ArticlePDF Available

Stress-Related Biosocial Mechanisms of Discrimination and African American Health Inequities

July 2018
Annual Review of Sociology 44(1)

DOI:10.1146/annurev-soc-060116-053403

Authors:

Bridget Goosby

University of Texas at Austin

Jacob E. Cheadle

University of Nebraska–Lincoln

This review describes stress-related biological mechanisms linking interpersonal racism to life course health trajectories among African Americans. Interpersonal racism, a form of social exclusion enacted via discrimination, remains a salient issue in the lives of African Americans, and it triggers a cascade of biological processes originating as perceived social exclusion and registering as social pain. Exposure to discrimination increases sympathetic nervous system activation and upregulates the HPA axis, increasing physiological wear and tear and elevating the risks of cardiometabolic conditions. Consequently, discrimination is associated with morbidities including low birth weight, hypertension, abdominal obesity, and cardiovascular disease. Biological measures can provide important analytic tools to study the interactions between social experiences such as racial discrimination and health outcomes over the life course. We make future recommendations for the study of discrimination and health outcomes, including the integration of neuroscience, genomics, and new health technologies; interdisciplinary engagement; and the diversification of scholars engaged in biosocial inequities research.

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Annual Review of Sociology

Stress-Related Biosocial

Mechanisms of Discrimination

and African American Health

Inequities

Bridget J. Goosby,1Jacob E. Cheadle,1

and Colter Mitchell2

1Department of Sociology, University of Nebraska–Lincoln, Lincoln, Nebraska 68588, USA;

email: bgoosby2@unl.edu, jcheadle2@unl.edu

2Institute for Social Research, University of Michigan, Ann Arbor, Michigan 48104, USA;

email: cmsm@umich.edu

Annu. Rev. Sociol. 2018. 44:319–40

First published as a Review in Advance on

May 16, 2018

The Annual Review of Sociology is online at

soc.annualreviews.org

https://doi.org/10.1146/annurev-soc- 060116-

053403

2018 by Annual Reviews.

Keywords

allostatic load, discrimination, genomics, HPA axis, racism, social exclusion

Abstract

This review describes stress-related biological mechanisms linking inter-

personal racism to life course health trajectories among African Americans.

Interpersonal racism, a form of social exclusion enacted via discrimination,

remains a salient issue in the lives of African Americans, and it triggers a

cascade of biological processes originating as perceived social exclusion and

registering as social pain. Exposure to discrimination increases sympathetic

nervous system activation and upregulates the HPA axis, increasing physio-

logical wear and tear and elevating the risks of cardiometabolic conditions.

Consequently, discrimination is associated with morbidities including low

birth weight, hypertension, abdominal obesity, and cardiovascular disease.

Biological measures can provide important analytic tools to study the inter-

actions between social experiences such as racial discrimination and health

outcomes over the life course. We make future recommendations for the

study of discrimination and health outcomes, including the integration of

neuroscience, genomics, and new health technologies; interdisciplinary en-

gagement; and the diversiﬁcation of scholars engaged in biosocial inequities

research.

319

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INTRODUCTION

Inequities in morbidity and mortality rates for African Americans compared to Whites are long-

standing and remain striking in the United States. Although the processes from which these

disparities arise are multifaceted, they are rooted in the historical legacy of racism that is woven

into the fabric of life in the United States. The United States is a racialized social system of

interlinked domains across layers of social organization (Reskin 2012), supported by practices and

behaviors that produce a network of relations at social, political, economic, and ideological levels

that together shape life chances and health inequities (Bonilla-Silva 2015). These forces act on

the bodies and minds of African Americans, eroding psychic resources and wearing bodies down.

We focus on a speciﬁc aspect of the United States’ racialized social system: the role of perceived

interpersonal discrimination over the life course. This review emphasizes how these negative social

experiences get under the skin via interactions with biological processes that support individuals’

capacities for responsivity and adaptation to stress.

Interpersonal discrimination is a mechanism of social exclusion that remains a pervasive prob-

lem in the United States (Priest & Williams 2018). In fact, in a 2017 national survey, 92% of

African Americans reported that discrimination exists in the United States today, and 75% of

those respondents believed that interpersonal discrimination is a signiﬁcant social problem (NPR

et al. 2017). This review, therefore, focuses on (a) the pathways by which health inequities emerge

through interactions between the negative social experiences of interpersonal discrimination and

stress biology; (b) how these interactions emerge and are understood at different periods of the

life course; and (c) important new directions for future research at the intersection of the bio-

logical and the social. Biosocial processes linking discrimination to health are not exclusive to

African Americans, but we use African Americans’ unique conditions in the United States as an

important example. Much of what we discuss here is likely relevant to other stigmatized social and

racial/ethnic groups who experience high rates of interpersonal discrimination and social exclu-

sion (Pescosolido & Martin 2015). Moreover, the problem of racism is not unique to the United

States, and other societies also present racial health inequities to which the biosocial processes

reviewed here likely apply (Paradies 2006, Pascoe & Smart Richman 2009).

DEFINING DISCRIMINATION

Discrimination is the unjust or prejudicial treatment of a category of people. Minority racial

status is not a prerequisite for discrimination, but it is an important dimension along which

groups of people experience systemic adverse treatment (Williams & Mohammed 2009). This

systematic component with respect to race in general and African Americans in particular reﬂects

racism, that is, “the social categorization and stratiﬁcation of social groups into races that devalues

and disempowers groups” (Priest & Williams 2018, p. 163). Racism is commonly conceptualized

across multiple levels. At the individual level, intrapersonal racism reﬂects individuals’ internalized

attitudes and beliefs about innate superiority or inferiority. Structural racism reﬂects the systematic

exclusion from institutions and markets, such as schools, employment, health, housing, credit, and

justice (Reskin 2012), as well as the withholding of symbolic resources within social institutions

and society more generally (Priest & Williams 2018).

Interpersonal racism, the focus of this review, is at a minimum a dyadic process of “discrimi-

nation between people, with varying degrees of frequency and intensity, including manifestation

from racially motivated assault to verbal abuse, ostracism, and exclusion” (Priest & Williams 2018,

p. 163). Such acts can reﬂect explicit biases (e.g., Jim Crow racism) and the aggressive acts of abuse

associated with racist ideologies, as well as implicit biases (e.g., aversive or colorblind racism) of

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which the perpetrator may not be aware (Bonilla-Silva 2017) and that produce subtler forms of

exclusion (e.g., microaggressions; Sue et al. 2007). Each of these dimensions of racism contributes

to African American health inequities, and each is interdependent with the others.

SOCIOLOGY AND HEALTH BIOLOGY

Systematic and meta-analytic reviews of traditional survey-based studies demonstrate that per-

ceived interpersonal discrimination is associated with a broad range of mental and physical health

outcomes (Paradies et al. 2015, Priest et al. 2013, Pascoe & Smart Richman 2009). These studies

document consistent correlations of perceived discrimination with psychological constructs such

as depressive symptoms, anxiety, anger, low self-esteem, and negative well-being, as well as as-

sociated physical manifestations including poor self-rated health, low birth weight, hypertension,

obesity, high blood pressure, and cardiovascular disease. Models linking discrimination to health

usually posit two global pathways. The ﬁrst pathway comprises physiological stress-related pro-

cesses, and the second reﬂects behavioral patterns (e.g., alcohol and substance use, diet, sexual

risk; e.g., Richman et al. 2018). This review focuses on the ﬁrst set of stress biology pathways.

The pervasive adverse inﬂuences of discrimination on health point to a complex set of in-

teractions between human biology, the human brain’s capacity for sociality, and our social in-

terdependencies on one another. Our brains process and prepare for environmental (i.e., social)

demands by monitoring, regulating, and coordinating internal systems in a process of predictive

regulation termed allostasis (McEwen 1998, Sterling 2012). Allostatic mechanisms manage en-

ergy and homeostatic parameters when confronted with a stressor (McEwen 1998). From a social

science perspective, these allostatic parameters—physiological states—are latent variables. Re-

vealing these physiological indicators (i.e., biomarkers) allows researchers to peer into processes

otherwise invisible to the observer and often to the participants themselves. Many biomarkers are

highly sensitive, making it possible to determine health status characteristics prior to the onset

of morbidity. Moreover, the latent nature of biological measures also assists in addressing re-

verse causality concerns (e.g., negative affect bias) through traditional survey measures that link

perceived interpersonal discrimination to different facets of self-reported health (Richman et al.

2018).

Processes in our bodies are typically affected before we get sick enough to consciously recognize

the change in our health condition. To the extent that stressors become chronic, the modulation of

allostatic regulation can begin to tax systems over time, placing strain on those systems and wearing

them out due to the accumulating allostatic load burden (see also McEwen 1998). Allostatic load

refers to the wear and tear on bodily systems that occurs from frequent allostatic modulation arising

from exposure to chronic stress. The ongoing strain can limit physiological adaptive capacity to

stress by causing a failure to adapt to repeated stressors, by halting neuroendocrine and autonomic

responses, and generally by limiting the ability to respond adequately to stressors (McEwen &

Gianaros 2010). In this way, we could say that allostatic states accumulate over the life course and

are, over time, converted into physiological allostatic load traits.

Biological measures, thus, hold potential for understanding how social conditions and experi-

ences adversely affect health over the life course and at different points within it. Such measures

allow researchers to peer back earlier into life before illness manifests, and to quantify the tolls

exacted by socioenvironmental conditions. Together, period-speciﬁc modulation and accumula-

tion processes are critical for characterizing the what, when, and why of health outcomes. We

cannot review all the biological pathways by which racism in the United States affects health (e.g.,

differential exposure to environmental toxins as a result of residential segregation, etc.), and we

focus instead on the subdomains of neurobiology, stress physiology, and genomic factors.

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Amygdala: a brain

region serving several

functions, including

processing basic

threats (including

physical pain and

social rejection),

memory, decision

making, and emotions

Dorsal anterior

cingulate cortex

(dACC): a subdivision

of the anterior

cingulate cortex

involved in appraising

social experiences,

including social pain,

physical pain, and

reward-based learning

and memory

Anterior insula (AI):

a limbic-related cortex

involved in processing

norm violations,

emotions, empathy,

social decision making,

interoceptive

awareness, and pain

Periaqueductal gray

(PAG): the primary

control center for

descending pain

modulation

Dorsomedial

prefrontal cortex

(DMPFC): a brain

region involved in

creating a sense of the

self and of the mental

states of others

(“theory of mind”) and

in processing social

threat and exclusion

Ventromedial

prefrontal cortex

(VMPFC): a brain

region involved in

social decision making

and emotion

regulation

DISCRIMINATION AND HEALTH OVERVIEW

Sociologists have long recognized the pivotal role of social support and connection in human

health (House et al. 1988). Durkheim’s (1951) argument that social dynamics pattern individual

pathologies, of which integration and anomie are critical factors, is a staple of sociological training.

Interpersonal racism and the associated exclusionary acts of discrimination, whether intentional

or due to insensitivity, withhold their targets’ opportunities for inclusion and support. Targets of

racism and discrimination are thereby denied the symbols of group membership and the motivating

positive emotional energy that individuals derive from successful social experiences (Collins 2014).

Because interpersonal discrimination is socially patterned by racism, these experiences contribute

to large-scale population health inequities by regulating stress exposure risk beyond other forms

of social disadvantage [e.g., socioeconomic status (SES)] that are also patterned by racism (Glass

& McAtee 2006, Phelan & Link 2015).

To characterize why these experiences are harmful, it is important to begin not with the body,

but with the brain. For a social stressor like perceived interpersonal discrimination to get under

the skin, it must ﬁrst get into the mind. Figure 1 presents a conceptual model illustrating the

stress-related pathways connected to interpersonal discrimination that we describe in the following

sections (see also Albert et al. 2013).

Neural Processing of Social Threats

In everyday language, negative social experiences are referred to as painful. When we have been

mistreated, we “feel hurt” by the experience (Eisenberger 2012). There is truth in these colloqui-

alisms. The neural structures supporting the emotional component of pain (as compared to the

somatic component) are shared with those supporting the experience of social pain that results

from social rejection and exclusion (Eisenberger 2012). Social connection is an important facet of

human survival. The mechanisms supporting protection from physical threats via physical pain

may have been conserved to support the feelings of social pain experienced when social inclusion

and therefore survival are threatened (Eisenberger 2013). The pathway between interpersonal dis-

crimination, neurobiological processes, and perceived discrimination is depicted in Figure 1.

A number of brain regions are responsible for processing different aspects of fear and pain,

including the amygdala, the dorsal anterior cingulate cortex (dACC), the anterior insula (AI),

and the periaqueductal gray (PAG). These regions detect and coordinate responses to perceived

threat, and along with the dorsomedial prefrontal cortex (DMPFC), they further support different

aspects of social exclusion processing (Eisenberger 2013), suggesting the shared basis for physical

and social pain mentioned above. These systems further interact with those that process safety in

the absence of negative outcomes, including the ventromedial prefrontal cortex (VMPFC) and the

posterior cingulate cortex (PCC) (Delgado et al. 2006, Schiller & Delgado 2010). Together, these

different systems monitor and respond to the social environment, including threats to inclusion,

and interact with key brain regions that mediate stress response systems.

These regions are embedded in large-scale intrinsic functional networks, including the salience

network (somatovisceral emotional experiences), the mentalizing network (“theory of mind”), and

the central executive network (cognition) (Barrett & Satpute 2013). The interactions within and

among these networks allow the social environment to be processed and monitored, support

socioenvironmental learning, and enable future social experiences and the anticipation of the po-

tential threats embedded in future encounters (Eisenberger & Lieberman 2004). Consequently,

whereas interpersonal discrimination can have localized harmful effects on a person via the im-

mediate needs it presents, the threat of such experiences is also a learning process, as depicted in

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Interpersonal racism

Perceived discrimination

Allostatic load

SNS/SAM Glucocorticoids Inammation

Epigenetic processes, gene expression

Low birth weight, hypertension, obesity,

diabetes, cardiovascular disease

Learning, anticipation,

vigilance, behavior

Genetics, individual

experiences, life course

development

Hypothalamus

Pituitary

Adrenals

Flow of external to internal processes

Bidirectional ow from internal to external

Figure 1

Visual description of the reviewed biosocial links between interpersonal discrimination and health. This

ﬁgure is a visual abstract of the themes discussed in the paper and is not representative of all possible

biosocial relationships. Arrow boxes indicate temporal processes, blue boxes capture a range of predictors

and outcomes, and ovals indicate speciﬁc physiological response products that, over time, reduce health. In

section () interpersonal discrimination is identiﬁed by the brain as a stressor requiring immediate

physiologic response, and also, over time, it becomes a learned process that creates anticipation and vigilance

towards possible future exposures. Sympathetic nervous system arousal occurs in response to discrimination

stress exposure () and in concert with the upregulation of the hypothalamic-pituitary-adrenocortical axis

(). Together, these systems initiate stress activation including sympathetic-adrenal-medullary (SAM),

glucocorticoid, and inﬂammatory responses. When stress exposure is chronic, these responses create

allostatic load, or wear and tear on the body, and increase risks for a variety of adverse health outcomes

throughout the life course. Epigenetic processes and gene expression () contribute to the process in a

bidirectional manner. Social stress can potentially moderate gene expression and epigenetic processes over

the life course and across biological systems. The temporal nature of this process is depicted in the left to

right ﬂow of Figure 1 and the epigenetic/expression feedback in Figure 1. Abbreviations: SAM,

sympathetic-adrenal-medullary system; SNS, sympathetic nervous system.

Posterior cingulate

cortex (PCC):

a brain region highly

interconnected with a

wide range of intrinsic

control networks,

including the

processing of emotions

and memory

Intrinsic functional

networks: widespread

brain regions that are

functionally

interconnected when

processing task

demands

the outward arrow box in Figure 1. These encounters shape how individuals understand their

experiences, form expectancies for future encounters, and therefore monitor and prepare the body

(i.e., predictive regulation) for the social interactions embedded in the social environments they

inhabit and pass through (i.e., vigilance; Blair & Raver 2012, Lewis et al. 2015).

These neural processes are therefore important for monitoring and recognizing discrimination

as a ﬁrst phase in the downstream stress-related physiological cascades that we have depicted in

the descending pathways in Figure 1. Several studies now document the links between activity in

the neural regions involving social exclusion–related brain areas and different aspects of the stress

process. These regions monitor the environment for social feedback, including threats to social

inclusion, and coordinate physiological responses (Eisenberger 2013).

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Salience network:

network involved in

detecting and ﬁltering

salient stimuli, with

anatomical

connections important

for autonomic nervous

system and hormonal

modulation

Mentalizing

network:

a network involved in

understanding the

mental states of self

and others that guide

or are responsible for

overt behavior

Central executive

network: a network

subserving basic

cognitive processes

such as attentional

control, cognitive

inhibition, inhibitory

control, working

memory, and cognitive

ﬂexibility

Central nervous

system (CNS): the

part of the nervous

system containing the

brain and the spinal

cord

Peripheral nervous

system (PNS): the

nerves and ganglia

outside the brain and

spinal cord that relay

information from the

CNS to the rest of the

body

Autonomic nervous

system (ANS):

a largely unconscious

PNS subsystem

regulating bodily

functions such as heart

rate, digestion,

respiratory rate,

pupillary response,

urination, and sexual

arousal

Sympathetic Nervous System

At the broadest level, the nervous system consists of the central nervous system (CNS), which

contains the brain and spinal cord, and the peripheral nervous system (PNS), which contains

nerves and ganglia outside of the CNS. An important subdivision of the PNS is the autonomic

nervous system (ANS), which controls a range of bodily functions (e.g., heart rate, respiration,

digestion). In the ANS, the sympathetic nervous system (SNS) prepares the body to deal with

the demands of the environment, including threats to social inclusion (Bosch et al. 2009), and it

is responsible for the ﬁght-or-ﬂight response. A related balancing branch, the parasympathetic

nervous system (PSNS), manages recovery (rest-and-digest response). The SNS and PSNS work

mostly, but not entirely, in opposition to one another. SNS modulation, in particular, can be

damaging to health when stress is chronic (see Figure 1).

CNS activity in the dACC, AI, PAG, and amygdala associated with social exclusion and inclu-

sion processing (Eisenberger 2013) is connected to increased SNS activity (e.g., blood pressure,

heart rate) (Critchley et al. 2003, McEwen & Gianaros 2010). Moreover, damage to the dACC

decreases reactivity to mental stressors (Critchley et al. 2003), suggesting that the dACC mediates

ANS activity. VMPFC activity during fear extinction tasks predicts decreased SNS activity (Phelps

et al. 2004) and reduced cardiovascular responses during a social stressor (Wager et al. 2009), pos-

sibly due to associations with the PSNS (H¨

ansel & von K¨

anel 2008). The hypothalamus mediates

SNS reactivity to social exclusion threats such as perceived discrimination. The hypothalamus is

a structure located in the limbic system composed of small nuclei that manage a variety of ANS

functions. Relevant hypothalamus-mediated SNS activity has been referred to as the sympathoa-

drenal or sympathetic-adrenal-medullary (SAM) system (Cohen et al. 2007). SNS-triggered SAM

activity releases the adrenal hormones epinephrine/adrenaline and norepinephrine/noradrenaline,

which increase blood sugar, heart rate, and blood circulation, and reallocates energy to be utilized

during the acute-phase response to a stressor.

An important consequence of this elevated SAM activity is increased wear and tear on the

cardiovascular system (Brotman et al. 2007). Cardiovascular responding shows different patterns

depending on whether the stressor is positive or negative. In the former case, heart rate increases

and blood vessels dilate, lowering total peripheral resistance while increasing cardiac output and

keeping blood pressure relatively stable. During negative stressors, by contrast, blood vessels con-

tract, restricting blood ﬂow for fast circulation and increasing blood pressure (Brondolo et al. 2003).

This elevated blood pressure, amounting to hypertension when chronic, is particularly dangerous

due to increased blood viscosity from elevated blood glucose levels and to increases in certain

cholesterol particles that contribute to arterial scarring and elevated cellular inﬂammation, which

are precursors to atherosclerosis (Sapolsky 2004). These conditions are all indications of higher

allostatic load in the body and markers of accelerated stress-induced wear and tear (McEwen 1998).

HPA Axis

Sociological research has sought to understand the stress process in terms of socially patterned

stressors that shape mental and physical health (Pearlin 2010). These studies have documented

stress typologies and characterized key mediators and moderators in the stress process, such

as social support (Pearlin 1999). The stress process model argues that the consequences of exposure

to stressors such as chronic economic hardships create psychological burdens that are challenging

for individuals to bear, leading to declines in health resulting from maladaptive psychological and

behavioral coping (Turner 2013). More recent stress process models include attention to physi-

ological stress reactivity, adaptation, and load via the hypothalamic-pituitary-adrenal (HPA) axis

( Jackson et al. 2010, Turner 2013), depicted in Figure 1.

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Sympathetic nervous

system (SNS):

the ﬁght-or-ﬂight

subsystem of the ANS

that accelerates the

heart rate, constricts

blood vessels, and

raises blood pressure

Parasympathetic

nervous system

(PSNS): a subdivision

of the ANS that serves

to slow the heart rate,

increase intestinal and

glandular activity, and

relax the sphincter

muscles

Sympathetic-

adrenal-medullary

(SAM) system:

hypothalamus-

mediated stress

response system that

controls adrenaline

and noradrenaline

release, upregulating

the SNS and

downregulating the

PSNS

Along with SNS/SAM processes, the HPA axis is a key mediator of stress responsivity and

long-term health outcomes. The HPA axis is a complex set of interactions comprising direct ef-

fects and feedback loops among the hypothalamus, the pituitary gland, and the adrenal glands.

The primary function of the HPA axis is to regulate metabolic (neuroendocrine) and immune

function (McEwen & Gianaros 2010). This system is primarily responsible for metabolizing car-

bohydrates, fats, and proteins; for gluconeogenesis (internal production of blood glucose); and

for inﬂammatory immune function regulation (Sapolsky 2004). The HPA axis elevates circulating

hormone levels, starting with the activation of corticotropin releasing hormone (CRH), which

triggers the production of adrenocorticotropic hormone (ACTH) into the bloodstream. ACTH

triggers the release of glucocorticoid hormones, including cortisol. Cortisol, a stress hormone,

regulates metabolic function (e.g., circulating blood glucose, fat storage, insulin response), immune

response (e.g., increased inﬂammation for wound healing), and mood (Sapolsky 2004). Cortisol

facilitates easy energy access by reducing the body’s sensitivity to insulin, the hormone responsible

for regulating uptake of blood glucose for storage in cells, while increasing gluconeogenesis. In

addition, cortisol promotes the breakdown of fats into fatty acids (lipolysis) and contributes to the

initial inhibition of inﬂammatory and acute-phase immune responses to infection (McEwen 2003).

Neural sensitivity to social exclusion and reactivity to negative social experiences such as per-

ceived interpersonal discrimination are linked directly to HPA axis activity. For example, social

stress experiments show increased HPA activity in response to social evaluative threats (Bosch

et al. 2009, Dickerson et al. 2009). Greater activity in the brain regions involved in processing

and monitoring for threat is also implicated. Activation in the dACC during a mental stress task

is associated with increased stress hormone output (Wang et al. 2005), and increased cortisol is

also predicted from dACC and DMPFC activity in response to social exclusion (Dedovic et al.

2009). Although such increases are adaptive in the short term, chronic increases in circulating

blood glucose, coupled with the dampened response to insulin regulated by higher cortisol lev-

els, heighten the risk for insulin resistance, abdominal obesity, and type 2 diabetes (Black 2003).

As with SNS/SAM, HPA pathways also create wear and tear on the arteries via an increase in

particle-dense blood. This increased blood viscosity is thought to cause inﬂammation and arterial

scarring, both of which are risk factors for cardiovascular disease and indicators of allostatic load

(Seeman et al. 2010).

Genomics

Genetic research is perhaps the most controversial area of biologically informed sociological re-

search. Concern that genetic research will be used to support racist agendas is a reﬂection of the

larger societal problem of racist ideologies, racial domination, and dehumanization (Zuberi et al.

2015). In practice, genomic research on African ancestry groups lags behind studies of European

ancestry groups, despite evidence that more multiethnic research is needed (Need & Goldstein

2009). This lag partly reﬂects the challenges of population stratiﬁcation and admixture resulting

from slavery, a reliance on nonrepresentative higher-SES European-ancestry samples, a genotyp-

ing technology tailored for the more genetically homogenous European ancestry, and the complex

politics of race (Bentley et al. 2017, M´

arquez-Luna et al. 2017, Popejoy & Fullerton 2016). Conse-

quently, Eurocentric estimates perform poorly for groups from different ancestral lineages and who

experience different environments (M´

arquez-Luna et al. 2017, Ware et al. 2017). Multiple reviews

document the current methods, results, and major concerns of genetic research for social scientists,

including the lack of diversity in study populations (Duster 2015, Freese 2008, Mitchell 2018).

The a priori rejection of genetic information based on the key (and well-documented) distinc-

tion between genetic ancestry and the social attribution of race impairs our understanding of how

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life in a racialized social system affects health through genetically inﬂuenced biological pathways.

Genetic variation, depicted in the entering arrow box in Figure 1, contributes to variability

of all the biological systems discussed above, and therefore it inﬂuences the individual capacities

underlying sensitivity to social exclusion and need for inclusion (Preller et al. 2016), emotional and

physiological reactivity (Mitchell et al. 2013, Moore & Depue 2016, Pluess 2015), and individual

differences in allostatic load accumulation (Brody et al. 2013). Moreover, the activity of genetic

networks varies during development, modulating the organism’s responses to the environment at

different life stages (Manuck & McCaffery 2014, Mitchell et al. 2013). Biosocial interactions likely

occur at a much higher level of biological organization than the gene, which is likely why most

genetic effects are exceptionally small and come from across the genome (Belsky et al. 2013). Be-

cause the genome evolved to set the parameters for environmental responsiveness, understanding

the underlying architecture of these biological processes provides clear beneﬁts. Further, genes

may be highly informative if we consider that some of the biological levels are too dynamic or

too invasive to measure, such as the neurotransmitter systems that regulate communication be-

tween nodes in the neural networks involved in monitoring and responding to social inclusion and

exclusion (Preller et al. 2016).

Moreover, it is more useful to think in terms of genomics and not just genes, as we have indi-

cated at the bottom of Figure 1. The gene is a predictor that can be linked to the environment via

gene by environment interaction (GxE), but other genome features occupy different locations in

causal models with environmentally dependent pathways. Gene expression is the process by which

the information contained on the chromosome (DNA, epigenetics, etc.) is used to assemble func-

tional gene products. Research indicates that social stress regulates gene expression, potentially

moderating allostatic response and load accumulation. For example, social stress is associated with

upregulated pro-inﬂammatory immune response and downregulated antiviral immune response

(Slavich & Cole 2013). Loneliness is also implicated in differential expression of the genes involved

in reward circuits in the CNS (Canli et al. 2017), and the social stress of loneliness is associated with

differential expression of genes containing glucocorticoid receptor response elements (Cole 2013).

Gene expression is also dependent on epigenetic processes, as indicated by the dashed feedback

loop in Figure 1. Epigenetics—for example, DNA methylation—is the study of the chromo-

somal alterations that inﬂuence gene activity and expression without changing the nucleotide

sequence (Champagne 2018). Methylation, the process by which methyl groups attach to DNA

by binding to a cytosine base, typically diminishes and can even turn off gene expression (less

commonly, genes can also be turned on). Interpersonal discrimination is associated with meth-

ylation patterns (Brody et al. 2016, Saban et al. 2014), as is stress more generally (Champagne

2010, Mitchell et al. 2015). Epigenetic regulation of the genome is environmentally dependent and

sensitive to social experience. Both methylation (Horvath 2013) and length of telomeres—DNA

sequences at the end of the chromosome that (generally) shorten with aging and stress (Shalev

et al. 2013)—appear to provide indications of the degree of cellular adversity and biological aging.

Interpersonal discrimination is associated with shorter telomere length in adults (Chae et al. 2014,

Lee et al. 2017) and in the placentas of newborns of women exposed to discrimination during

pregnancy ( Jones et al. 2017). Further, it is well documented that all of these genomic processes

(from epigenetics to gene expression) are highly developmental and change throughout the life

course (Champagne 2010, Manuck & McCaffery 2014, Mitchell et al. 2015, Shalev et al. 2013).

DISCRIMINATION AND HEALTH OVER THE LIFE COURSE

The stress process model provides an important heuristic guide for understanding the conse-

quences of socially stratiﬁed and patterned stressors for well-being (Pearlin 2010). Of particular

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importance is how exposure to chronic stress is regulated by ascribed characteristics of varying

social value (i.e., race) and their convergence with role statuses (i.e., student, parent, employee

etc.) over the life course (Pearlin 1999). Over their lives, individuals move from birth (when ad-

verse birth outcomes shape health and developmental trajectories), to childhood (when social

networks remain small and dependency on parents remains high), through adolescence (when

social networks expand and youth individuate from parents), and into adulthood (with its myriad

roles, demands, and dependencies). For stigmatized groups like African Americans, it is worth

considering whether some periods may be more sensitive to social rejection and exclusion than

others and how health deﬁcits accumulate over that time (Colen 2011). The social exclusion of

interpersonal discrimination is a moment of learning that conditions how future social interactions

are experienced. It is also a moment of allostatic responding via SNS/SAM, HPA, and genomic

mechanisms that, when viewed over the life course, contribute to a stress-response time series

over which allostatic loads accumulate. Considering this process over the life course is important

to understand the when, why, and what of physiological functioning and therefore to identify

the ﬁrst emergence of the biological manifestations of health disparities documented by midlife.

The temporal nature of this process is depicted in the left to right ﬂow of Figure 1 and the

epigenetic/expression feedback in Figure 1.

Birth

African Americans experience substantially disparate birth outcomes compared to Whites. Birth

disparities have not improved signiﬁcantly since the Jim Crow era (Sullivan 2013), and the odds

of low birth weight (<2.5 kg) and preterm birth for African Americans remain respectively 1.6

and 1.9 times larger than they are for Whites, even after controlling for a variety of factors

like SES (Schempf et al. 2007). Notably, the odds of unfavorable birth outcomes among African

immigrants in the United States decline substantially as time spent in the country increases,

converging with those of African American women by the third generation (David & Collins

1997). African American women exposed to discrimination during pregnancy have elevated blood

pressure, and their offspring have lower birth weights and higher preterm delivery risks (Hilmert

et al. 2008, 2014; Slaughter-Acey et al. 2016), outcomes strongly correlated with infant mortality

(Collins & David 2009, Schempf et al. 2007).

The in utero environment is a critical period shaping health risk trajectories.Exposure to stress-

ful conditions inﬂuences the neural and physiological stress pathways of the fetus via cascading

metabolic, epigenetic, and gene expression alterations (Champagne 2010, Godfrey & Barker 2001,

Mitchell et al. 2015, Thayer & Kuzawa 2015). Poor birth outcomes are associated with abdominal

obesity, insulin resistance, hypertension, type 2 diabetes, and cardiovascular disease (Nobili et al.

2008, Singhal et al. 2003), conditions for which African Americans are disproportionately at risk

(CDC 2005, Zhang et al. 2009). Though these conditions represent health risks, they are the

body’s way of preparing the offspring for the environmental stressors that may be experienced

outside the womb. In this way, the environment in the womb mirrors maternal stress-related

factors, preparing the child for the mother’s social environment.

For example, women who experience stress while pregnant secrete higher levels of CRH from

both brain and placenta, upregulating fetal neuroendocrine and HPA axis response during key

developmental periods of gestation (Collins & David 2009). Consequently, the fetus may be ex-

posed to higher levels of stress hormones, including cortisol, which can restrict growth and elevate

preterm delivery risk (Shapiro et al. 2013). When the fetus is exposed to high levels of stress hor-

mones through the placenta, glucocorticoid (i.e., stress hormones) receptors are downregulated

in the hippocampus, disrupting a key pathway modulating HPA axis activation. At the same time,

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receptor density in the amygdala is increased, affecting a key region involved in SNS/SAM and

HPA responsivity and activation (Wadhwa 2005). These inﬂuences may emerge through epige-

netic processes that prepare the offspring for life in a high-stress environment. In other words,

the in utero environment prepares the offspring stress reactivity proﬁle for stressful environ-

mental conditions outside the womb (Kuzawa & Sweet 2009, Mitchell et al. 2015, Shalev et al.

2013).

Childhood and Adolescence

In many ways, African American children in the United States are not given the same opportunities

to enjoy childhood as White youth (Goff et al. 2014). By the time they reach three or four years

of age, young children of color are able to discern the members of dominant social groups and to

perceive negative racial stereotypes (Averhart & Bigler 1997, Branch & Newcombe 1986). This

awareness may reﬂect African American experiences of discrimination in the form of racial slurs and

taunts, bullying and social exclusion, harassment by the police, and the disproportionate allocation

of punitive treatments in school (Perry & Morris 2014, Sanders-Phillips 2009). Consequently,

African American children are at risk of experiencing elevated feelings of danger, social isolation,

and psychological distress (Sanders-Phillips 2009). Together, these factors work to upregulate

stress response systems via brain-mediated pathways, and in combination with greater stress across

life domains due to factors such as residential segregation and other features of the United States’

racial hierarchy (e.g., Massey & Denton 1993), they may exceed some individuals’ ability to cope

and respond effectively (Sanders-Phillips et al. 2009).

In their systematic review, Priest and colleagues (2013) found that exposure to discrimination

from birth through age 18 was linked to a range of negative mental health outcomes. Early life

stress is linked to higher blood pressure, blood glucose, body mass index, and pro-inﬂammatory

immune function in childhood and adolescence, thus elevating chronic disease risk as youth age and

physiological insults accumulate (Goosby et al. 2016, Miller & Chen 2010). In children as young as

9 or 10 years old, exposure to discrimination is associated with elevated blood pressure and higher

inﬂammatory markers (Goosby et al. 2015) as well as ﬂatter diurnal cortisol curves (Martin et al.

2012). Moreover, a number of studies now document genomic (i.e., GxE, epigenetics, telomere

length, etc.) correlates of social experiences disproportionally experienced by African American

children that may modify stress-health pathways in the long term (Champagne 2018, Mitchell

et al. 2017, Notterman & Mitchell 2015, Shalev et al. 2013).

Adolescence is marked by a host of interlinked physiologic and social transitions, including

neural sensitivity to social exclusion (Masten et al. 2009). Motivated by the biological changes due

to pubertal onset and development, youth become increasingly aware of their status in peer social

hierarchies as they shift from parents to peers as their primary socializing agents (Goosby et al.

2013). They may also become aware that they inhabit highly racialized systems of oppression as

they are exposed to discriminatory experiences in the expanding range of social environments their

autonomy allows them to navigate (Hope et al. 2015, Morris & Perry 2016). Also during this time,

adolescents may be exposed to more discrimination and become increasingly cognizant of the

vicarious discrimination and microaggressions experienced by themselves, their family members,

friends, peers, and others (Wickrama et al. 2017). Such experiences may add to or exacerbate their

existing stress burden, increasing allostatic load earlier in life and setting the stage for morbidity

and mortality inequities including obesity, hypertension, and cardiovascular disease (Goosby &

Heidbrink 2013).

Studies examining African American/White differences from adolescence into adulthood sug-

gest that the secretion of cortisol among African American adolescents is higher at bedtime and

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ﬂatter during the day, indicating higher levels of stress activation (DeSantis et al. 2007). These

proﬁles are also possible indications of reduced allostatic responding due to stress cascade modi-

ﬁcations resulting from persistent stressor anticipation and exposure (DeSantis et al. 2007, 2015).

Consequently, adolescent reports of discrimination are associated with ﬂatter cortisol curves in

adulthood (Adam et al. 2015). Importantly, diurnal cortisol curves appear to peak during days

characterized by positive affect, as indicated by a steeper decline during the day (Hoyt et al.

2015). Interpersonal discrimination is also positively associated with higher allostatic load (Brody

et al. 2013) and elevated pro-inﬂammatory cytokine markers (Brody et al. 2015), an indicator of

inﬂammation.

Adulthood

Adulthood is generally the time when illness manifests. Earlier life course stages set up the health

patterns during adulthood, altering aspects of CNS social processing, moderating health physi-

ology and genomic mechanisms, and accumulating wear and tear. Stressors broaden and deepen

with age, social roles become more complicated, and family and other interdependencies become

more crucial. Given these many challenges, early adversity sets the individual baseline upon which

the unique stressors of adulthood continue building.

Emerging adulthood. Emerging adulthood (∼ages 18–29) involves various transitions or turn-

ing points, including education, employment, parenthood, and marriage, all of which can transpire

in the context of interpersonal discrimination (Hope et al. 2015). Such disruptive exposures can

exacerbate the existing stress burden associated with normative transitions during this period.

Indeed, the African American/White allostatic load gap is already pronounced at ages 18–24 and

continues to widen through middle age (Geronimus et al. 2006). In one functional magnetic res-

onance imaging (fMRI) study on discrimination, adults in this age range showed greater social

pain–related CNS activity and reduced neural activity associated with emotion regulation in re-

sponse to negative social treatment, though discrimination was associated with lower social pain

but greater regulatory CNS activity (Masten et al. 2010).

Important experimental laboratory studies have demonstrated that exposure to discrimination

for African American college students is linked to ANS and SNS responses. Blood pressure,

an indicator of SNS activation, is positively associated with discrimination in individuals with

lower Afrocentric orientation relative to college students with stronger Afrocentric orientation

(Neblett & Carter 2012). Perceived discrimination among African American (but not White)

college students is linked to lower heart rate variability, an indicator of SNS-PSNS modulation

and a cardiovascular risk factor (Hill et al. 2017, Williams et al. 2017). These laboratory studies

provide important clues regarding the physiological load accumulated by minority college students

in predominantly White spaces.

As they transition into parental roles, African Americans must consider their children’s ex-

periences with race-related stressors such as discriminatory experiences in schools and with law

enforcement (Dow 2016). Though little is known about how these worries affect parents’ health,

there is evidence that such conditions can lead to psychological stress and rumination (Murry

et al. 2001). Indeed, according to one estimate among college-educated adults, African Ameri-

cans’ allostatic load levels are 32% higher than those of comparable Whites (Howard & Sparks

2015). However, it is not clear how much of this disparity is due to the unique contributions of

parenting stress, to the high probability of contacts with Whites for this group of relatively advan-

taged African Americans (i.e., interpersonal discrimination), and to other factors (i.e., structural

or intrapersonal racism, behaviors, etc.).

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Middle age through senescence. By middle age, African American adults show numerous signs

of accelerated aging. For example, as measured by telomere length, African American women aged

49 to 55 are estimated to be 7.5 years biologically older than SES-comparable White counterparts

(Geronimus et al. 2010). There is recent evidence indicating that African American adults aged

51 and older who reported the highest lifetime discrimination exposures had shorter telomere

lengths relative to those who reported low to moderate levels of lifetime discrimination (Lee et al.

2017). Discrimination among middle-age and older African Americans is also associated with

other health-related markers predictive of chronic stress–related conditions such as diabetes, heart

disease, and stroke. Discrimination is associated with higher levels of the inﬂammatory marker

C-reactive protein (Lewis et al. 2010), elevated stress hormones (Fuller-Rowell et al. 2012),

abdominal/visceral fat (Lewis et al. 2011), high blood pressure (Lewis et al. 2009), oxidative stress

(Szanton et al. 2012), and coronary artery calciﬁcation (Everage et al. 2012). These outcomes are

important to note given the acute differences in health outcomes between African Americans and

Whites during middle age, and they likely reﬂect patterns of wear and tear accumulation over

many years.

African American adults have persistently higher allostatic load relative to Whites until they

reach age 60–65, at which point such disparities appear to reduce in magnitude, perhaps due

to mortality selection (Levine & Crimmins 2014). When comparing the allostatic load levels of

African American and White adults, Duru and colleagues (2012) found evidence that the disparities

in diabetes- and cardiovascular-related mortality were partially explained by allostatic load, and

these differences were independent of SES (Duru et al. 2012). These ﬁndings are signiﬁcant given

that African Americans are also more likely to experience earlier onset of age-related chronic

diseases and fatal chronic conditions (Levine & Crimmins 2014). In fact, 28% of cardiovascular

deaths among African Americans occur at less than 65 years of age compared to 13% for Whites,

a difference that persists after controlling for SES (Jolly et al. 2010).

It is important to recognize the intersecting life-course pathways that come to shape African

American health disparities, including factors such as improved SES that may lead to additional

race-related stressors. Indeed, a recent study using the 1979 National Longitudinal Survey of

Youth (NLSY79) showed both that African Americans reported higher rates of discrimination

as they moved up the socioeconomic ladder relative to their SES-stable counterparts and that

the high rates of discrimination explained the racial disparity in health outcomes among upwardly

mobile adults (Colen et al. 2018). Additionally, an important and understudied area requiring more

attention is the role of death and bereavement as an extension of systemic racial inequality that

interpersonal discrimination likely contributes to. African American health inequities contribute

to the likelihood of experiencing the loss of multiple loved ones over the life course, which is a

traumatic and acute stressor that appears to exacerbate individual and intergenerational health

risks within African American families (Umberson et al. 2017).

FUTURE ISSUES

In this review we have emphasized stress-related processes modulated by experiences of inter-

personal discrimination, so we now focus on promising directions within this domain. There

remain a number of important avenues for continuing to illuminate the harsh inequities of life

in a racialized social system. We have focused on African Americans in this review, but research

on other marginalized social groups exists (though substantially smaller), and at a time of in-

creased aggression and hostility toward people of color, immigrants, sexual minorities, and people

of non-Christian faiths, more research is needed. In this ﬁnal section, we discuss important de-

velopments emerging across a variety of disciplines that hold promise for better measurement

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of racial inequality and the dynamic, adaptive biosocial pathways through which social condi-

tions shape health trajectories. Rather than reifying disciplinary boundaries, we see great value in

incorporating biological assessments into sociological research.

Neurobiology

We began our review of biosocial mechanisms noting the importance of the CNS as the mediator

of social experience and regulator of SNS/SAM and HPA axis activity. Neurosociological progress

since Massey (2002) in his 2001 presidential address to the American Sociological Association in-

troduced the limbic system and its role in cognition has been limited. That is not to say, however,

that there has been no progress. Theorists have grappled with the role of social encounters in

positive emotions and motivation (Collins 2014) and with the relationships between emotions and

neurobiology for social organization (Turner 2007). A more recent wave of scholars is becoming

involved in neuroscience research using brain imaging to answer sociological questions (Kalkhoff

et al. 2016; Kiat & Cheadle 2017; Kiat et al. 2016, 2017; Melamed et al. 2017). At the same time,

there is a growing interest in combining demographic population perspectives with neuroscientiﬁc

frameworks (Falk et al. 2013). We have argued that because the brain is the key mediator of both

experience and physiological regulation (McEwen 1998, Sterling 2012), a deeper understanding of

it is necessary for broadly conceptualizing stress-related and experiential emotion-based processes.

Such understandings are likely important for genetic and some genomic pathways, because many

pathways that are considered sociologically relevant (e.g., 5-HTTLPR) underlie neurobiological

systems. Imaging technologies may, in the future, shed light on how discrimination affects struc-

tural and functional neural network connectivity and may thereby illuminate important aspects

of social and emotional processing. Currently, the neuroscience of discrimination exposure is in

its infancy if compared to general experiences of social exclusion, and more work is needed to

determine how these experiences inﬂuence the brain to modify the ways individuals experience

and process complex social environments and interactions (Kiat et al. 2016, Masten et al. 2010).

The brain is the organ that decodes and responds to social experiences and is an important new

frontier for sociological researchers.

Sensor-Based Health Measurement

The knowledge base for understanding the basic biological pathways supporting health has de-

veloped rapidly and continues to do so. New assays and technologies will continue to provide

greater insight into speciﬁc mechanisms within different systems as the utility of saliva, blood,

and other tissues continues to expand. Whereas biological researchers seek to peer into different

processes in the body, sociologists often seek more global indicators and indexes, for example

when they use multiple biomarkers to estimate allostatic load. Although many of the biological

underpinnings already in place have utility in sociological research, looking forward sociologists

may begin considering noninvasive biosignals as compared to, or for use in conjunction with,

biomarkers. Rapid technological development is quickly expanding the nature and type of tools

available to researchers thanks to the tremendous diffusion of smartphones and wearable devices

as technology companies seek to capitalize on these markets.

The tools of ambulatory research (Trull & Ebner-Priemer 2014), such as ecological momentary

assessment, promise to more accurately characterize the nature of discriminatory experiences, their

frequencies, and the ways they are experienced. Discrimination research has mostly relied on scales

with item categories that provide only gross estimates of exposure rates. Cell phone frameworks

are now available for passive data collection (Ferreira et al. 2015), along with applications for

collecting real-time social contact networks within which individuals’ social experiences can be

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situated (Fournet & Barrat 2014). Wearable devices are also receiving a great deal of attention,

with consumers using a range of sensors to gather data about themselves with the goal of informing

their health decisions (Swan 2013). Health assessment devices currently use signals measured on

the body, such as photoplethysmography (PPG) sensors for heart rate (Lu et al. 2009), changes in

skin conductance due to SNS activity (Boucsein 2012), and accelerometers (Goosby et al. 2018).

These approaches provide detailed information on aspects of the CNS, the PSNS, and physical

activity and sleep. Taken together, this engineering-based side of biological assessment holds

promise for monitoring emotional lability, activity and sleep recovery, social contacts, and high-

frequency participant reports on these and other factors. The timescales of some of these processes,

sometimes of the order of seconds, can be much ﬁner than they are for traditional biomarkers,

which can span minutes or years. However, these measures assess state-based allostatic processes

and will need to be linked to longer-term measures of trait-based traditional biomarkers of allostatic

load to clarify how dynamic dimensions of interpersonal discrimination are associated with health

biology to form biosocial signals of sociological signiﬁcance.

Genomics

As described above, the vast majority of work linking genetics to health outcomes has been con-

ducted on White European-ancestry populations (Need & Goldstein 2009, Popejoy & Fullerton

2016), and in their current state many of these genetic correlates do not perform as well in

non-European-ancestry populations (Ware et al. 2017). Nevertheless, as more African and other

non-European genetic work is conducted, the CNS underpinnings of social exclusion sensitivity

and vigilance, HPA reactivity, and behavioral or health outcomes may help detect the effects of

discrimination by controlling how genes and experiences interact to regulate the risks of poor

health outcomes. Discrimination may, like other social stressors, be moderated by genotype (i.e.,

by GxE). Finding those GxE will be challenging, and understanding the stress dynamics by which

interpersonal discrimination affects health-related processes may require greater use of molecu-

lar approaches such as epigenetics and gene expression. Further, in nearly all genomic research,

ancestry will continue to be an incredibly complex confounder. Ancestry is strongly correlated

with genotype frequency, and it may be strongly correlated with, but not be the same as, socially

ascribed race (Guo et al. 2014), which is what typically deﬁnes health inequities. Extremely careful

and thoughtful research is needed to disentangle GxE factors and explain how discrimination

interacts with the body to dysregulate physiological systems and increase allostatic load, thereby

becoming embodied.

The relatively recent use of genomic mechanisms in stress—and especially discrimination—

research has not afforded sufﬁcient time to fully determine which measures are robust biological

mechanisms and which are symptoms of health decline. For example, is telomere shortening

associated with discriminatory stress resulting in higher rates of cancer, or is telomere shortening

simply a summary of chronic systemic dysregulation (especially at younger ages)? Work in the

next decade will likely begin by separating the extent to which these measures are acting as

mechanisms or biomarkers. This distinction almost certainly varies by stressor and health outcome

combination. Biosocial researchers are ﬁnally harnessing the necessary longitudinal data in non-

White samples to address these types of questions with respect to the unique constellations of

stressors experienced by non-European-ancestry populations (see Popejoy & Fullerton 2016), and

such research is supported by a recent NIH funding opportunity for social epigenetics research

on minority health and health disparities. The models resulting from this research will provide

new opportunities for understanding how social and genetic factors interact to shape complex

behavioral phenotypes and disease susceptibility.

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Training

As biological data expand into sociology, there is a tremendous need for collaboration between

biological scientists and health inequality and discrimination researchers across a range of increas-

ingly relevant ﬁelds, such as computer science and engineering, molecular biology, immunology,

and neuroscience. Biosocial problems are hard problems. Scholars in these areas will continue to

explore the links between stress and health alongside their colleagues in the social sciences, and

it is worth considering how this research will beneﬁt from the inclusion of sociologists in inter-

disciplinary teams. Sociological perspectives that emphasize the role of discrimination at multiple

levels of social organization have much to offer because they inherently recognize that discrim-

ination today reﬂects ongoing historical processes whose roots spread deep and wide within our

culture. In the same way that sociologists are unfamiliar with the complexity of biological systems,

biologists and health scientists tend to be reductionist with respect to social context. Furthermore,

the sociologists who study different facets of discrimination themselves come from diverse back-

grounds, experiences, and perspectives. In particular, just as the biological data have often been

examined in White or European-ancestry samples, the vast majority of researchers in this area are

White. We strongly encourage scholars of color to lend their experience, knowledge, and skills

to this work, and we believe that broad and inclusive participation will help protect the future

of biosocial science from the mistakes of the past. In short, biosocial work—even concerning

discrimination—will continue to expand rapidly, and we argue it will be far more consequential

and accurate if sociologists are signiﬁcantly involved.

CONCLUSION

This review has focused on an important dimension of the United States’ racialized social sys-

tem: the role of interpersonal discrimination and how this social experience becomes embodied.

Through stress process mechanisms, social experiences are translated into short-term physiological

states; over time, through learning processes and repeated experiences, the allostatic modulation

of physiological states accumulates allostatic load and potentially modiﬁes and is modiﬁed by

genomic processes. The health inequities experienced by African Americans over the life course

begin at birth, when reproductive processes program the newborn for the stressful environment

experienced by the mother, whose level of physiological stress is the result of a life-long adapta-

tion process. Although we have pointed to some promising directions for future research, other

scholars would almost certainly have pointed in other directions and emphasized discrimination

at other levels of social organization. The mechanisms conducive to poor health are many, and

large-scale patterns of racial inequity have long been embedded in different facets of the racist so-

cial organization of the United States. However, even if we strip away the broad macro-structural

patterns of inequality in the United States and focus instead on the systemic yet small-scale in-

terpersonal interactions in which discrimination is enacted face-to-face, differential treatment via

exclusionary acts has large-scale consequences for population health.

SUMMARY POINTS

1. The majority of African Americans believe interpersonal discrimination is an important

social issue.

2. Interpersonal racism is enacted through discrimination, a form of social exclusion that is

processed in the brain as social pain in the same regions associated with the emotional

components of physical pain.

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3. Activity in the neural regions that process social exclusion is associated with increased

SNS and HPA axis activity.

4. SNS and HPA activity increase the risk of cardiometabolic conditions and cardiovascular

wear and tear.

5. Genomics can be an important analytical tool to investigate the interactions between

experiences of racial inequality and life-course health outcomes.

6. Discrimination against African Americans is associated with adverse birth outcomes,

hypertension, abdominal obesity, cardiovascular disease, and other associated morbidities

over the life course.

7. In the future, sociologists are encouraged to integrate neuroscience, genomics, and new

health technologies; to engage in interdisciplinary collaboration; and to diversify the pool

of scholars engaged in biosocial health inequities research.

DISCLOSURE STATEMENT

The authors are not aware of any afﬁliations, memberships, funding, or ﬁnancial holdings that

might be perceived as affecting the objectivity of this review.

ACKNOWLEDGMENTS

The authors would like to thank Doug Massey and the anonymous reviewer for their helpful

comments on earlier drafts.

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ANNUAL REVIEWS

Connect With Our Experts

New From Annual Reviews:

Annual Review of Criminology

criminol.annualreviews.org • Volume 1 • January 2018

Co-Editors: Joan Petersilia, Stanford University and Robert J. Sampson, Harvard University

The Annual Review of Criminology provides comprehensive reviews of signicant developments in the multidisciplinary eld of

criminology, dened as the study of both the nature of criminal behavior and societal reactions to crime. International in scope, the

journal examines variations in crime and punishment across time (e.g., why crime increases or decreases) and among individuals,

communities, and societies (e.g., why certain individuals, groups, or nations are more likely than others to have high crime or

victimization rates). The societal effects of crime and crime control, and why certain individuals or groups are more likely to be

arrested, convicted, and sentenced to prison, will also be covered via topics relating to criminal justice agencies (e.g., police, courts,

and corrections) and criminal law.

TABLE OF CONTENTS FOR VOLUME 1:

THE DISCIPLINE

• Reﬂections on Disciplines and Fields, Problems, Policies, and Life,

James F. Short

• Replication in Criminology and the Social Sciences,

William Alex Pridemore, Matthew C. Makel, Jonathan A. Plucker

CRIME AND VIOLENCE

• Bringing Crime Trends Back into Criminology: A Critical Assessment

of the Literature and a Blueprint for Future Inquiry, Eric P. Baumer,

María B. Vélez, Richard Rosenfeld

• Immigration and Crime: Assessing a Contentious Issue,

Graham C. Ousey, Charis E. Kubrin

• The Long Reach of Violence: A Broader Perspective on Data, Theory,

and Evidence on the Prevalence and Consequences of Exposure to

Violence, Patrick Sharkey

• Victimization Trends and Correlates: Macro‑ and Microinﬂuences

and New Directions for Research, Janet L. Lauritsen, Maribeth L. Rezey

• Situational Opportunity Theories of Crime, Pamela Wilcox,

Francis T. Cullen

• Schools and Crime, Paul J. Hirschﬁeld

PUNISHMENT AND POLICY

• Collateral Consequences of Punishment: A Critical Review and Path

Forward, David S. Kirk, Sara Wakeﬁeld

• Understanding the Determinants of Penal Policy: Crime, Culture,

and Comparative Political Economy, Nicola Lacey, David Soskice,

David Hope

• Varieties of Mass Incarceration: What We Learn from State Histories,

Michael C. Campbell

• The Politics, Promise, and Peril of Criminal Justice Reform in the

Context of Mass Incarceration, Katherine Beckett

THE PRISON

• Inmate Society in the Era of Mass Incarceration, Derek A. Kreager,

Candace Kruttschnitt

• Restricting the Use of Solitary Conﬁnement, Craig Haney

DEVELOPMENTAL AND LIFE‑COURSE CRIMINOLOGY

• Desistance from Offending in the Twenty‑First Century,

Bianca E. Bersani, Elaine Eggleston Doherty

• On the Measurement and Identiﬁcation of Turning Points

in Criminology, Holly Nguyen, Thomas A. Loughran

ECONOMICS OF CRIME

• Gun Markets, Philip J. Cook

• Offender Decision‑Making in Criminology: Contributions from

Behavioral Economics, Greg Pogarsky, Sean Patrick Roche,

Justin T. Pickett

POLICE AND COURTS

• Policing in the Era of Big Data, Greg Ridgeway

• Reducing Fatal Police Shootings as System Crashes: Research, Theory,

and Practice, Lawrence W. Sherman

• The Problems With Prosecutors, David Alan Sklansky

• Monetary Sanctions: Legal Financial Obligations in US Systems of

Justice, Karin D. Martin, Bryan L. Sykes, Sarah Shannon, Frank Edwards,

Alexes Harris

• Forensic DNA Typing, Erin Murphy

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Annual Review

of Sociology

Volume 44, 2018

Contents

Prefatory Article

On Becoming a Mathematical Demographer—And the Career

in Problem-Focused Inquiry that Followed

Jane Menken pppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp1

Theory and Methods

Historical Census Record Linkage

Steven Ruggles, Catherine A. Fitch, and Evan Roberts ppppppppppppppppppppppppppppppppppppp19

Interpreting and Understanding Logits, Probits, and Other Nonlinear

Probability Models

Richard Breen, Kristian Bernt Karlson, and Anders Holm ppppppppppppppppppppppppppppppppp39

Social Processes

Consumer Credit in Comparative Perspective

Akos Rona-Tas and Alya Guseva ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp55

Control over Time: Employers, Workers, and Families Shaping Work

Schedules

Naomi Gerstel and Dan Clawson ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp77

Silence, Power, and Inequality: An Intersectional Approach to Sexual

Violence

Elizabeth A. Armstrong, Miriam Gleckman-Krut, and Lanora Johnson pppppppppppppppppp99

Formal Organizations

Globalization and Business Regulation

Marie-Laure Djelic and Sigrid Quack ppppppppppppppppppppppppppppppppppppppppppppppppppppp123

Transnational Corporations and Global Governance

Tim Bartley pppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp145

Political and Economic Sociology

Boundary-Spanning in Social Movements: Antecedents and Outcomes

Dan Wang, Alessandro Piazza, and Sarah A. Soule pppppppppppppppppppppppppppppppppppppp167

Globalization and Social Movements

Paul Almeida and Chris Chase-Dunn ppppppppppppppppppppppppppppppppppppppppppppppppppppp189

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Political (Mis)behavior: Attention and Lacunae in the Study of

Latino Politics

Michael Jones-Correa, Hajer Al-Faham, and David Cortez ppppppppppppppppppppppppppppp213

Differentiation and Stratiﬁcation

Credit, Debt, and Inequality

Rachel E. Dwyer ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp237

Environmental Inequality: The Social Causes and Consequences

of Lead Exposure

Christopher Muller, Robert J. Sampson, and Alix S. Winter ppppppppppppppppppppppppppppp263

Occupations, Organizations, and Intragenerational Career Mobility

Arne L. Kalleberg and Ted Mouw pppppppppppppppppppppppppppppppppppppppppppppppppppppppppp283

Poverty in America: New Directions and Debates

Matthew Desmond and Bruce Western pppppppppppppppppppppppppppppppppppppppppppppppppppp305

Stress-Related Biosocial Mechanisms of Discrimination and African

American Health Inequities

Bridget J. Goosby, Jacob E. Cheadle, and Colter Mitchell ppppppppppppppppppppppppppppppppp319

Individual and Society

The Reversal of the Gender Gap in Education and its Consequences

for Family Life

Jan Van Bavel, Christine R. Schwartz, and Albert Esteve ppppppppppppppppppppppppppppppp341

Demography

Integrating Biomarkers in Social Stratiﬁcation and Health Research

Kathleen Mullan Harris and Kristen M. Schorpp ppppppppppppppppppppppppppppppppppppppppp361

The Sociology of Refugee Migration

David Scott FitzGerald and Rawan Arar ppppppppppppppppppppppppppppppppppppppppppppppppp387

Policy

Modern Trafﬁcking, Slavery, and Other Forms of Servitude

Orlando Patterson and Xiaolin Zhuo ppppppppppppppppppppppppppppppppppppppppppppppppppppppp407

Redistributional Policy in Rich Countries: Institutions and Impacts

in Nonelderly Households

Janet C. Gornick and Timothy M. Smeeding ppppppppppppppppppppppppppppppppppppppppppppp441

Sociology and World Regions

Families in Southeast and South Asia

Wei-Jun Jean Yeung, Sonalde Desai, and Gavin W. Jones pppppppppppppppppppppppppppppp469

vi Contents

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From Chicago to China and India: Studying the City in the

Twenty-First Century

Xuefei Ren ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp497

Globalization of Quantitative Policing: Between Management and

Statactivism

Emmanuel Didier ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp515

Latin America, a Continent in Movement but Where To? A Review of

Social Movements’ Studies in the Region

Mar´ıa Incl ´an ppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppppp535

Indexes

Cumulative Index of Contributing Authors, Volumes 35–44 ppppppppppppppppppppppppppp553

Cumulative Index of Article Titles, Volumes 35–44 ppppppppppppppppppppppppppppppppppppp557

Errata

An online log of corrections to Annual Review of Sociology articles may be found at

http://www.annualreviews.org/errata/soc

Contents vii

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The Influence of Racial Discrimination as a Chronic Stressor on Type 2 Diabetes Risk and Self-Management Behaviors among Black Adults: A Scoping Review

Article

Full-text available

Dec 2024
Curr Diabetes Rep

Alana Ewen

Purpose of Review This literature review highlights the behavioral and biological mechanisms that link racial discrimination to type 2 diabetes (T2D) risk, self-management, and related complications in the Black population in the United States. Next steps are discussed and include recommendations for disease mitigation. Recent Findings Black Americans are exposed to high levels of stress, with many stressors rooted in racial discrimination, a psychosocial factor that inhibits positive behavior change and disrupts bodily systems and functioning. T2D is a largely preventable disease, yet Black Americans experience known structural and systemic barriers (i.e., structural racism) that profoundly impact diabetes onset and progression. While causal mechanisms that link racial discrimination and T2D have become a more recent focus of study, a dearth of research on racial discrimination-related stress, and the role it plays in the onset and self-management of T2D, remains. Summary Identifying the structural and contextual factors, specifically racial discrimination, that influence diabetes risk and self-management among Black adults is important in closing the gap in health disparities. Findings on coping strategies adopted across the African diaspora are also warranted as policy makers, researchers, and clinicians work together to create an actionable path forward.

Epigenome-wide association study of perceived discrimination in the Multi-Ethnic Study of Atherosclerosis (MESA)

Article

Full-text available

Jan 2025

Perceived discrimination, recognized as a chronic psychosocial stressor, has adverse consequences on health. DNA methylation (DNAm) may be a potential mechanism by which stressors get embedded into the human body at the molecular level and subsequently affect health outcomes. However, relatively little is known about the effects of perceived discrimination on DNAm. To identify the DNAm sites across the epigenome that are associated with discrimination, we conducted epigenome-wide association analyses (EWAS) of three discrimination measures (everyday discrimination, race-related major discrimination, and non-race-related major discrimination) in 1,151 participants, including 565 non-Hispanic White, 221 African American, and 365 Hispanic individuals, from the Multi-Ethnic Study of Atherosclerosis (MESA). We conducted both race/ethnicity-stratified analyses as well as trans-ancestry meta-analyses. At false discovery rate of 10%, 7 CpGs and 4 differentially methylated regions (DMRs) containing 11 CpGs were associated with perceived discrimination exposures in at least one racial/ethnic group or in meta-analysis. Identified CpGs and/or nearby genes have been implicated in cellular development pathways, transcription factor binding, cancer and multiple autoimmune and/or inflammatory diseases. Of the identified CpGs (7 individual CpGs and 11 within DMRs), two CpGs and one CpG within a DMR were associated with expression of cis genes NDUFS5, AK1RIN1, NCF4 and ADSSL1. Our study demonstrated the potential influence of discrimination on DNAm and subsequent gene expression.

Socios y socias de las Big Four que han auditado empresas IPSA 2015-2022

Article

Full-text available

Jan 2025

Gabriela Alejandra González Valles

Desde el inicio de la profesión contable, las mujeres han tenido dificultades en la integración a esta y en ser consideradas profesionales cualificadas para enfrentar cualquier reto en los negocios, lo cual evoca los límites establecidos por los estereotipos de género que aun persisten en la sociedad. A pesar de la femilización que ocurrió en la carrera de Contador Público y Auditor en pleno siglo XXI, se ha identificado que los altos cargos de las empresas siguen estando fuera de alcance para las mujeres. Este ejercicio de investigación revisó las memorias anuales y estados financieros de las empresas del IPSA entre 2015-2022 con el objetivo de identificar si las mujeres están participando de estos escenarios profesionales o siguen siendo excluidas. Se encontró que, si bien hay pocas mujeres auditando dichas empresas, estas se ubican en la industria retail, segmentando su participación dentro del mercado de servicios profesionales de contabilidad y auditoría en Chile.

Zur Evolution der sozialen Ungleichheit

Chapter

Jan 2025

Do African Americans overreport or underreport their experiences of discrimination? Evidence from list experiments

Article

Oct 2024
EUR SOCIOL REV

Akira Igarashi

Discrimination is one of the largest barriers that immigrants and racial/ethnic minorities face in contemporary society. Social scientists have developed and applied field experimental methods to detect the existence and prevalence of discrimination in various domains. In addition, researchers have utilized questionnaires to directly ask discrimination victims about their experiences and the frequency of discrimination they encounter. However, self-reports of discrimination may be biased due to judgment errors in attributing mistreatment to discrimination and intentional overreporting (vigilance) or underreporting (minimization) of discrimination. In this study, we propose a two-stage model that distinguishes between these judgment and reporting biases. We argue that vigilance and minimization stem from sensitivity concerns. We conducted a list experiment with African American respondents who asked about their experiences of employment and everyday discrimination. Comparing the list experiment and direct question estimates, we find no evidence of systematic underreporting or overreporting of employment discrimination. For everyday discrimination, we find overreporting concentrated among ideologically liberal African Americans. These results provide new insights into biases in self-reported discrimination and suggest researchers should be attentive to the conditions under which these biases arise.

Relations Between Optimism-Pessimism and Loneliness in Sexually Minoritized Men: The Moderating Role of Chronicity-Based Discrimination

Article

Dec 2024
J HOMOSEXUAL

A closer examination of the “rural mortality penalty”: Variability by race, region, and measurement

Article

Aug 2024
J RURAL HEALTH

Background Racial health disparities are well documented and pervasive across the United States. Evidence suggests there is a “rural mortality penalty” whereby rural residents experience poorer health outcomes than their urban counterparts. However, whether this penalty is uniform across demographic groups and U.S. regions is unknown. Objective To assess how rural–urban differences in mortality differ by race (Black vs. White), U.S. region, poverty status, and how rural–urban status is measured. Methods Age‐standardized mortality rates (ASMRs)/100,000 by U.S. county (2015–2019) were obtained by race (Black/White) from the CDC Wonder National Vital Statistics System (2015–2019) and were merged with county‐level social determinants from the US Census Bureau and County Health Rankings. Multivariable generalized linear models assessed the associations between rurality (index of relative rurality [IRR] decile, rural–urban continuum codes, and population density) and race‐specific ASMR, overall, and by Census region and poverty level. Results Overall, average ASMR was significantly higher in rural areas than urban areas for both Black (rural ASMR = 949.1 per 100,000 vs. urban ASMR = 857.7 per 100,000) and White (rural ASMR = 903.0 per 100,000 vs. urban ASMR = 791.6 per 100,000) populations. The Black‐White difference was substantially higher ( p < 0.001) in urban than in rural counties (65.1 per 100,000 vs. 46.1 per 100,000). Black–White differences and patterns in ASMR varied notably by poverty status and U.S. region. Conclusion Policies and interventions designed to reduce racial health disparities should consider and address key contextual factors associated with geographic location, including rural–urban status and socioeconomic status.

The Role of Trust in Mental Health: Vulnerability and Trust-Building in Theory and Practice

Book

Nov 2024

Gerard Leavey

This book offers a comprehensive examination of trust and its relationship with mental illness and wellbeing. Engaging with a broad range of mental health research, theory, and practice through various transdisciplinary theoretical models of trust, this book highlights the social and family contexts surrounding the making and breaking of trust and mental health. It examines various sociological conceptual and theoretical frameworks of risk and trust while also engaging with evolutionary perspectives on the human need for cooperation and trust. The author describes how, in a world of constant connectivity, the drawing of boundaries assigns some people as strangers, using stigma as a form of power. The book concludes by considering the future of mental health and where trust-building may be possible. Each chapter is interspersed with observations and insights from the author’s personal research covering many populations, communities, and issues over several decades. Drawing on a wide range of interdisciplinary literature, the book will be of interest to mental health practitioners, researchers, and scholars interested in the psychosocial aspects of mental illness and stigma. ‘Professor Leavey’s book throws light on a far too long neglected factor with a powerful impact on structures of society and the management of problems ranging from care for people with diseases to the continuation of war or the maintenance of peace’. – Professor Norman Sartorius (MD, PhD, FRCPsych) is a leading international expert in psychiatry. He has been the President of the World Psychiatric Association and of the European Psychiatric Association, and Director of the Mental health Division of the World Health Organization ‘This remarkable book takes the concepts of trust and mental health and moves them around each other as if they were reciprocal moons of our planetary existence. Trust is a concept perfectly central to individuals, families, communities and society. For almost a thousand years the idea of ‘trust’ has grown from the ancient roots of meaning that include: integrity, alliance, faithful, steadfast, shelter, safety, hope, and consolation. This book is a fascinating tour-de-force which gazes at trust and hope, and their inversions, from multiple perspectives, and asks how we can strengthen trust and hope and mental health in the future’. – Sir Graham Thornicroft is Emeritus Professor of Community Psychiatry at King’s College London. He was Knighted in 2017 for services to mental health; Graham has authored over 30 books and written over 670 peer-reviewed scientific papers, shaping global mental health policies.

Strategies and Insights for Women Leaders in Higher Education: A Guide to Driving Positive Transformation

Book

Nov 2024

Wafa Hozien

This book delves into critical factors for women’s success in academia, offering strategies, and counsel anchored in a robust theoretical framework. Hozien’s thoughtful, interdisciplinary approach to women leadership culminates in a comprehensive understanding of the critical factors that can influence career success in higher education. Grounded by an intersectional lens and data-driven analysis, the book’s focus on minority female populations informs the inherent challenges and shifting representation in educational leadership. Each chapter integrates real-world examples, case studies, and immediately actionable advice to advocate for and support current and aspiring female leaders, administrators, and policymakers. A masterful blend of theory and practice, this book’s timely insights empower women to take charge of their leadership journeys with the intention of fostering a generation of confident and capable academic leaders who can drive positive transformation.

Age-Friendliness as a Framework for Equity in Aging

Chapter

Nov 2024

Place performs a powerful role in shaping experiences of aging. Aims of the age-friendly movement have changed dramatically since the inception of the Global Age-friendly Cities Project in 2006, and the aging demographic has simultaneously become more diverse and complex. Growing economic disparities, climate crises, and the global pandemic have amplified challenges to aging well across the lifespan. This chapter provides an overview of the age-friendly movement both internationally and within the United States. It examines how the concept of age-friendliness has grown into a framework that guides placemaking in a variety of settings and calls attention to contemporary criticism of the movement related to diversity, equity, and inclusion. The chapter examines the intersectional nature of the social, economic, and environmental challenges tied to aging and considers age-friendliness as an ecological framework with a unique capacity to address historic barriers in new, significant ways. The chapter locates the age-friendly movement in the context of the widening of socioeconomic and health disparities and presents a case of need to refocus the lenses of equity and participation in order to expand health and social justice in the design of places.

Heterogeneity in polygenic scores for common human traits

Preprint

Full-text available

Feb 2017

Perceived Discrimination and Adolescent Sleep in a Community Sample

Article

Full-text available

Apr 2018

Sleep is a key restorative process, and poor sleep is linked to disease and mortality risk. The adolescent population requires more sleep on average than adults but are most likely to be sleep deprived. Adolescence is a time of rapid social upheaval and sensitivity to social stressors including discrimination. This study uses two weeks of daily e-diary measures documenting discrimination exposure and concurrent objective sleep indicators measured using actigraphy. We assess associations between daily discrimination and contemporaneous sleep with a diverse sample of adolescents. This novel study shows youth with higher average discrimination reports have worse average sleep relative to their counterparts. Interestingly, youth reporting daily discrimination have better sleep the day of the report than youth who do not.

Diversity and inclusion in genomic research: why the uneven progress?

Article

Full-text available

Oct 2017
J Community Genet

Conducting genomic research in diverse populations has led to numerous advances in our understanding of human history, biology, and health disparities, in addition to discoveries of vital clinical significance. Conducting genomic research in diverse populations is also important in ensuring that the genomic revolution does not exacerbate health disparities by facilitating discoveries that will disproportionately benefit well-represented populations. Despite the general agreement on the need for genomic research in diverse populations in terms of equity and scientific progress, genomic research remains largely focused on populations of European descent. In this article, we describe the rationale for conducting genomic research in diverse populations by reviewing examples of advances facilitated by their inclusion. We also explore some of the factors that perpetuate the disproportionate attention on well-represented populations. Finally, we discuss ongoing efforts to ameliorate this continuing bias. Collaborative and intensive efforts at all levels of research, from the funding of studies to the publication of their findings, will be necessary to ensure that genomic research does not conserve historical inequalities or curtail the contribution that genomics could make to the health of all humanity.

Rumination Moderates the Association Between Resting High-Frequency Heart Rate Variability and Perceived Ethnic Discrimination

Article

Full-text available

Sep 2017

Ethnic discrimination (ED) is both an unfortunate and uncontrollable phenomenon that uniquely impacts African Americans (AAs) and other individuals of ethnic minority status. Perceived ethnic discrimination (PED), defined as the degree to which an individual consciously perceives a negative event as discriminatory and threatening, largely determines the impact that ED can have on target individuals. However, research has not yet considered how individual differences in both emotion regulation abilities, as indexed by resting high-frequency heart rate variability (HF-HRV), and rumination, a maladaptive emotion regulation strategy, may predict PED in AAs. The following investigation examined this relationship in a sample of 101 college-aged students (45 AAs and 56 Caucasian Americans). Resting HF-HRV was assessed via electrocardiogram during a 5-minute-resting period. Rumination was assessed using the ruminative responses scale and everyday PED was assessed using the perceived ethnic discrimination questionnaire. Results showed a significant negative relationship between resting HF-HRV and PED in AAs only. Rumination significantly moderated this relationship, such that lower HF-HRV was related to higher PED only in AAs who reported moderate to higher, β = 0.417 (0.125), p <.01, levels of trait rumination. These results suggest that greater HF-HRV and lesser ruminative tendencies are key factors in reducing PED and therefore possibly, negative consequences associated with ED.

The Neural Bases of Status-Based Influence

Article

Full-text available

May 2017

Status characteristics theory provides a theoretical explanation for why social status promotes social influence in collectively oriented task groups. It argues that status differences produce differences in expectation states, which are anticipations of task-related contributions. Those with an expectation advantage are more influential, contribute more often to group discussions, and so on. The authors conducted the first experimental test of status characteristics theory while participants were in a magnetic resonance imaging machine. This permitted the measurement of neural activity in brain regions found to be associated with processing social status. The results indicate that neural activity does not explain the effect of status on behavior.

The Impact of Individuation on the Bases of Human Empathic Responding

Article

Full-text available

May 2017

While there is substantial overlap in the neural systems underlying empathy for people we know as opposed to strangers, social distance has been shown to significantly moderate empathic neural responses towards the negative experiences of others. Intriguingly however, variance in empathic neural responses towards known and unknown targets has not been reflected by behavioral differences as indexed by self-reported empathic ratings. One explanation for this disconnect is that empathic evaluations of known and unknown individuals draw on different bases (e.g. target identity/reactions) within the empathic process. To test this hypothesis, we utilized high density EEG to assess how individuating targets with personal names moderated the link between behavioral pain ratings and attentional processing oriented towards (a) initial target processing and (b) subsequent expressions target discomfort. Consistent with prior findings, no differences in pain ratings between individuated and unindividuated targets was observed. However, individual mean pain rating differences for individuated targets was strongly positively related to attentional processing levels, indexed by the P300, during the initial presentation of those targets, a relationship absent for unindividuated targets. In contrast, pain ratings for unindividuated targets was positively related to levels of attentional processing, indexed by the Late Positive Potential (LPP), during the subsequent discomfort expression stage. Furthermore, the LPP response to individuated target discomfort was positively linked to behavioral measures of emotional expressivity whereas the LPP response to unindividuated target discomfort was positively associated with cognitive appraisal. These findings suggest that individuation can significantly shift the bases of empathic responding.

The genetics of human behavior: A hopeless opus?

Chapter

Mar 2018

C. Mitchell

Multiethnic polygenic risk scores improve risk prediction in diverse populations

Article

Nov 2017

Methods for genetic risk prediction have been widely investigated in recent years. However, most available training data involves European samples, and it is currently unclear how to accurately predict disease risk in other populations. Previous studies have used either training data from European samples in large sample size or training data from the target population in small sample size, but not both. Here, we introduce a multiethnic polygenic risk score that combines training data from European samples and training data from the target population. We applied this approach to predict type 2 diabetes (T2D) in a Latino cohort using both publicly available European summary statistics in large sample size (Neff = 40k) and Latino training data in small sample size (Neff = 8k). Here, we attained a >70% relative improvement in prediction accuracy (from R2 = 0.027 to 0.047) compared to methods that use only one source of training data, consistent with large relative improvements in simulations. We observed a systematically lower load of T2D risk alleles in Latino individuals with more European ancestry, which could be explained by polygenic selection in ancestral European and/or Native American populations. We predict T2D in a South Asian UK Biobank cohort using European (Neff = 40k) and South Asian (Neff = 16k) training data and attained a >70% relative improvement in prediction accuracy, and application to predict height in an African UK Biobank cohort using European (N = 113k) and African (N = 2k) training data attained a 30% relative improvement. Our work reduces the gap in polygenic risk prediction accuracy between European and non-European target populations.

Father Loss and Child Telomere Length

Article

Jul 2017

Background and objectives: Father loss during childhood has negative health and behavioral consequences, but the biological consequences are unknown. Our goal was to examine how father loss (because of separation and/or divorce, death, or incarceration) is associated with cellular function as estimated by telomere length. Methods: Data come from the 9-year follow-up of the Fragile Families and Child Wellbeing Study, a birth cohort study of children in 20 large American cities (N = 2420). Principal measures are as follows: salivary telomere length (sTL), mother reports of father loss, and polymorphisms in genes related to serotonergic and dopaminergic signaling. Results: At 9 years of age, children with father loss have significantly shorter telomeres (14% reduction). Paternal death has the largest association (16%), followed by incarceration (10%), and separation and/or divorce (6%). Changes in income partially mediate these associations (95% mediation for separation and/or divorce, 30% for incarceration, and 25% for death). Effects are 40% greater for boys and 90% greater for children with the most reactive alleles of the serotonin transporter genes when compared with those with the least reactive alleles. No differences were found by age at father loss or a child's race/ethnicity. Conclusions: Father loss has a significant association with children's sTL, with the death of a father showing the largest effect. Income loss explains most of the association between child sTL and separation and/or divorce but much less of the association with incarceration or death. This underscores the important role of fathers in the care and development of children and supplements evidence of the strong negative effects of parental incarceration.

Racial disparities in health among nonpoor African Americans and Hispanics: The role of acute and chronic discrimination

Article

May 2017
SOC SCI MED

Stress-Related Biosocial Mechanisms of Discrimination and African American Health Inequities

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