General, research

childhood poverty, stress, and the brain

—disclaimer: I am certainly not an expert on this topic, but I’m trying to learn more because this topic intersects interests I have with my students’ interests, and writing helps me organize what I’ve learned.—

Research expands our knowledge and (should) ultimately solve problems. One of the world’s current wicked problems is poverty. In 2016, the poverty rate was 12.7% in the United States, or, in other words, 40.6 million people were living in poverty. Poverty rates are higher yet among young folks, with 17.4% of males and 18.4% of females under 18 living in poverty. Yet societal systems reinforce poverty and make socioeconomic mobility exceedingly difficult. In fact, many poverty interventions fail because they do not take into account the complexity of the problem. For example, providing educational interventions to parents is likely fruitless when they do not have the time to participate in educational programming or the transportation to get there. There is no one solution to a wicked problem. But arguably, what we know about the brain and neuroplasticity should motivate us to fix systemic problems, such as poverty traps, that harm children and make it exceedingly challenging to escape poverty.

The human brain is uniquely “underdeveloped” when we are born, setting the stage environmental sensitivity. Total brain volume doesn’t peak until ages 11-14. Gray matter peaks earlier, around ages 9-11 and then undergoes extensive pruning to eliminate unnecessary synapses. Gray matter peaks latest in brain regions involved in higher order cognition, such as the dorsolateral prefrontal cortex. These late-developing regions are also known as association areas because they help integrate signals from many other brain regions, playing a critical role in learning and judgment. White matter volume continues to increase into our early 20s, as does ventricular size. Reflecting these structural changes, functional neural networks markedly change throughout childhood and adolescent development.

Brain development is intertwined with social and environmental context. As the brain develops, it responds to environmental challenges and demands. For example, past research suggests that rats raised in enriched environments have more cortical growth in dorsal regions and rats raised in impoverished environments have deficits in cortical growth in lateral regions. The ability of the brain to change in response to experience is called plasticity. Molecular, cellular, systems, behavioral, and cognitive research demonstrates that the brain is highly plastic.

One of the most critical environmental contexts that can impede neural development is early life stress. Stress is like a transaction with the environment. Stressors are physical and psychological stimuli that are perceived as a threat, and poverty and low SES are associated with more stressors.

Stress activates the sympathetic nervous system (e.g., the four F’s: fight, flight, fear, and sex OR tend & befriend) and the hypothalamus-pituitary-adrenal (HPA) axis. When the HPA axis activates, this leads to the release of norepinephrine, epinephrine, and glucocorticoids (a steroid hormone). Glucocorticoids bind to and activate receptors throughout the body and the brain, including in the hypothalamus, hippocampus, and the prefrontal cortex.

Stress is biologically adaptive and necessary for survival. Therefore, the stress response prepares the body to deal with the stressor. To do so, the stress response mobilizes energy stores and dampens immune and inflammatory responses. We become alert, aroused, and ready to deal with our stressor.

This is helpful if we are dealing with an acute stressor. However, early life trauma and chronic stressors can overload the ability of the individual to cope with and respond to stressors on both physiological and psychological levels.

High levels of glucocorticoids over time can dampen long term potentiation (LTP) and facilitate long term depression (LTD). LTP is activity-dependent strengthening of a synapse – a trace of a neuron’s past experiences. Synapses are strengthened through several mechanisms such as increasing receptor activity, adding more receptors to the postsynaptic neuron, and gene transcription. LTP exerts its effects most notably in the hippocampus, where it is considered at least one mechanism for memory formation. LTD, on the other hand, weakens synapses may lead to memory decay. Glucocorticoids can also act as transcription factors (TF), which coordinate gene expression, leading to long-term changes in brain function.

Long term effects of stress include increased susceptibility to mental illness, such as depression or posttraumatic stress disorder. Early life exposure to trauma or chronic stress lead to brain changes that increase vulnerability to later stressors by creating long lasting changes in neuroendocrine reactivity. This vulnerability hypothesis suggests that early life stress lead to reduced hippocampal volume, which is a risk factor for later life stress disorders.

Early life (postnatal) stressors include a host of adverse childhood experiences such as living in poverty, physical, sexual, and emotional maltreatment, parental mental illness, and maternal separation. For example, children exposed to severe trauma show lower basal levels of glucocorticoids but children who experience maternal separation (such as full day-day care) show higher levels of glucocorticoids. Brain regions undergoing developmental changes are likely more sensitive to the effects of stress. For example, the prefrontal cortex and amygdala have prolonged developmental periods (into the teens and early 20s), therefore stress exposure through adolescence may have detrimental effects on prefrontal cortex development.

Epigenetics are a possible mechanism for the effect of early life stress on later mental health. Three epigenetic factors (DNA methylation, postranslational histone modifications, and small non-coding RNAs) may be key molecular mechanisms for increased mental health risks. Epigenetic factors create the neural groundwork that impacts later life ability to cope with stressors. In addition the the vulnerability hypothesis (above), the neurotoxicity hypothesis suggests that extended exposure to stress and glucocorticoids lessens neuronal resistance to stressors. Therefore, chronic stress leads the brain to be more susceptible to effects from any added stress endured later in life.

Our interpretation of stressors is key to determining how we physiologically and psychologically cope with stress. Our early life models for responding to stressors, too, have an impact on our perception of stressors. Predictability and control are two critical factors for understanding whether we interpret a stimulus as a stressor. For example, an unpredictable early life environment signals to a child that s/he cannot reliably depend on resources (financial, emotional, social, or otherwise) being available later on. In other words, poverty and early life stress lead to psychological consequences that reinforce poverty, making it difficult to escape.

The brain regions most susceptible to stress effects early in life are the prefrontal cortex and the hippocampus. The prefrontal cortex plays an important role in self control, impulsivity, valuation, and higher order cognition. The hippocampus is important for declarative memory. Beyond the effects of stress discussed above, research suggests that lower SES is associated with lower dopamine receptor availability. Behaviorally, research suggests that lower childhood SES is associated with more impulsivity in ambiguous/uncertain situations. Impulsivity is a highly adaptive response given the circumstances (e.g., take what’s available now because the future is uncertain), but is less adaptive when provided more resources. Yet, humans are phenomenal at learning and our early life learning sets the stage for how we respond to future challenges. Therefore it is incredibly challenging to “unlearn” to respond impulsively if that behavior has been reinforced throughout childhood. Relatedly, dispositional self control seems to be associated with better psychosocial outcomes among children with lower SES, but it comes at the cost of physical health, as if the demands of self control tip the individual into an allostatic overload.

So what are we to do? SES relates to prenatal factors, parental care, and cognitive stimulation, all of which impact brain development resulting in differential socioemotional and cognitive development. What’s more, the disparities in SES are incredibly concerning. Childcare, education, material resources, and parental well being are critical to improving outcomes of children in low SES homes. But fixing the problem of early life stress, low SES, and poverty needs to meet folks where they are at. Yet many “interventions” or policies require high agency (i.e., they require work by the individual). High agency interventions completely miss the point.

Some people might argue that most research on SES and poverty is correlational and therefore we cannot infer a direction of causality. This is the social causation versus social selection hypothesis (i.e., does being poor cause cognitive/mental health problems or vice versus?). Ample research favors social causation. In other words, folks are NOT predisposed to poverty. In fact, moving folks out of poverty alleviates many cognitive and emotional challenges they faced. In a quasi-experimental longitudinal study, researchers found that increased income (such that a family moved from below to above poverty levels) had a major influence on the development of several personality disorders. Similar longitudinal research finds similar results, where an income intervention improves parental relationships and benefits childhood mental health.

In other words, minimizing and ideally eliminating poverty could improve cognitive and mental health and well being of society as a whole. This is important because approximately 20% of Americans have been diagnosed with a mental illness in the past year.

Poverty itself seems to reinforce poverty because of how the ecology of poverty challenges healthy neural and behavioral development. Growing up in impoverished, often highly stressful environments negatively affects neural development. Children exposed to early life stress have an exhausted neural reservoir. Interventions to alleviate poverty should focus on childhood poverty. This may include targeting prenatal factors, parental care, and educational interventions. But it also may include directly increasing family incomes. Importantly, interventions need to be low agency (i.e., they don’t require work by the individual) and accessible.

 

References and further reading

Akee, R., Copeland, W., Costello, E. J., & Simeonova, E. (2018). How Does Household Income Affect Child Personality Traits and Behaviors? The American Economic Review, 108(3), 775–827. https://doi.org/10.1257/aer.20160133

Bureau, U. C. (n.d.). Income and Poverty in the United States: 2016. Retrieved July 5, 2018, from https://www.census.gov/library/publications/2017/demo/p60-259.html

Diamond, M. C., Rosenzweig, M. R., Bennett, E. L., Linder, B., & Lyon, L. (1972). Effects of environmental enrichment and impoverishment on rat cerebral cortex. Journal of Neurobiology, 3, 47-64.

de Kloet, E. R., Joëls, M., & Holsboer, F. (2005). Stress and the brain: from adaptation to disease. Nature Reviews. Neuroscience, 6(6), 463–475. https://doi.org/10.1038/nrn1683

Giedd, J. N., & Rapoport, J. L. (2010). Structural MRI of Pediatric Brain Development: What Have We Learned and Where Are We Going? Neuron, 67(5), 728–734. https://doi.org/10.1016/j.neuron.2010.08.040

Hackman, D. A., & Farah, M. J. (2009). Socioeconomic status and the developing brain. Trends in Cognitive Sciences, 13(2), 65–73. https://doi.org/10.1016/j.tics.2008.11.003

Haushofer, J., & Fehr, E. (2014). On the psychology of poverty. Science, 344(6186), 862–867. https://doi.org/10.1126/science.1232491

Insel, T. R. (2008). Assessing the Economic Costs of Serious Mental Illness. American Journal of Psychiatry, 165(6), 663–665. https://doi.org/10.1176/appi.ajp.2008.08030366

Kundakovic, M., & Champagne, F. A. (2015). Early-Life Experience, Epigenetics, and the Developing Brain. Neuropsychopharmacology, 40(1), 141–153. https://doi.org/10.1038/npp.2014.140

Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10(6), 434–445. https://doi.org/10.1038/nrn2639

Miller, G. E., Yu, T., Chen, E., & Brody, G. H. (2015). Self-control forecasts better psychosocial outcomes but faster epigenetic aging in low-SES youth. Proceedings of the National Academy of Sciences, 112(33), 10325–10330. https://doi.org/10.1073/pnas.1505063112

Mittal, C., & Griskevicius, V. (2014). Sense of control under uncertainty depends on people’s childhood environment: A life history theory approach. Journal of Personality and Social Psychology, 107(4), 621–637. https://doi.org/10.1037/a0037398

Pepper, G. V., & Nettle, D. (2017). The behavioural constellation of deprivation: Causes and consequences. Behavioral and Brain Sciences, 40. https://doi.org/10.1017/S0140525X1600234X

Power, J. D., Fair, D. A., Schlaggar, B. L., & Petersen, S. E. (2010). The Development of Human Functional Brain Networks. Neuron, 67(5), 735–748. https://doi.org/10.1016/j.neuron.2010.08.017

Wiers, C. E., Shokri-Kojori, E., Cabrera, E., Cunningham, S., Wong, C., Tomasi, D., … Volkow, N. D. (2016). Socioeconomic status is associated with striatal dopamine D2/D3 receptors in healthy volunteers but not in cocaine abusers. Neuroscience Letters, 617, 27–31. https://doi.org/10.1016/j.neulet.2016.01.056

 

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