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College of Arts, Humanities & Social Sciences

Department of Psychology

Psychology Matters

Diversity Matters

dversitymattersBy Alex Dufford
Doctoral Candidate




There is increasing evidence that stressful experiences during childhood can have long-lasting relationships with physical and mental health later in life. However, to attempt to mitigate this relationship, there is a need to understand its possible underlying mechanisms. The developing brain has become a recent mechanism of interest as it is both influenced by environmental factors and plays a key role in the maintenance of physical and mental health. The brain is also a potential important mechanistic pathway as it has a 'protracted' development and therefore childhood experience may have a particularly strong associated with its developmental trajectory. Aligning with the research goals of the Stress Early Experiences and Development research center, the Family and Child Neuroscience lab, seeks to understand how individual differences in stressful early experiences may be associated with brain development and developmental outcomes later in life.

The Family and Child Neuroscience (FCN) lab focuses on socioeconomic disadvantage (SED) as a particularly stressful early life experience that has been shown to have a robust relationship with brain development. There is consistent evidence that childhood SED is associated with the gray matter structure of a brain region involved in memory known as the hippocampus. While this relationship has been established, it is unclear how it is related to specific behaviors. Typically, studies focus on the SED-hippocampus relationship and its further associations with cognitive outcomes such as memory and learning. However, in a recent study published by Dr. Pilyoung Kim and I, the SED-hippocampus relationship was extended to focus on socioemotional outcomes. In the study (Dufford, Bianco, & Kim, 2019), childhood SED in middle childhood (8-10) was associated with hippocampus gray matter volume and the gray matter volume of another structure known as the 'amygdala'. Participants in the study also participated in a measure of their attentional bias to threat or their likelihood to orient their attention to threatening face stimuli. Interestingly, lower hippocampal volume was associated with greater attentional bias to threat. As attentional bias to threat is an early cognitive marker for anxiety disorders, this study has found preliminary evidence for pathways of association between childhood SED, hippocampus volume, and attentional bias to threat. Therefore, the hippocampal associations with childhood SED may not be unique to cognitive outcomes but may? further extend to socioemotional outcomes. This is critical as experiencing childhood SED has been associated with an increased likelihood of experiencing anxiety and depression in adulthood.

My colleagues and I also extended the knowledge about childhood SED and brain development beyond gray matter in the brain. The gray matter of the brain is primarily responsible for the computation of the brain, however white matter is the information 'super highways' of the brain. White matter is the pathways in which brain regions communicate information between one another. White matter development is also protracted and does not complete it development until a person is in their mid-20s. In a study of childhood SED and white matter, the study found that there was a relationship between childhood SED and white matter organization in several white matter tracts in the brain (Dufford & Kim, 2017). Specifically, this relationship was found in white matter tracts that are involved in socioemotional processing, language, and executive functioning. In a subset of these regions, greater exposure to multiple risk factors had an inverse relationship with the white matter organization. This study provided preliminary evidence that white matter organization in the brain is associated with both childhood SED and the cumulative amount of multiple risk factors in childhood.

These and other studies have led to a focus on the 'cumulative risk exposure' as a potential mechanistic pathway underlying the association between childhood SED and brain development. The cumulative risk model suggests exposure to multiple risk factors may have an overwhelming impact on development (and neurodevelopment) due to the multiple risks exceeding the adaptive capacities of the individual. Any given person may have exposure to few risk factors, however; SED is a unique experience which is usually associated with exposure to multiple risks at given time. Some examples of risk factors include exposure to: noise, crowding, poor housing quality, family violence, family turmoil, and separation from the family. The cumulative risk model treats exposure to risks equally and provides a single score representing the additive cumulative risk exposure. The cumulative risk model has been studied as a potential mechanistic pathway underlying the relationship between childhood SED and physiological measures (such as allostatic load). However, recently it has become a potential mechanism of interest for studies of brain development. The FCN lab's future work will include examining childhood cumulative risk exposure as a mediator of the relationship between childhood SED and brain structure in adulthood.

Overall, there is a relationship between childhood SED and brain development. This relationship may contribute to physical and mental health disparities across the lifespan. Therefore, to disrupt this relationship, mechanistic relationships must be identified, and interventions must be targeted while realizing that intervention will not be "one size fits all". Neurodevelopment and its relationship to environmental influences is enormously complex and a focus on individual differences will be paramount. Like the relationship between height and body weight, there is individual variation in the association between childhood SED and brain development and therefore these relationships are 'on average' and cannot provide information about any given person. Further, we highlight that these associations are not fixed or immutable. The ability of the brain to adapt to adverse circumstances is enormous and there is increasing evidence that environmental interventions (such as a parenting intervention) may act as 'buffers' of this relationship. Therefore, a focus on individual differences in early experiences will be key in understanding way in which to effectively mitigate income-related health disparities.


  • Dufford, A. J., Bianco, H., & Kim, P. (2019). Socioeconomic disadvantage, brain morphometry, and attentional bias to threat in middle childhood. Cognitive, Affective, & Behavioral Neuroscience, 19(2), 309-326.
  • Dufford, A. J., & Kim, P. (2017). Family income, cumulative risk exposure, and white matter structure in middle childhood. Frontiers in human neuroscience, 11, 547.