The concept of “poverty poisons the brain” has become a major area of research in neuroscience and the health sciences, and an increasingly utilized metaphor to argue for the importance of addressing inequality and poverty in the United States. This article systematically presents the research behind poverty poisons the brain, which includes the impact of socioeconomic status on human development, the developmental models used to understand how poverty impacts children, and the proximate social factors and brain mechanisms that represent the core causal model behind this research. This overview examines the uses of this research for neuroanthropology, highlighting the impact of inequality and how experience becomes embodied. Nevertheless, a simplistic cause–effect approach and the reduction of the social to the biological often hamper this type of research. A critical approach to how poverty poisons the brain provides the basis for making the shift to a more robust neuroanthropological approach to poverty. Neuroanthropology can utilize social embodiment, the dynamics of stress, and the production of inequality to transform research on poverty and children, and to make policy recommendations, do applied research, and craft and test interventions to deal with the pernicious impact of poverty.
In February 2008, Paul Krugman, Nobel laureate economist and New York Times columnist, wrote an op-ed entitled, “Poverty Is Poison.” He summarized research presented at the American Association for the Advancement of Science annual conference by Martha Farah, a University of Pennsylvania neuroscientist, and her colleagues. These data showed that “unhealthy” levels of stress hormones in poor children can harm neural development. Krugman then argued:
The effect is to impair language development and memory—and hence the ability to escape poverty—for the rest of the child's life. So now we have another, even more compelling reason to be ashamed about America's record of failing to fight poverty [Krugman 2008].
This theme of connecting neuroscience research with the discussion of poverty is one that has repeated itself several times in the intervening years. In 2009, Gary Evans and Michelle Schamberg, scientists at Cornell, published “Childhood Poverty, Chronic Stress, and Adult Working Memory” in the Proceedings of the National Academy of Sciences. At the popular Wired magazine site, journalist Brandom Keim followed suit with “Poverty Goes Straight to the Brain.” The opening to Keim's article reads,
Growing up poor isn't merely hard on kids. It might also be bad for their brains. A long-term study of cognitive development in lower- and middle-class students found strong links between childhood poverty, physiological stress and adult memory [Keim 2009].
In Keim's reporting, being “bad for kids’ brains” deserves separate emphasis, beyond poverty itself.
At the start of 2012, journalist Nicholas Kristof penned his own New York Times op-ed, “A Poverty Solution that Starts with a Hug.” Once again the equation of poverty, stress, and damaged brain development in childhood comes into play. His piece opens, “Perhaps the most widespread peril children face isn't guns, swimming pools or speeding cars. Rather, scientists are suggesting that it may be ‘toxic stress’ early in life, or even before birth.” This time the public conclusion draws not just on research, but on what Kristof calls a “landmark warning” from the American Academy of Pediatrics. This well-respected group of pediatricians had just published a policy statement in their own journal, Pediatrics: “Early Childhood Adversity, Toxic Stress, and the Role of the Pediatrician: Translating Developmental Science into Lifelong Health.”
Pediatricians are now armed with new information about the adverse effects of toxic stress on brain development, as well as a deeper understanding of the early life origins of many adult diseases. As trusted authorities in child health and development, pediatric providers must now complement the early identification of developmental concerns with a greater focus on those interventions and community investments that reduce external threats to healthy brain growth [Committee on Psychosocial Aspects of Child and Family Health et al. 2012:e224].
I call this consistent linkage of children living in poverty and negative brain development the “poverty poisons the brain” model (Lende 2008). This model provides a powerful framing for thinking about how “experience gets under the skin” and how social factors like class and race negatively impact individuals. The poverty poisons the brain model is also “compelling” to people who argue in public about poverty—toxic stress is presented as a terrible peril early in life because it is bad for brain development.
This article will present the research behind “poverty poisons the brain,” critically analyze the model and its social uses, and finally examine how to make it into a more robust neuroanthropological approach. The first half moves through the basic research paradigm behind poverty poisons the brain, which uses multifactorial etiology and a nested model of causation to understand how poverty does affect the brain. This research offers potential strengths for neuroanthropologists interested in how culture and society shape development. Similarly, research in biological and medical anthropology that examines individual outcomes with respect to social conditions can gain theoretical and applied insights for work that examines poverty, health disparities, and other similar domains. The second half of the article examines the poverty poisons the brain paradigm in a critical light. By placing important social dynamics in the background, this research often hides both actual poverty and the political economy of inequality from view. The approach can reinforce essentialist understandings of social class, and assume that by fixing poisoned brains, social problems can largely be solved. I finish by outlining research questions and additional model elements that could transform this approach in ways that match the holistic and comparative fundamentals at the core of anthropology.
FROM POVERTY TO THE BRAIN
Research linking poverty and the brain starts by establishing that there is a problem first—that lower socioeconomic status (SES) during childhood does indeed lead to negative outcomes in adults. That established, the research presents a developmental framework to understand that linkage. Next comes the heart of the poverty poisons the brain story—the combination of proximate environmental factors that shape childhood development and internal neurological mechanisms that translate proximate factors into structural and functional brain changes and associated capabilities and deficits. As shown in Figure 1, the core of the model is centered on local mediators and brain development.
In the move to considering the proximate factors shaping development, SES is generally placed to one side. SES is not seen as a proximate mechanism that can interact directly with people's brains and bodies; rather, SES is embodied through social relationships, personal experiences, and local material and social conditions that can impact the individual. This reduction generally strikes researchers as normal and appropriate—SES is a macro factor, and can only interact through local factors that constitute the broader SES indicator. More importantly, the brain is seen as only intersecting with SES through these individual-level factors, such that psychology, environmental health, and individual development become the primary lenses to explain how the poisoning actually happens.
SES and Negative Outcomes
Researchers generally establish that there is a significant problem in the first place that is in need of an explanation. Indeed, there is robust evidence that links SES in Western settings to negative outcomes (Duncan et al. 1994; Noble et al. 2007). Researchers are then careful to define SES. It is presented as an indicator of status and position in society, and often gets measured in two basic ways in western countries, level of income and level of education (not coincidentally, these are among the easiest aspects of SES to measure). Still, researchers hedge their bets by acknowledging that SES is a “complex construct” which derives from “household income, material resources, education and occupation, as well as related neighborhood and family characteristics” (Hackman et al. 2010:651). As another example, Evans et al. (2012) describe SES as having “associated physical/material, financial, educational, and social environmental features” but label its “primary constituents” as “income, education, [and] occupation.”
Researchers also highlight the specific types of negative outcomes that are linked to lower SES. These generally fall into three areas: physical health, mental and behavioral health, and intelligence and academic success. Lower childhood SES is linked to lower ratings of health, greater cardiovascular disease, and increased mortality in adulthood (Adler and Stewart 2010). For mental and behavioral health, Hackman and colleagues document that, “children and adolescents from low-SES backgrounds show higher rates of depression, anxiety, attention problems and conduct disorders, and a higher prevalence of internalizing (that is, depression- or –anxiety-like) and externalizing (that is, aggressive and impulsive) behaviours, all of which increase with the duration of impoverishment” (Hackman et al.:652). On the intelligence side, lower SES is associated with lower IQ scores, less academic success, and less language ability. Recent research is pointing to links from childhood adversity to lower intelligence and cognitive success over the lifespan, which in turn is linked to greater mortality (Jokela et al. 2009).
The Causal Models Linking SES to Negative Outcomes
The link between SES and different types of negative outcomes is supported by multiple studies. The next step in this research has been to account for why there is this association between SES and negative outcomes: What mechanisms account for it? How does SES specifically lead to negative outcomes? This research first assumes that the linkage is a causal relationship, that SES does have direct and indirect effects on success and health. Then a model involving human development and multifactorial etiology is used to examine the causal factors. One of the most recent versions of this combination is the American Academy of Pediatrics’ explicit embrace of an “ecobiodevelopmental” framework, which combines together an ecological model of development with a biodevelopmental focus on the child (Committee on Psychosocial Aspects of Child and Family Health et al. 2012).
The overall model is one that combines a distal to proximate conceptualization of the developing child, where multiple causes can come into play to influence development. In practice, the poverty poisons the brain research establishes that distal factors—SES —matters, and then moves to focus on the proximal factors that mediate the impact of SES in local environments like the home. Then it also examines the internal mechanisms, particularly the neurobiological systems, that are seen to account for the negative outcomes. In other words, the causal flow goes from SES to local mediators, and from local mediators to the altered development of the brain, and finally that altered development accounts for the negative outcomes experienced by the person later in life (see Figure 1). In this causal flow, the reason that neuroscience matters is that “in contrast to sociological and epidemiological approaches, neuroscience can identify the underlying cognitive and affective systems that are influenced by SES …[and provide] candidate mechanisms for the cause-effect relationships between SES and neural development” (Hackman et al. 2010:651).
Theories of human development play a central role in advanced versions of the “poverty poisons the brain.” These models go beyond asserting that “toxic stress” or some other cause is to blame for damaged brains. Rather, these developmental models aim to account for how experiences during development actually lead to positive and negative changes in neural development, function, and capability. There are four basic causal models used. Although they are often used in conjunction to explain specific outcomes, they are nonetheless distinct in how they understand the role of development in shaping biology (Hackman et al. 2010). These four models emphasize different dimensions of development: early experience, cumulative experience, selective achievement, and interactive experience. Each draws on research in human development that establishes how sensitive periods, an increasing number of risk factors, and behavior can shape the functioning of the person.
The first model—emphasizing the role of early experience—is often described as an embedding or developmental origins model. The key point is that early experience embeds itself in biological function during critical formative periods, leading to altered development over the lifespan. For poverty, it is clear that early experiences of deprivation are influential over the lifespan, often leading to health problems and reductions in lifetime income (Adler and Stewart 2010; Hackman et al. 2010). The second model is typically described as an accumulation of risk factors or adverse experiences. For example, the longer children spend in poverty, the worse in general are the adult outcomes across a range of indicators, from cardiovascular health to academic achievement to adult income (Adler and Stewart 2010; Hackman et al. 2010). In contrast to an emphasis on formative early experiences, the second model focuses on the developmental pathways children take, where pathways marked by adversity can lead to negative outcomes. The cumulative negative effects pave the way to bad health and adult capacity.
The selectionist model is one of the most determinist. It posits that individuals are born with certain traits and capacities and that these neural limits lead to a selective effect (Hackman et al. 2010). High-skill individuals end up with greater SES, whereas individuals born with lower abilities end up in lower classes. The selective effective is often seen as twofold: low-SES parents had lesser ability, however measured, and their cognitive abilities got passed onto their child; the child, in turn, was only able to progress so far along the SES scale because he or she did not have the same level of brain power as other children.
Although this model, put so baldly, might seem more a part of social discourse—we live in a meritocracy, people get their just desserts, and so forth—it actually appears more often in psychology and neuroscience research than might be expected. For example, recent work on neuroimaging and addiction among siblings compared to controls highlights a lack of executive control, or the ability to inhibit behavior, as a central feature in the risk of developing substance abuse (Ersche et al. 2012). “Abnormalities in fronto-striatal brain systems implicated in self-control” among confirmed addicts and their nonaddicted siblings point to an “underlying neurocognitive endophenotype” for addiction (Ersche et al. 2012:601). The implication is that this shared trait comes from family, and thus from genetics; in the media, this turns into the explanation for why individuals with low executive function, marked by abnormal brains, end up as substance abusers (Hamilton 2012; Szalavitz 2012). As Hamilton (2012) puts it, “Addicts’ brains may be wired at birth for less self-control.”
The final model is an interactive model, where behavior and feedback from the environment place individuals in different developmental niches. By changing the proximal environments that shape development, individuals thereby change their own growth and development (Worthman 2010). This feedback effect from the local environment can have both positive and negative effects. For example, a child that seeks out supportive relationships that he or she does not have at home can buffer the negative effects of the home environment. In contrast, an individual that seeks out drug-using friends to escape from home can create a cascade of negative effects on his development. The interactive model is the one needing the most development, and closest to a neuroanthropological approach that aims to link social and cultural research with brain function, child development, and the enculturation and socialization of brains (Odden 2009; Worthman 2009). Ideas about neural plasticity and neural reuse, links between experiences in the environment and epigenetic regulation of development, the concept of a zone of proximal development and of important sociocultural niches with human development can come together in this type of interactive developmental approach.
Hackman and colleagues (2010) provide comprehensive coverage of the proximate mechanisms that research has shown relate to brain development and negative outcomes. These include parenting quality, in utero environment, home environment, toxin exposure (e.g., lead), nutrition, and stress (both chronic and acute). Research on how these proximal factors directly interact with the developing child generally focuses on direct insults or problems, for example, exposure to lead having a negative impact on brain development and leading to lowered cognitive ability, or how a lack of resources, whether malnutrition or books, can place limits on development.
Nevertheless, some researchers recognize that neighborhood quality can make a difference, and provide a link to understanding how inequality and deprivation affect childhood outcomes. Hertzman and Boyce (2010) outline one major study they have undertaken in British Columbia on early child development and neighborhood socioeconomic characteristics. In this research, evidence shows that more than 40 percent of the variance for health vulnerabilities, as measured by early development indicators, can be attributed to neighborhood socioeconomic characteristics. Furthermore, inequality can get under the skin through the experience of social status. Hertzman and Boyce write that, “Findings on the health correlates of subjective social status and peer group subordination suggest that the health disparities associated with SES may be at least partially attributable to differences in individuals’ sense of identity, respect, and position within societies, small or large, marked by nonegalitarian structures and values” (Hertzman and Boyce 2010:332).
However, in most neuroscience research, the main proximal factors considered are social relationships and educational opportunities. For example, descriptions of the home environment often focus on “familial conflict and problematic parental behaviour,” including “harsh and inconsistent discipline, less sensitivity to the needs of the child, [and] reduced verbal communication” (Hackman et al. 2010:654). In other words, they are bad parents, while SES remains a distal cause: “The important point is that broader social and economic context can influence the quality of parental care, which then influences the activity of the neural systems that regulate stress reactivity and cognition in offspring” (Hackman et al. 2010:655).
The other area that often receives attention is “the level of cognitive stimulation in the home” (Hackman et al. 2010). Stimulation includes “the availability of books (and other literacy resources), computers, trips, and parental communication. Together, these factors can explain the effects of SES on cognitive ability in children (for example, on reading and mathematics skill), even when maternal IQ has been controlled for” (Hackman et al. 2010:655). Thus, SES gets reduced to parenting and home quality, which are then associated with the negative outcomes. However, this causal move effectively washes SES from sight; the availability of books is the relevant indicator, not how greater or lesser SES might affect access to books, computers, and museum trips.
Finally, researchers focus on local stressors in the environment and local experiences with status as two ways that SES can impact the developing individual. As McEwen and Gianaros describe it, “the chronic experience of low SES at the individual level could involve enduring financial hardships, a sense of insecurity regarding future prosperity, and the possible demoralizing feelings of marginalization or social exclusion attributable to comparative social, occupational, or material disadvantage” (McEwen and Gianaros 2010:192). They also highlight subjective social status, the person's “perception of her or his relative standing or ranking in a social hierarchy” (McEwen and Gianaros 2010:192), as something that can affect emotional and physiological processes, thus implicitly making the negative experience of subjective social status into a problem of stress.
To understand how “experience gets under the skin” researchers focus on biological mechanisms that mediate experience and can change over time because of this experience. Hertzman and Boyce (2010) provide a useful two-piece framework for understanding this process—social causation and biological embedding. Social causation, unlike the typical cause–effect relation taught in basic science, is nonlinear and often nonspecific. A child might have a general vulnerability to adversity, and subsequently, dynamic interactions with the environment affect the cumulative impact of experience on development. Social causation often involves mundane experiences and relies on repeated exposures over time. This linkage of dynamic interactions and mundane experiences can lead to contingent lines of causation, for example, divorce leading to a drop in earning power leading to more economic stress leading to more drinking by a parent. Finally, social causation involves interpretive processes—meaning and emotion matter in experience. The impact of an adverse experience often depends as much on how the person interprets it as it does on some intrinsic aspect of the event itself.
Hertzman and Boyce (2010) present biological embedding as the complement to social causation. Biological embedding occurs when experience alters biological function, which can lead to long-term stable changes over development. Biological embedding does not work indiscriminately; rather, Hertzman and Boyce (2010) propose that biological systems have to meet several basic characteristics for embedding to occur: (1) the system in question can be influenced by daily experience and (2) responds to experience over the lifecourse; (3) its functioning (or dysfunction) has significant impacts on health, learning, and/or behavior, and (4) the differences in outcome can derive in part from early experience. Although Hertzman and Boyce highlight several systems that meet these criteria—the autonomic nervous system and the prefrontal cortices, for example—they present stress and the hypothalamic–pituitary–adrenal (HPA) axis as the best model for how biological embedding happens.
The American Academy of Pediatrics (Committee on Psychosocial Aspects of Child and Family Health et al. 2012) also places “toxic stress” at the center of how early childhood adversity affects childhood development and adult health and capability. Toxic stress is defined largely in biological terms: “excessive or prolonged activation of the physiologic stress response systems” and “disruptive physiologic responses (ie, toxic stress) that produce ‘biological memories’ that increase the risk of health-threatening behaviors and frank disease later in life” (Committee on Psychosocial Aspects of Child and Family Health et al. 2012:e225). Although “stable, responsive relationships” with caregivers can buffer early adversity, the American Academy of Pediatrics highlights stress as the principal mediating cause of inequality, writing that growing evidence “links childhood toxic stress to the subsequent development of unhealthy lifestyles (eg, substance abuse, poor eating and exercise habits), persistent socioeconomic inequalities (eg, school failure and financial hardship), and poor health (eg, diabetes and cardiovascular disease)” (Committee on Psychosocial Aspects of Child and Family Health et al. 2012:e225). Toxic stress becomes the focal point of rhetoric, research, and policy.
Stress is not an idle choice—it does represent an excellent system to demonstrate that poverty can indeed poison the brain. At a mechanistic level inside the person, the physiology of stress involves both brain and body and is often driven by reactions to environmental stressors, both real (e.g., a fistfight) and perceived (e.g., thinking a fistfight could happen). Thus, the physiology lends itself to metaphorical understanding, as a way to think and talk about how poverty is damaging. But the technical details back that talk up. To use the language of McEwen and Gianaros, “stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior” (McEwen and Gianaros 2010:190). McEwen and Gianaros (2010) then present the concept of allostasis, in which short-term activation of the stress system to deal with adversity can lead to long-term costs because of wear-and-tear with chronic stress, as a way to understand how a relatively constant condition like SES can produce negative effects over time.
Stress also becomes a way to both examine and evoke other biological mechanisms that play a role in how development adapts to experience, both positively and negatively. The loss of neuroplasticity through glucocorticoid exposure as a fetus or infant is one main way researchers like McEwen and Gianaros (2010) and Hackman et al. (2010) explain how the poisoning happens—high levels of glucocorticoids can lead to greater neuronal loss and less proliferation of connections among neurons, leading to a less-effective brain. Epigenetics is another major way to talk about how stress, and experience more broadly, can alter brain development. Lupien and colleagues (2009) argue that through epigenetics, genes get expressed differently because of timing and exposure to stress coupled with previous exposure to adversity. Recently, Essex and colleagues (2011) demonstrated differential DNA methylation, a crucial epigenetic mechanism, in adolescents exposed to childhood adversities earlier in life.
Beyond stress, researchers also focus on the mechanistic links between childhood poverty and adverse outcomes with respect to academic achievement. Generally, the link is made between compromised language acquisition and cognitive development and later IQ–cognitive ability and educational success. For example, a recent prospective study by Najman and colleagues concluded, “Children experiencing family poverty at any developmental stage in their early life course have reduced levels of cognitive development, with the frequency that poverty is experienced predicting the extent of reduced cognitive scores” (Najman et al. 2009:284). Similarly, Hackman and Farah write, “Language ability differs sharply as a function of SES … SES gradients have been observed in vocabulary, phonological awareness and syntax at many different stages of development” (Hackman and Farah 2009:65).
A final area where internal mechanisms can play a role is in behavior, particularly the impact of poverty on mental and behavioral health, where greater rates of problems are found among low SES children and adolescents (Hackman et al. 2010). Often these problems are linked to the effect of early maltreatment and conflict-filled relations in the home, which can impact the development of emotional regulation and cognitive control in the limbic and prefrontal areas of the brain. There is also evidence that directly links the experience of lower SES to threat appraisal and fear within the individual, pointing to a more direct way that inequality might shape children's brains (McEwen and Gianaros 2010). In this research, lower perceived parental social standing was linked to greater amygdala reactivity to angry faces and lower subjective social status was associated with reduced volume in the anterior cingulate cortex. As McEwen and Gianaros argue, these areas affect the regulation of behavior, and compromised function here can “increase vulnerability to psychiatric and medical syndromes characterized by dysregulated emotion-related behaviors and physiology” (McEwen and Gianaros 2010:207).
In summary, the mechanistic approaches use stress, epigenetics and neuroplasticity, language acquisition, and emotion regulation as ways that social causes can alter biological function through biological embedding. A key system here is the HPA axis, and the concept of “toxic stress” that can drive continued overactivation of the axis with an associated impact on the brain. Toxic stress becomes how poverty poisons the brain.
APPROACH TO INTERVENTIONS
Hackman and Farah write, “societal investment in reducing the impact of childhood poverty on cognitive ability is far more efficient [early in life] than programs designed to reverse its effects later in life” (Hackman and Farah 2009:71). This basic point—that the greatest payoff comes from early investment, and that this early investment can help mitigate lifelong effects of poverty—is the strongest policy point that emerges from the “poverty poisons the brain” model.
Beyond this important conclusion, different researchers propose different interventions for early childhood. Hackman and Farah (2009) highlight providing additional income to families of poor children, which has been linked to improved language function. They also argue that interventions can directly target specific neurocognitive systems, describing the example of the “Tools of the Mind” program, a computerized game aimed at enhancing executive function in children. Hackman et al. (2010) paint in broader brushstrokes, mentioning direct changes to SES, improving access to medical care and nutritional supplements, and also direct interventions through cognitive training and enhancement. They also present “poverty poisons the brain” as a public health problem that requires shaping the environments of these children. “Precedence should be given to improving care for children and to providing enriching environments during pre- and postnatal development. Therefore, policies and programmes that reduce parental stress, enhance parental emotional well-being and provide adequate resources for parents and communities should be prioritized” (Hackman et al 2010:656).
McEwen and Gianaros (2010) present an approach aimed specifically at reducing chronic stress and allostatic load. They highlight basic things like increasing physical activity and social integration, both of which can buffer the person against chronic stress. They argue that pharmaceutical interventions should be considered, even with potential side effects. Finally, they point to “top-down effects of policies,” where “education, housing, taxation, setting of a minimum wage, and addressing occupational health and safety and environmental pollution regulations are all likely to affect the brain and health via a myriad of mechanisms” (McEwen and Gianaros 2010:212).
The American Academy of Pediatrics is most explicit on the policy side, advocating a “broad-based, multisector commitment” that aims to reduce toxic stress in children (Committee on Psychosocial Aspects of Child and Family Health et al. 2012). Part of this commitment can come through pediatricians themselves, who should shift to this new approach emphasizing toxic stress while continuing to draw on their strengths in developmental approaches to health, understanding the importance of prevention, and having a powerful role as advocates for change. Besides more extensive training about toxic stress, the Academy recommends recognizing the limits of an office-based approach to “full address the new morbidities effectively” (Committee on Psychosocial Aspects of Child and Family Health et al. 2012:e226) and the urgent need for the development of more evidence-based strategies.
Although these broad-based approaches are often advocated, it is clear that medications and brain-based training are already at the forefront of what will count as “effective interventions.” These types of intervention studies are easy to construct as “evidence based,” requiring a double-blind approach that washes away the complexity of engaging specific communities or aiming for large-scale programs to achieve change.
“POVERTY POISONS THE BRAIN”—USES FOR NEUROANTHROPOLOGY
Before turning to a critical analysis of the “poverty poisons the brain” approach, I want to highlight four potential uses for neuroanthropologists concerned with the links between inequality, development, children, and health. First, the interactive elements of the overall approach offer useful conceptual tools for neuroanthropologists. Social causation, the interactive model of development, biological embedding, and neuroplasticity and epigenetics provide a cascading approach to understanding just how poverty poisons the brain, and thus how unequal social outcomes and health disparities come to be. Second, the “poverty poisons the brain” model gets at central anthropological questions, such as how do culture and social structure shape the individual. This research highlights the need for us to think seriously about how experience gets under the skin, from processes of enculturation to the impact of inequality. Anthropologists like Gravlee (2009) and Worthman (2009) are actively examining the embodiment of social inequality and the development of emotion regulation through childhood experience. The “poverty poisons the brain” approach offers ways to further link embodiment to development, and thus produce even more robust anthropological models for how social inequality and cultural experience shape us into the people we are.
Third, “poverty poisons the brain” offers a powerful rhetorical model that anthropologists might use to argue publicly about the need to address systemic inequality, structural violence, and health disparities. As a metaphor, it can help policy makers and the public understand the high costs that these systemic social inequalities can create, and also to tease out and explain away some of the obvious objections—that behaviors like drug use or violence are to blame, or that these people simply reached some preordained limits, and resources would be better spent elsewhere. Inequality is toxic is a compelling line, and locating that toxicity inside people—inside their brains—can help researchers convince often-skeptical audiences that social forces do indeed matter and should be addressed. Negative outcomes like drug use and low educational achievement are just that, outcomes linked to toxic stress and other neurobiological reactions to what children face. Although this approach does offer a double-edged sword, which will become apparent below, “poverty poisons the brain” can cut through to issues that anthropologists consider central to applied efforts.
Fourth, the “evidence-based” approach offers potential uses for anthropologists. The American Academy of Pediatrics emphasizes prevention, collaborating with the community, and thinking outside the office setting. Anthropologists, armed with a neuroanthropological approach, can help design interventions that can make a difference in families’ and children's lives. These types of interventions can be just as easily subjected to an evidence-based approach as brain-based training. Thus, “poverty poisons the brain” can help frame an overall approach to developing effective applied anthropology that can show demonstrable effects and thus become incorporated into the work of broader societal institutions like the American Academy of Pediatrics.
THE NEUROANTHROPOLOGY OF “POVERTY POISONS THE BRAIN”
A Critical Failing
The first and most obvious problem with “poverty poisons the brain” is how it effectively works to conceal the social forces—both the actual poverty suffered by people and the systemic effects and politics of inequality—from view. This flaw is almost enough to undercut the entire approach. Although these researchers do aim to highlight the pernicious effects of poverty during childhood on the rest of the lifecourse, they don't actually focus on poverty much. As Figure 1 shows explicitly, SES becomes prenatal factors, parental care, and cognitive stimulation, which in turn becomes brain development, and that leads to cognition, academic achievement, and mental health. The effect is to wash away social considerations and theory from the model, and thus essentialize social difference in the family and the individual. As researchers move from social inequality to the proximate factors, neighborhood quality and SES get reduced to low-quality parenting, household conflict, and other local manifestations of “toxic stress.” The social level of analysis gets left behind, even though in reality, the social is part-and-parcel of the household and the child's experience.
Researchers like Hackman and Farah do warn that the neuroscience is open to “blaming the victim,” writing “Characteristic differences between individuals of higher and lower SES have been used by some to argue that low SES individuals are intrinsically less deserving or less valuable members of society. The biological nature of the differences documented by cognitive neuroscience can make these differences seem all the more ‘essential’ and immutable” (Hackman and Farah 2009:71). Nevertheless, they seem blithely unaware of how their own models facilitate such blaming. How else are we supposed to read the transition from SES to brain development and academic achievement? Simply contradicting ideas about “fixed, innate programs” and stating “there is little evidence to suggest differences are essential or immutable” is not good enough. As ethnographic research on the “disease model” of addiction has shown, social actors like law enforcement can easily incorporate supposedly liberating biology-based models to justify increased criminalization and prosecution of drug users (Garriott 2011). After all, they have a disease—a biological problem, whether that pathology came through an innate genetic program or “specific causal pathways by which socioeconomic deprivation can affect brain function” (Hackman and Farah 2010:71).
The same model—where socioeconomic deprivation comes down to brain function—also supports existing approaches to dealing with brain problems, from pharmaceuticals to education that “treat” or “enhance” brain function. A massive capitalist enterprise already exists for developing pharmaceuticals for children. A new market is rapidly taking shape for “brain training” initiatives to shape the newly conceived “plastic” brain, building on existing therapeutic and educational enterprises. All these endeavors will take the “poverty poisons the brain” model and seek to both profit and assert societal control through this new causal metaphor to understand children's development.
Thus, neuroanthropologists who plan to use a “poverty poisons” approach need to be aware of the double-edged sword of the metaphor. We are not the only actors who will use it, and although it might cut toward confronting inequality, it also cuts toward essentializing difference and favoring already existing forms of social control and biology-driven management of “poisoned brains.” To counteract these considerable drawbacks, neuroanthropologists must be explicit on making the “poverty poisons” model into one that moves far beyond a focus on how SES gets lodged in the brain, thereby losing social theory through an intrinsic focus on the individual. Three ways exist to reform this approach, and make it into something that can do considerable anthropological work.
The Social Embodiment of Inequality
One way to bring the social into view is to recognize, as I wrote above, that inequality itself (and not just “the impact” of inequality) will be manifest in the environment and in development. The embodiment of inequality offers an approach to better understand how proximate factors and dynamics include social and cultural forces (Gravlee 2009; Krieger 2005). Such an approach can draw on (1) radical contextualization, where the use of ethnography, studying up, and biosocial analysis can help highlight how social processes underpin health disparities (Chapman and Berggren 2005); (2) the anthropology of adverse environments, which incorporate “a range of physical, social, and temporal factors that are highly localized and sensitive to community-level influences on growth and health” (Moffat and Galloway 2007:676); (3) the social embodiment of biology, to understand how context and environment can get under the skin (Gravlee 2009; Kuzawa and Sweet 2009); (4) risk focusing, where culture plays a fundamental role in the cumulative experience of disadvantage over development (Schell 1992); and (5) the everyday practices of privilege, discrimination, and status that play a role in perpetuating inequality (Schultz et al. 2006; Stephens and Gillies 2012; Sweet 2010). Together, these approaches offer the way to understand, first, how the social is present in the everyday life of inequality, and second, to connect that to a much wider range of proximate factors and local environments that shape development and embodied biology.
FROM “TOXIC STRESS” TO THE DYNAMICS OF STRESS AND INEQUALITY
Stress is the lynchpin around which much of the “poverty poisons the brain” discourse revolves. “Toxic stress” does the poisoning, while the HPA axis is exhibit number one to show how connected the brain is to the body and the environment, and thus vulnerable to poverty. The main problem is that “toxic stress affects vulnerable biology” does not change either reductive cause–effect thinking or move beyond a mechanical conceptualization of what stress is. Still, decades of research on stress provide the grounding for a better model of stress that can link easily to social theory and to the everyday reality of inequality.
First, anthropological research has consistently linked the experience of social status to stress, such that incongruity with social norms (McDade 2008), a lack of consonance with societal ideals (Dressler 2011), the sense of social alienation and social worth (Blakey 1998), negotiating social conflicts in relationships (Flinn 2007), and the inability to achieve major social goals for a “good life” (Brown et al. 2009) all impact stress. Second, anthropologists have also reformulated environmental stressors as cultural, particularly through the interpretive frameworks brought to bear to understand and cope with adversity (Eggerman and Panter-Brick 2010; Snipes et al. 2007). Together, this research shows that the ability to realize collective goals in one's life, not being able to “find a way out” of difficult social situations or conflicting demands, and feelings of despair and hope matter deeply in what stress is and does.
The next step is to link this anthropological work on stress with psychological and neurobiological research. This research, often done with animal models or in controlled situations in university laboratories, resonates deeply with the anthropological research. This research highlights how uncertainty and unpredictability are stressful; that a lack of control, or the ability to do something about one's situation, exacerbates stress; and that lower social status, particularly in social interactions where that status is judged and reinforced, is intrinsically stressful (Matthews and Gallo 2011; Miller et al. 2009; Sapolsky 2005). These findings are remarkably close to the anthropological work. Uncertain and unpredictable interactions with people of higher status (e.g., waiting for the other shoe to drop); a lack of control and feeling despair; few if any means to do anything about one's social situation—the joint social and neural dynamics make stress poisonous. “Toxic stress” is toxic not simply through the accumulation of stressors, but because there is a match between sociocultural forces and neuropsychological forces.
Thus, a neuroanthropology of poverty shows that poverty is not bad simply because of lower social status, increased environmental stressors, and a lack of resources. Poverty is bad because it unites individual and societal lack of control, creates unpredictable adversity, sets conditions that leave people unable to respond, and creates a sense of helplessness and despair. Yet there is a flip side to this neuroanthropological approach. The dynamic view also provides recommendations for what to do. Given people options, reducing uncertainty, and generating more equal relations are all ways to change the neuroanthropology of stress. Doing that requires tackling inequality in both its proximate and societal dimensions.
THE PRODUCTION OF SOCIAL FACTS
The flow of causality in the basic “poverty poisons the brain” model is from SES to the individual brain, where changes in neural structure and function are then assumed to largely account for individual outcomes like educational achievement. This reductionist approach assumes that assembling a group of underachieving, brain-compromised individuals is the central key to understanding how social class and inequality come about. These researchers overlook how the brain can and does play a role in the social production and reproduction of class and patterns of social inequality and health disparity. Indeed, if we think about Bourdieu's habitus, that internal collection of habits and tastes and practices, the brain becomes a particularly important way to understand how we actually come to have a habitus, rather than simply assume that it is given, sui generis, by social forces (Downey 2010; Hay 2009). The brain contributes to the production and reproduction of our social lives, and that perspective offers a truly important way to understand how poverty, social experience, and brain development come together in helping to create social class and the reproduction of social structure. The social organization of inequality happens through how social forces shape our neuroplastic and embodied brains. Opening up questions for how this process happens is a crucial next step for really understanding what we mean by “poverty poisons the brain.”
As neuroscience shows, poverty literally can be anatomy, something that cannot be fixed simply by money or by declarations of human rights. This view challenges typical liberal policy. Inequality runs through families, through development and through behavior and biology. Standard liberal solutions often assume that changing the environment—affecting policy or providing better information—is enough. It is not. People themselves take part in reproducing inequality. It is in their bones, in their hearts, in the brains. This reality makes both “blame the victim” and social justice approaches equally viable. To move beyond this easy dichotomy, a good first step is to draw on the multifactorial etiology approach to understanding the conjunction of social environments, behavioral biology, and human development. A crucial next step is to incorporate measures of higher level social causes into this model, and to also develop measures that better examine the sociocultural dimensions and neuroanthropological processes present at the proximate level of explanation. This second step opens up an evidence-based approach to showing how the social matters at all levels represented in Figure 1, and for showing better how poverty truly does poison the brain. Alongside this empirical approach, it is important to develop multilevel and multisited interventions that are tied together by a holistic applied anthropology focused on the neuroanthropology of poverty.
However, better measurements and interventions using a multifactorial model will not solve the culture versus biology or mind–body dichotomies present in both anthropology and neuroscience. Understanding the role that the brain plays in generating social structure is not as simple as recognizing that neuroscience can contribute to our understanding of concepts like habitus or aid in understanding how inequality gets reproduced generation to generation. It also requires a wholesale shift in how many anthropologists and many neuroscientists conceive of the brain. The mechanistic research done by neuroscience is often done from the perspective of the brain, for example, that stress is largely psychobiological, an internal and individual state shaped by the “fight-or-flight” evolution of the stress system. This view might be useful in the laboratory, the scientific gaze to fix on a certain neurological function. But it is not how the brain works in the real world. The social and the meaningful become part of how the brain functions. That requires a fundamental shift in how we understand what the brain does.
One of the most problematic issues with “poverty poisons the brain,” and much of brain research in general, is that the brain becomes a fetish. We point to the neuroanatomical changes in the brain, and then say, this stuff about poverty being bad for children must be true. Recall the opening of the Wired piece, “Growing up poor isn't merely hard on kids. It might also be bad for their brains.” Here children are placed to one side in favor of our new marker of individuality, the brain. Social relationships between people, from the structural to the everyday, become reduced to how they are expressed, mediated, and transformed by mechanical processes—objects—within the brain. Referencing the brain as the central mediator of poverty hides the larger truths of inequality and distorts our understanding of what poverty really is. To take a more extreme example to illustrate the same point, it is like saying slavery is both harmful to people and morally wrong because it impacts brains.
The brain has become like property, something a person possesses and that poverty—somehow separate from the person, a naturalized thing that causes stress—negatively impacts. This view is in need of a radical change. The social system does flow through the brain, among other material and symbolic substrates; the brain works in such a way that its function is, at least in part, social. Put differently, taking the perspective of human meaning and social relations as the way to understand brain function is an area in need of urgent development.
The brain is not anatomy alone. Taking the combination of neuroscience and anthropology seriously means that social environments, in all their complexity, become as important as any brain part. Still, anthropology does need to go through an unsettling shift in our understanding of inequality, given the central role that development and neural function do play in what poverty is and means for people. In anthropology, often social forces become the privileged way we understand social suffering. Neuroanthropology challenges that view. The embodiment that runs through the brain—this sociobiological embedding of our experiences and our social relations—is indeed a core cause, a central hub, around which inequality is created. The embodied brain is not just a fundamental place of suffering, it is a fundamental cause of social suffering. The way our brains work, their openness to social causation and biological embedding; the way the dynamics of the stress system can meet the dynamics of the social system—these mean that suffering from poverty is not reducible to social theory alone. People suffer through their embodied brains, through despair and toxic stress and destructive behavior. The brain suffers poverty. We can build research that examines how and why neuroanthropological dynamics play a role in social suffering, the reproduction and impact of inequality, and the disparities in health and well-being that children experience by growing in unequal conditions.