Inequality and Early Childhood Adversity

Toxic Stress and Its
Epigenetic Effects

Bruce McEwen

Rockefeller University

increases the odds that children will not be ready for school at age 5, will not complete high school and will be poor as adults (Roos, Wall-Wieler & Boram 2019, Duncan & Brooks-Gunn 1997, Chmielewski & Reardon 2016, Reardon & Portilla 2016, Wagmiller & Adelman 2009)  Clearly, lack of pre-schooling, poorly funded and ineffective schools, challenging neighborhoods, and limited parental resources to promote child development, among other variables, contribute to these odds.


Another important mechanism shaping these odds is the early childhood “embodiment of inequality” resulting from toxic stress. That mechanism and its implications are the focus of our talk.  Joining the perspectives of neuroscience and sociology focuses us on early-childhood adversities that result from social inequality, as well as from troubled relationships in the household and beyond. These adversities, in turn, can produce toxic stress that has profound impacts on the ways that the brain and body develop and thus on life trajectories. 


Sociology helps us see how childhood adversity is patterned and connected to larger social inequalities. The “developmental neuroscience of early stress and disadvantage” (Boyce et al. 2012) alerts us to the probabilistic consequences of those adversities – for example, more difficulties with self-control and thus of behavioral issues, as well as greater trouble in planning, organizing and sequencing thinking and actions in cognitive tasks and problem-solving. Neuroscience and epigenetics also help us understand the biological mechanisms by which childhood adversities can impact children’s bodily systems and brain development through recurrent stress which becomes toxic when there are inadequate protective relationships to cushion the impact of stressful environments. 


As we connect sociology and biology/neuroscience, we resist biological determinism.  Indeed, we examine biological processes not as primary causes of social outcomes but rather as mechanisms that are shaped by social structures, relationships and interactions and that, in turn, affect life trajectories. Brain plasticity also means that ill-effects of stressful circumstances can be prevented or mitigated by strong social networks and relationships. This means that at the same time that we seek to understand adversities and their social distribution, we also need to examine the differential availability of socially structured systems of support and intervention that can protect against or compensate for the early biological effects of toxic social environments.


This is a probabilistic world; although there is greater likelihood of lower school readiness, dropping out of school, and behavioral and health issues for children growing up in poverty than for kids with little or no exposure to poverty, early adversity and chronic stress do not always have deleterious effects. Some of that variation in responses to adversity may be accounted for biologically – genetic differences that make some children much more responsive to their environments and others relatively immune from the effects of adversity (Obradovic et al 2010). Some of that variation depends on the differential availability of protective relationships with nurturing adults.


How does stress get under the skin (Evans et al. 2004)?  Unlike normal stress, which we all experience, toxic stress involves the frequent or sustained activation of the hypothalamic–pituitary–adrenal axis (HPA axis) and other mediators of adaptation, which are responsible for our biological response to stress (McEwen 1998). Toxic stress can result from chronic exposure to stressors such as economic marginality, racism, abusive social relationships or continuing exposure to the threat of violence. Supportive and nurturing interpersonal relationships as well as healthy lifestyle behaviors (for example, regular exercise and good diet), however, can prevent or reduce toxic stress in the face of continuing stressors.  This means that social environments – both negative and positive – matter for the body’s responses to stress.


An adaptation process (“allostasis”) preserves homeostasis in the body. Optimal adaptation occurs when responses to stress turn on and off efficiently. However, frequent or chronic stressors distort the normal balance of the components of allostasis (for example, too little or too much adrenalin, cortisol, cytokines, metabolic hormones or neurotransmitters).  This imbalance results in wear-and-tear on the body and brain that changes the prefrontal cortex’s architecture as well as that of other brain regions.  This spiral is called “allostatic load” or when it is most severe “allostatic overload.” (McEwen 1998, McEwen & Wingfield 2003).   Toxic stress leading to allostatic overload has significant consequences:   


… it disrupts brain architecture, affects other organ systems, and leads to stress-management systems that establish relatively lower thresholds for responsiveness that persist throughout life, thereby increasing the risk of stress-related disease and cognitive impairment well into the adult years (Shonkoff et al 2009).


Toxic stress is well-documented in neuroscience research on poverty and SES, clearly summarized by Martha Farah (Farah 2018). For example, that research demonstrates “the realities of SES disparities in neurocognitive function … and provide(s) more direct evidence of the involvement of prefrontal cortex in the observed SES disparities” (Hackman et al 2010). The slow development of the prefrontal cortex which controls decision making, working memory,  impulsivity and emotion (Casey et al 2011, McEwen & Morrison 2013) makes it particularly vulnerable to toxic early life stress but also subject to “rewiring” through later interventions (Pechtel & Pizzagalli 2011). Hanson et al. (2013) have shown that the gray matter in the brain grows more slowly for infants from poor families than for those infants from more advantaged families.  The prefrontal cortex plays a vital role in managing responses to stress, but toxic stress alters both its structure and functioning as a result of release of hormones and neurotransmitters by nerve cells (McEwen & Morrison 2013).  The consequences appear to include compromised capacities for behavioral and emotional self-regulation, including working memory and executive function (Shonkoff & Garner 2012).


Neuroscience research thus points to biological mechanisms that explain how inequalities can “get under the skin” with potential life-long consequences for health and life trajectories. It also helps us to imagine the social interventions that can protect against these effects.  However valuable we find the insights of biology and neuroscience, we must be cautious about how narrowly or broadly they are applied in the worlds of practice and policy. Medicalization is one common response – that is, defining the problems of adversity primarily as medical conditions requiring diagnosis and treatment of individuals.  Sociological perspectives encourage a broader look at causation, emphasizing the social structures and practices that give rise to adversities and the resources that can protect against their potential impact on bodies and brains. This perspective turns attention to social policies to reduce adversities and to development of community resources to protect against them. 



Boyce WT, Sokolowski MB, Robinson GE. 2012. Toward a new biology of social adversity. PNAS 109: 17143-17148

Brady D, Finnegan RM Hubgen S. 2017. Rethinking the Risks of Poverty: A Framework for Analyzing Prevalences and Penalties, Amer J Sociology
123: 740-786

Casey BJ, Somerville LH, Gotlib IH, Ayduk O, Franklin NT, et al. 2011. Behavioral and neural correlates of delay of gratification 40 years later.
     Proc Natl Acad Sci USA 108: 14998-5003

Chmielewski AK, Reardon SF. 2016. Patterns of Cross-National Variation in the Association Between Income and Academic Achievement.
     AERA Open 2, 3: 1-27.

Duncan G, Brooks-Gunn J. 1997. Income Effects across the Life-Span: Integration and Interpretation." In Consequences of Growing Up Poor, ed. G   
     Duncan, J Brooks-Gunn. New York: Russell Sage

Evans GW, Chen E. Miller GE, Seeman T. 2012 How poverty gets under the skin: a life-course perspective. In The Oxford Handbook of Poverty and
     Child Development
, ed. V Maholmes, RB King, pp. 13-36. New York: Oxford Univ. Press

Farah MJ. 2018. Socioeconomic status and the brain: prospects for neuroscience-informed policy. Nat Rev Neurosci 19: 428-38

Hackman DA, Farah MJ. 2009. Socioeconomic status and the developing brain. Trends Cogn. Sci. 13:65-73

Hanson JL, Adluru N, Chung MK, Alexander AL, Davidson RJ, Pollak SD. 2013. Early neglect is associated with alterations in white matter integrity
     and cognitive functioning. Child Dev 84: 1566-78

McEwen BS. 1998. Protective and Damaging Effects of Stress Mediators. New England J.Med. 338: 171-79

McEwen BS, Morrison JH. 2013. The Brain on Stress: Vulnerability and Plasticity of the Prefrontal Cortex over the Life Course. Neuron 79: 16-29

McEwen BS, Wingfield JC. 2003. The concept of allostasis in biology and biomedicine. Horm. & Behav. 43: 2-15

McEwen CA, McEwen BS. 2017. Social Structure, Adversity, Toxic Stress and Intergenerational Poverty: An Early Childhood Model.
     Ann Rev Sociology 2017: 445-472

Obradovic J, Bush NR, Stamperdahl J, Adler NE, Boyce WT. 2010. Biological sensitivity to context: the interactive effects of stress reactivity and
     family adversity on socioemotional behavior and school readiness. Child Dev 81: 270-89

Pechtel P, Pizzagalli DA. 2011. Effects of early life stress on cognitive and affective function: an integrated review of human literature.
     Psychopharmacology 214: 55-70

Reardon SF, Portilla, XA. 2016. Recent trends in income, racial, and ethnic school readiness gaps at kindergarten entry. AERA Open 2 (3 )1-18

Roos LL, Wall-Wieler E, Boram J. 2019. Poverty and Early Childhood Outcomes. Pediatrics 143: e20183426

Shonkoff JP, Boyce WT, McEwen BS. 2009. Neuroscience, molecular biology, and the childhood roots of health disparities. JAMA 301: 2252-59

Shonkoff JP, Garner AS. 2012. The lifelong effects of early childhood adversity and toxic stress. Pediatrics 129: e232-46

Wagmiller RL, Adelman RM. 2009. Childhood and Intergenerational Poverty: The Long-Term Consequences of Growing up Poor.
     New York: Nat’l Center Child Poverty

Brothers Bruce McEwen and Craig McEwen will present "Inequality and Early Childhood Adversity:  Toxic Stress and Its Epigenetic Effects" on Thursday, November 21, 4:30-6:00 pm, 133 S. 36th Street, Room 250 (The Forum).


Bowdoin College

THE REVERBERATIONS OF INEQUALITY ARE TOO OFTEN FELT BY CHILDREN growing up in poverty in many societies, but especially in the United States (Brady et al. 2017).  In the U. S. early childhood poverty significantly