physical well-being

Allostasis Bodily systems maintaining stability by adapting to change.

Allostatic load Wear and tear experienced by the body as a consequence of inefficient shutting down or turning on of responses stressors to maintain allostasis.

HPA axis (Hypothalamic- pituitary-adrenal axis)

Feedback interactions between hypothalamus and the pituitary and adrenal glands. Controls responses to stress and regulates immune system, mood and emotion, and energy storage/expenditures.

Cortisol Glucocorticoid hormone released in response to stress; increases blood sugar (glucose) circulation, suppresses immune system, aids in fat, protein, and carbohydrate metabolism.

Metabolism Chemical reactions that occur in the human body that maintain life.

Metabolic Syndrome Combination of co-ocurring medical conditions that elevate the risk of cardiovascular disease and diabetes.

Atherosclerosis Thickening and inflammation of artery walls as a consequence of accumulation of cholesterol or other fatty materials.

Insulin Hormone produced by the pancreas that helps regulate fat and carbohydrate metabolism by causing certain cells to take up glucose (blood sugar) circulating in blood.

Insulin Resistance Condition where cells do not respond to insulin causing blood glucose to rise. If not regulated can elevate risk of Type 2 diabetes and cardiovascular disease.

Phenotype An organism’s observable traits and characteristics.

Genotype Genetic composition of a cell, organism, or individual, made up of alleles or various forms of the same gene.

Epigenetics Heritable changes in gene expression without changing underlying DNA sequence

Telomere Region at the ends of a chromosome containing repetitive neucleotide sequences that protect chromosome from deterioration. Telomeres become shorter over time due to cell division

Oxidative stress Imbalance in a biological system’s ability to repair damage or detoxify reactive conditions within a cell. Associated with conditions such as cancer, cardiovascular disease, chronic fatigue.

Fetal Environment Gestational conditions during prenatal development.

Low Birth Weight (Microsomia)

birth weight of less than 2,500 grams (5.8 pounds)

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