THE BIOLOGY OF THE POVERTY TRAP: How Genetic Modifications Perpetuate Socioeconomic Inequality

Tabata Amaral is the daughter of a bus fare collector and a housemaid who once lived in one of the poorest neighborhoods of São Paulo, Brazil. Only 1.6% of Brazilians who, like Tabata’s family, lived in slums ever attain a college degree. Yet she completed a double major in Political Science and Astrophysics at Harvard, after winning numerous Brazilian science competitions and securing a scholarship to attend one of the best-regarded preparatory high schools in the country. Narratives of individuals overcoming hardship appeal to our hearts—it is the hero’s journey manifesting itself in the real world, bringing justice through the reconciliation of exceptional talent and success.

However, these stories retain their power because they are the exception, after all, if they weren’t, there would be no wonder or amazement at the protagonist’s victory. The data shows that the reality for most families is years—or even centuries—of struggle against hardship to attain better living conditions. According to the 2018 Organization for Economic Cooperation and Development (OECD) report on social mobility, it takes, on average, 4.5 generations for a low-income family to achieve mean income in an average OECD country. In developing nations such as Tabata’s, it can take as many as 9 generations [1], which amounts to 135-180 years of toil to reach the Brazilian average income of 17,000 U.S. dollars per year for a family of 4. The lack of social mobility is caused by what the report calls a “sticky floor” and a “sticky ceiling” in our social hierarchy: the poor struggle to move up in the wealth pyramid, and the rich are unlikely to move down. This poverty trap results in a dysfunctional feedback loop through which the poor stay poor because their lack of wealth hinders their acquisition of wealth. After all, while Tabata had to win a national mathematics competition to be able to afford a top high school, wealthy qualified students could substitute a merit scholarship for the “merit” of being able to pay tuition.

Narratives of individuals overcoming hardship appeal to our hearts—it is the hero’s journey manifesting itself in the real world, bringing justice through the reconciliation of exceptional talent and success.

This paradox in our social system is one of the issues that is important for most ideological frameworks. From a social justice perspective, it promotes the exploitation of the most vulnerable and perpetuates an unjust social hierarchy where opportunities are distributed based on previous wealth. From an economic standpoint, the poverty trap also decreases productivity by impeding meritocratic selection and underutilizing low-income talent.

As important as this issue is, tackling it is a serious challenge. Access to high quality education is an important component of any solution, as it is a good predictor of lifetime earnings independent of family wealth [2]. Thus, it appears to follow that an efficient way to break the feedback loop is to provide every student with the same educational opportunities independent of their financial situation. However, although this measure is indisputably crucial to improve social mobility, its effectiveness can be curtailed by interactions between students’ socioeconomic status and their health. Poorer communities are especially vulnerable to disease because of sanitation conditions and hardship-related stress which compromises the immune response [3]. As these low-income students are more likely to have their physical well-being compromised, they are also more likely to suffer from academic underachievement [4]. This diminishes potential earnings relative to their peers and, thus, with decreased wealth after graduation, they are more likely to be ill, further hindering their chances to increase their wealth—a biomedical manifestation of the poverty trap.

The data shows that the reality for most families is years—or even centuries—of struggle against hardship to attain better living conditions.

The OECD report dedicates approximately 1% of its pages to discussion of the effects of health on social mobility, and mainly focuses on how “labor market withdrawal,” “out-of-pocket expenses,” and developmental problems due to malnourishment affect wealth outcomes [1]. These are definitely important issues, which is why it is concerning that developed nations such as the United States still have not eradicated issues outlined in the report such as food insecurity [5] and lack of access to prenatal care [6].  Due to the magnitude of OECD’s influence, it is also concerning that the report fails to contemplate and emphasize the more nuanced effects that emerge from the fact that humans are fundamentally biological entities and are therefore bodily and biologically affected by socioeconomic factors.

Taking into account some of these biological factors in economic predictions does indeed yield robust results. Incorporating standard epidemiological models for disease in a model that predicts population wealth based on the number of diseased individuals accurately recapitulates real wealth distributions, indicating the strong relationship between disease and socioeconomic success. Apart from showing the explanatory power of this biological variable, the study also shows that, all else being equal, there are two competing tendencies—one being the accumulation of wealth and reduction of disease, and the other being impoverishment and increase of disease prevalence. The destiny of a community, in this model, depends on the initial conditions of a community relative to a threshold [7]. Although this tendency is not deterministic in real life due to natural fluctuations in external parameters, the overall trend it suggests is daunting.

…the study also shows that, all else being equal, there are two competing tendencies—one being the accumulation of wealth and reduction of disease, and the other being impoverishment and increase of disease prevalence.

The results of this study also assume that wealth determines nutrition and access to hygiene, and that worker productivity is fixed. Fortunately, although these assumptions can be true in some contexts, it is possible to intervene in these areas and adjust these parameters.  Multiple policies exist around the world to do so: an increase in healthcare accessibility and sanitation infrastructure would limit the deterministic relationship between wealth and access to hygiene. Additionally, food stamps and cash transfer have been shown to be somewhat effective in limiting low-income malnutrition in different countries [8,9]. However, although these policies are invaluable, the limited success they have had so far [9] point to more complex underlying social and biomedical issues. Making them a priority would still not be enough.

To understand why, we must go back to the second World War, during which a brutal German siege against the Dutch created the longest and arguably most important human experiment that no ethical circumstances could recreate. Because of wartime famine, a cohort of socioeconomically diverse individuals from all ages was subjected to malnourishment. No child, pregnant woman, or elder was spared. From this disgrace emerged the founding experiment of modern epigenetic theory, the key to understanding the most worrisome effects of poverty in our development.

A 2008 study that followed up with the people whose mothers had been affected by the famine verified that individuals whose mothers were in early pregnancy during the event had a different pattern of methylation marks in their genomes than their siblings who were born before or after the siege. This effect was observed over six decades after the famine [10], showing that it had long-term staying power and that hardship in early life could cause molecular changes that last a lifetime. Effectively, hardship can shape a genome from birth.

Genome methylation—the addition of a methyl group to DNA—is a central part of the study of epigenetics, which is concerned with changes in gene expression that are not caused by mutations of the genomic sequence. Generally, methylation of a gene or its promoter inhibits the expression of the gene. Additionally, because altering one gene can subsequently change the expression of many genes, these changes can create complex downstream effects [11]. Understanding these interactions is an important part of contemporary biochemical and bioinformatic research.

…modern epigenetic theory, the key to understanding the most worrisome effects of poverty in our development.

The body’s stress response system is tightly regulated by epigenetics. The hypothalamic-pituitary-adrenal (HPA) axis is the chain of interactions that controls and coordinates the stress response. In a well-functioning organism, the hypothalamus, a part of the brain, releases an initial “signal,” corticotropin release hormone (CRH), to the bloodstream. After binding to its receptor, CRH acts as a signal that indirectly stimulates the release of cortisol, popularly known as the stress hormone, to the bloodstream. Cortisol then activates the intracellular glucocorticoid receptor, which travels to the nucleus and directly interacts with DNA to cause gene expression changes through methylation, as well as acetylation, another type of epigenetic mark. To avoid overproduction of the stress signal, cortisol also inhibits the production of CRH, thus indirectly moderating its own secretion. This negative feedback loop is crucial for the homeostasis, or stability, of the stress response system [12].

However, multiple studies have shown that early life experiences can disrupt this equilibrium, resulting in an imbalanced stress response. Childhood maltreatment by parents is one critical factor in early life development that is negatively correlated with socioeconomic status [13]. Studying the effects of childhood maltreatment can therefore give insight into the biochemical mechanisms that relate early-life stress to its long-term consequences along socioeconomic lines. In rats, lack of maternal caregiving has been shown to increase methylation of the promoter region of the glucocorticoid receptor in the pituitary gland [14]. In this tissue, this epigenetic change decreases the body’s ability to detect and regulate increases in stress levels. Therefore, rats who do not receive maternal care have more intense and poorly regulated stress responses. A similar study found that humans who were subjected to childhood maltreatment showed less methylation in the CRH receptor gene [15], which makes the body more sensitive to CRH and can cause the over-secretion of cortisol. Therefore, childhood maltreatment—which is associated with socioeconomic status—has been shown to be linked to perturbations of the equilibrium of the HPA axis through epigenetic changes in both rats and humans.

Effectively, hardship can shape a genome from birth.

These epigenetic findings are even more worrisome when considering that low socioeconomic status is associated with stress [16]. Because low-income individuals are more likely to suffer childhood maltreatment and therefore have dysregulated HPA axes, increased stress can become a chronic problem. Increased stress is known to diminish immune function and therefore increase individuals’ susceptibility to disease, [3] thus reinforcing the disease-poverty feedback loop. Chronic stress, somewhat ironically, also makes it more likely for inflammatory [3] and chronic diseases to develop [17]. As we would expect, poor counties have been observed to have increased incidences of chronic disease [18]. Beyond these immediate physiological and disease-related outcomes, continued stress is also associated with addiction [19] and impaired working memory [20], both of which, along with chronic disease, are associated with decreased worker productivity [21]. This is especially unsettling, as worker productivity is one of the parameters that allows populations to escape the disease-poverty feedback loop within the aforementioned model.

Epigenetic changes, therefore, contribute to the hindrance of social mobility. Moreover, such modifications have also been shown to be inheritable in plants [22], and there is evidence suggesting that heritability is also possible in humans [23,24]. If a detrimental epigenetic change due to hardship were indeed inheritable, it would create an intergenerational problem, where the socioeconomic effect of hardship would be transmitted generation after generation through the genome. This raises important questions: how far into the future could we expect those changes to be detectable? And how do events such as genocide or slavery affect the great-grandchildren of the people who directly suffered those past traumas?

This raises important questions…how do events such as genocide or slavery affect the great-grandchildren of the people who directly suffered those past traumas?

These are pressing questions, but the most pressing of all, in my opinion, is how we should respond to what we already know to be true about the epigenetic perpetuation of income inequality. There are possible pharmacological approaches that we can take: the previously mentioned rat study showed that the methylation differences caused by parental neglect were reversible using a histone deacetylase inhibitor. Using such methods to address these issues, however, is still a distant possibility given our current understanding of the epigenome. It is made even more distant by the fact that, currently, most resources are being directed towards more “traditionally” biological problems such as directly curing diseases and increasing longevity. Only around 7% of the National Institute of Health’s budget is currently being devoted to health disparities [25]. Given that non-medical factors and interventions account for most of the decrease in disease mortality in the past century [26], and that there is a tangible relationship between inequality and health as discussed above, not dedicating resources to the mitigation of biology-inequality interactions seems to be a significant gap in contemporary research efforts.

On the other hand, even a panacea might not be a panacea. Even if a treatment against HPA dysregulation were to be produced, it could potentially benefit the wealthy without much positive impact on the poor, and thus reinforce the stratified socioeconomic system we see today. There exist multiple historical examples in which health interventions and biomedical breakthroughs have reached different social strata to different extents, resulting in widening gaps among social classes. For example, the development of the germ theory of disease in the 19th century is known for changing common hygiene practices and is credited with an unparalleled reduction in infectious disease rates. However, if we look closer at the data for the United States, we can see that, while professional classes did see a steep decrease in child mortality, the working classes were practically unaffected by this new paradigm of knowledge. Because of that, this breakthrough created an unprecedented gap between those groups in terms of child mortality [27]. Similarly, a recent study on the use of cancer treatment in Nordic countries indicated that, even with universal access to healthcare, less educated individuals were less likely to seek treatment options that were shown to increase survival [28].

Yet purely economic measures may be similarly ineffective. In the aforementioned OECD document, which is meant to be taken as reference in policymaking, the complex impacts of health in social mobility are largely ignored or seen as secondary. Although the 2018 report on social mobility recommends several economic and educational measures to mitigate the “sticky floor” effect, it barely considers the impact of poverty on a person’s health and economic prospects, dedicating only 3 out of its 355 pages on the subject and thus not presenting the nuance this subject requires. The report also contains sections that would greatly benefit from a wider perspective of the issue at hand. For example, though the document considers educational measures and access to information as tools for professional development, it misses an opportunity in failing to also identify these as mechanisms through which health inequities could be alleviated. Within this narrow framework, the possibility of an economic reform with the primary objective of mitigating inequities in health status, or a health policy drafted to improve social mobility seems small; both would be considered heterodoxic at best.

The lack of a real solution to the epigenetic perpetuation of inequality, the historic inability of healthcare and health interventions to transcend social boundaries, and the insufficient attention the OECD dedicates to promote access improvement make one thing startingly apparent: our currently disjoint areas of knowledge cannot adequately support real solutions to address the complex and multidisciplinary problem of the biology-poverty cycle. Though it may seem counterintuitive or “unnatural” to involve biologists in economic discussions, and vice versa, the definition of any boundary between areas of knowledge is arbitrary. For example, 300 years ago, much of what we today understand as “science” was called “natural philosophy.” Furthermore, many of these “natural philosophers” who formed the basis of our current scientific thinking also engaged in questions of metaphysics that would seem out-of-place given our current conception of scientific inquiry. In the 1800s, chemists still described the atom without the use of physical models, something that would now be unfeasible given how the field has evolved since then. More recently, neuroscience has become an interdisciplinary and independent field of inquiry, following the realization that neither psychology nor neuroanatomy alone could fully describe the human brain [29].

It is an illusion to believe that…it would be enough to rely solely on the behavioral aspect of human functioning and ignore the basic biological principles that governs it.

A similar paradigm shift must come to address the poverty trap, and we are past the time to do so: The rat study was performed in 2004, and the Dutch famine cohort has been studied for the last 50 years. It is an illusion to believe that, in modeling human behavior and the distribution of wealth, it would be enough to rely solely on the behavioral aspect of human functioning and ignore the basic biological principles that govern those. Foucault, building on foundations similar to Thomas Kuhn, discussed how the use of words forms the concept that to which those words refer, and how this can delimit the questions that can be asked inside an area of knowledge. This can be useful, as it provides a set of questions that can be addressed methodologically. However, we have taken these conceptual delimitations too far. Even at Yale, which strives for interdisciplinarity, each area has its own physically independent building or territory on campus. When applying for grants, one must request funds from a subject-specific institution, which, almost by definition, must focus its attention on the newest developments of its own area. Furthermore, the OECD and other policymaking research institutions’ job posting require “relevant” professional experience [30], and the definition of relevant must depend on the delimitation of an array of knowledge and activities, which is done through the lenses of the current way of thinking. Thus, they fall short by not properly incorporating different bodies of knowledge and thought. To address that, it is time for biologically-minded economics, or the creation of any new term that will allow for the concept to be formed, and, just like neuroscience, allow for the use of all necessary tools to solve this problem.

Work Cited:

  1. OECD. “A Broken Social Elevator? How to Promote Social Mobility.” 2018, doi:10.1787/9789264301085-en.
  2. Tamborini, Christopher R., et al. “Education and Lifetime Earnings in the United States.” Demography, vol. 52, no. 4, 2015, pp. 1383–1407., doi:10.1007/s13524-015-0407-0.
  3. Dhabhar, F. S. (2009). Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection and Immunopathology. Neuroimmunomodulation, 16(5), 300–317. doi: 10.1159/000216188.
  4. California Department of Education. Getting Results: Developing Safe and Healthy Kids Update 5: Student Health, Supportive Schools, and Academic Success. 2005. [Accessed: 2 May 2018].
  5. UNITED STATES DEPARTAMENT OF AGRICULTURE. “Food Security and Nutritional Assistance”. 2018,…
  6. Phillippi, J. C. (2009). Womens Perceptions of Access to Prenatal Care in the United States: A Literature Review. Journal of Midwifery & Womens Health, 54(3), 219–225. doi: 10.1016/j.jmwh.2009.01.002
  7. Bonds, Matthew H., et al. “Poverty Trap Formed by the Ecology of Infectious Diseases.” Proceedings of the Royal Society B: Biological Sciences, vol. 277, no. 1685, Sept. 2009, pp. 1185–1192., doi:10.1098/rspb.2009.1778.
  8. Collins, A. M., & Klerman, J. A. (2017). Improving Nutrition by Increasing Supplemental Nutrition Assistance Program Benefits. American Journal of Preventive Medicine, 52(2). doi: 10.1016/j.amepre.2016.08.032.
  9. Groot, R. D., Palermo, T., Handa, S., Ragno, L. P., & Peterman, A. (2017). Cash Transfers and Child Nutrition: Pathways and Impacts. Development Policy Review, 35(5), 621–643. doi: 10.1111/dpr.12255.
  10. Heijmans, B. T., et al. “Persistent Epigenetic Differences Associated with Prenatal Exposure to Famine in Humans.” Proceedings of the National Academy of Sciences, vol. 105, no. 44, 2008, pp. 17046–17049., doi:10.1073/pnas.0806560105.
  11. Greenberg, M. V. C., & Bourc’His, D. (2019). The diverse roles of DNA methylation in mammalian development and disease. Nature Reviews Molecular Cell Biology, 20(10), 590–607. doi: 10.1038/s41580-019-0159-6.
  12. Oakley, R. H., & Cidlowski, J. A. (2013). The biology of the glucocorticoid receptor: New signaling mechanisms in health and disease. Journal of Allergy and Clinical Immunology, 132(5), 1033–1044. doi: 10.1016/j.jaci.2013.09.007.
  13. Lefebvre, R., Fallon, B., Wert, M. V., & Filippelli, J. (2017). Examining the Relationship between Economic Hardship and Child Maltreatment Using Data from the Ontario Incidence Study of Reported Child Abuse and Neglect-2013 (OIS-2013). Behavioral Sciences, 7(4), 6. doi: 10.3390/bs7010006.
  14. Weaver, Ian C G, et al. “Epigenetic Programming by Maternal Behavior.” Nature Neuroscience, vol. 7, no. 8, 2004, pp. 847–854., doi:10.1038/nn1276.
  15. Jiang, Shui, et al. “Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma.” Frontiers in Psychiatry, vol. 10, Aug. 2019, doi:10.3389/fpsyt.2019.00808.
  16. Cohen, Sheldon, et al. “Socioeconomic Status Is Associated With Stress Hormones.” Psychosomatic Medicine, vol. 68, no. 3, 2006, pp. 414–420., doi:10.1097/01.psy.0000221236.37158.b9.
  17. Renzaho, Andre M. N., et al. “Stressful Life Events and the Onset of Chronic Diseases among Australian Adults: Findings from a Longitudinal Survey.” European Journal of Public Health, vol. 24, no. 1, July 2013, pp. 57–62., doi:10.1093/eurpub/ckt007.
  18. Shaw, Kate M., et al. “Chronic Disease Disparities by County Economic Status and Metropolitan Classification, Behavioral Risk Factor Surveillance System, 2013.” Preventing Chronic Disease, vol. 13, Jan. 2016, doi:10.5888/pcd13.160088.
  19. Sinha, Rajita. “Chronic Stress, Drug Use, and Vulnerability to Addiction.” Annals of the New York Academy of Sciences, vol. 1141, no. 1, 2008, pp. 105–130., doi:10.1196/annals.1441.030.
  20. Evans, G. W., and M. A. Schamberg. “Childhood Poverty, Chronic Stress, and Adult Working Memory.” Proceedings of the National Academy of Sciences, vol. 106, no. 16, 2009, pp. 6545–6549., doi:10.1073/pnas.0811910106.
  21. Fouad, Ahmed Mahmoud, et al. “Effect of Chronic Diseases on Work Productivity.” Journal of Occupational and Environmental Medicine, vol. 59, no. 5, 2017, pp. 480–485., doi:10.1097/jom.0000000000000981. 
  22. Sano, H., & Kim, H.-J. (2013). Transgenerational Epigenetic Inheritance in Plants. Epigenetic Memory and Control in Plants Signaling and Communication in Plants, 233–253. doi: 10.1007/978-3-642-35227-0_11.
  23. Vassoler, F., & Sadri-Vakili, G. (2014). Mechanisms of transgenerational inheritance of addictive-like behaviors. Neuroscience, 264, 198–206. doi: 10.1016/j.neuroscience.2013.07.064.
  24. Pembrey, M. E., Bygren, L. O., Kaati, G., Edvinsson, S., Northstone, K., Sjöström, M., & Golding, J. (2005). Sex-specific, male-line transgenerational responses in humans. European Journal of Human Genetics, 14(2), 159–166. doi: 10.1038/sj.ejhg.5201538.
  25. National Institute of Health. “Estimates of Funding for Various Research, Condition, and Disease Categories (RCDC)”. 2020,
  26. Preston, S. H. (1996). American Longevity: Past, Present, and Future. SSRN Electronic Journal. doi: 10.2139/ssrn.1824586.
  27. Preston S. “American Longevity: Past Present and Future,” Distinguished Lecturer in Aging Series, Center for Economic Policy, Syracuse University Policy Brief 7/1996.
  28. Fiva, J. H., Hægeland, T., Rønning, M., & Syse, A. (2014). Access to treatment and educational inequalities in cancer survival. Journal of Health Economics, 36, 98–111. doi: 10.1016/j.jhealeco.2014.04.001.
  29. Cowan, W. M., Harter, D. H., & Kandel, E. R. (2000). The Emergence of Modern Neuroscience: Some Implications for Neurology and Psychiatry. Annual Review of Neuroscience, 23(1), 343–391. doi: 10.1146/annurev.neuro.23.1.343.
  30. OECD. “Staff Categories”. 2018,