- Title: (Ms., Mr., Dr., Prof.)
- First Name
- Last Name
- University of Minnesota
- United States
- Postal Code
- dejos002 AT umn.edu
- Membership Status
- Student Member
- Title of Symposium
- ADAPTATION, NOT DEFICIT: HOW THE TYPE AND TIMING OF POVERTY INFLUENCES NEURODEVELOPMENT
- List the Chair(s) and All Presenter Names and Email Addresses
Annie Brandes-Aitken ([email protected])
Meriah DeJoseph ([email protected]) Chair and Presenter
LillyBelle Deer ([email protected])
Jamie Hanson ([email protected])
Eric Finegood ([email protected]estern.edu)
- Topics to be Addressed:
- Physiological Processes including hormonal modulation, Neurodevelopment and Plasticity including imaging work, Stress, Adversity
- Ages of Research Subjects
- infancy, adolescence
- Details of Research Subjects
- Ethical Agreement
- I agree
- Symposium Proposal Text (type or paste from Word doc)
Burgeoning research at the intersections of development and psychobiology has advanced our understanding of the potentially deleterious impacts of childhood poverty. In so doing, however, the field has often inadvertently adopted a deficit model, prompting recent calls for a move towards understanding how children adapt to heterogenous environmental demands present in the context of poverty. In this Young Investigators Symposium, we examine the role of several poverty-relevant contextual factors implicated in neurobiological development. Starting in infancy, Annie Brandes-Aitken will discuss how chronic parent stress influences early markers of infant regulation. Meriah DeJoseph then examines how the dose and timing of poverty-related adversity calibrates stress physiology systems in middle childhood, followed by LillyBelle Deer who compares the predictive utility of multiple indices of socioeconomic inequalities on child inflammation and reactivity. Moving into adolescence, Dr. Jamie Hanson will discuss learning-based contextual adaptations among youth experiencing high levels of economic stress, and Dr. Eric Finegood will explore how neighborhood violence shapes immune and inflammatory biomarkers in adolescence. Embedded throughout the talks are a variety of methods (adrenocortical, autonomic, immunological, EEG, MRI) and statistical approaches (causal inference models, computational modeling) that strengthen the scientific and social impacts of the findings. A new generation of interdisciplinary researchers across diverse institutions offer a unique perspective to addressing socially relevant questions with implications for policy that support today’s youth. The collective insights gleaned will generate meaningful discussion among ISDP members, inspiring future research aimed at elucidating the neurodevelopmental processes of adaptation in the context of economic hardship.
PARENT CORTISOL AND THE NEURAL UNDERPINNINGS OF ATTENTION AND EMOTION REGULATION IN INFANCY
Brandes-Aitken1 (Primary Presenter), S. Braren1, A. Greaves1, K. Kozak1, & N.H. Brito1
1New York University, New York, NY
Research suggests that parent stress is an important factor contributing to the development of child self-regulation abilities. In particular, infancy is a sensitive period for brain development during which the effects of parent stress may be especially pronounced. Thus, in the current study we investigated longitudinal associations of parent cortisol and neural markers of attention and emotion regulation from 3- to 9-months of age. Parents and their infants (N=100) were recruited from a wide range of socioeconomic backgrounds in the New York City area to participate in the study. Families visited the lab at infant ages 3 and 9 months. At the 3-month visit, caregiver hair was sampled and assayed for cortisol. Infant EEG was recorded during an attention eliciting video paradigm and theta power was calculated as a neural indicator of attention. At the 3- and 9-month visits resting EEG was recorded and alpha asymmetry was calculated as a neural indicator of emotion regulation. Between-person analyses indicated that higher levels of caregiver cortisol were associated with lower theta power at 3-months and decreased alpha asymmetry at 9-months of age. Within-person analyses indicated that higher cortisol levels were associated with a longitudinal decrease in alpha asymmetry across infancy. Results suggest that chronic parent stress predicts differences in the neural underpinnings of infant attention at 3-months and emotion regulation at 9-months of age. Examining associations between caregiver stress physiology and infant neural activity may help elucidate early mechanisms connecting environments of risk to differences in infant cognitive and emotional development.
A CAUSAL INFERENCE APPROACH FOR EXAMINING THE TIMING AND CHRONICITY OF POVERTY-RELATED ADVERSITY ON PROFILES OF CHILD STRESS RESPONSIVITY
M.L. DeJoseph1 (Primary Presenter), I.C. Stallworthy1, E.D. Finegood2, C.C. Raver3, C.B. Blair3,4, & D. Berry1
1University of Minnesota, Minneapolis, MN
2Northwestern University, Evanston, IL
3New York University, New York, NY
4New York University School of Medicine, New York, NY
The many environmental exposures often associated with childhood poverty—such as material scarcity, sociocognitive resources, and home and community violence—are theorized to alter stress response systems through the process of biological embedding. However, extant research remains mixed due to limitations with study design and the ways in which traditional statistical approaches examine the dosage and timing effects of poverty. The current study aims to fill this gap by presenting findings from a home-based Trier Social Stress Test (TSST-H) among a prospective, population-based longitudinal sample of children (N = 1,292; M age = 13.2 yrs; 48% female; 45% African American) in low-income communities. Separate latent profile models of salivary cortisol, alpha amylase, respiratory sinus arrhythmia, and blood pressure each revealed responsivity patterns that illustrated differential sensitivity to experience. To examine the extent to which the type, timing, and chronicity of poverty-related adversity (i.e. material deprivation, sociocognitive stimulation, emotional threat) predicts class membership, we applied a causal inference approach—marginal structural models—to empirically isolate the timing effects of each exposure while controlling for time-varying confounding variables. Specifically, we examined the effects of different sequences of exposure (no adversity, chronic adversity, and adversity isolated to infancy, toddlerhood, early childhood, and concurrent middle childhood) on latent profile membership. The combined methodological and substantive contributions of this study elucidate the temporal and cumulative dimensions of how the lived experiences of children in poverty become biologically embedded. Findings have implications for developmental science as well as for programs that support families experiencing economic inequalities.
SOCIOECONOMIC DISADVANTAGE, INFLAMMATION, AND CORTISOL REACTIVITY
L.K. Deer1 (Primary Presenter), A.M. Parenteau1, N.V. Alen1, & C.E Hostinar1
1University of California, Davis, Davis, CA
Children’s socioeconomic circumstances can influence the development of their stress-responsive systems like the HPA axis and immune system. However, socioeconomic status (SES) is a multifaceted construct operationalized in various ways across studies. Thus, it is unclear which SES facet is most strongly related to the activity of these systems. The present study sought to clarify this issue. Children ages 9-11 years old (M=9.92, SD=0.58; 49.1% female) provided salivary cortisol samples before and after the Trier Social Stress Test-Modified and serum cytokines (IL-6, IL-10, TNF-alpha), which were standardized and combined to create a composite measure of baseline inflammation. Parents provided information on parental education, family income, the use of government assistance (e.g., SNAP, WIC) and whether the family qualified for housing assistance from the Department of Housing and Urban Development. Sample size ranged from 100 to 175 across analyses. All analyses controlled for child age and sex. Analyses revealed that traditional measures of SES such as parental education and family income were not associated with inflammation, cortisol reactivity, or baseline cortisol. Receipt of government assistance was associated with higher inflammation, F(1,98)=5.17, p=.025, and higher baseline cortisol, F(1,171)=4.99, p=.027, but not with cortisol reactivity, p=.15. Participants who qualified for housing assistance showed higher cortisol reactivity, F(1,95)=6.35, p=.01. These results indicate that aspects of socioeconomic disadvantage such as use of government and housing assistance may be more strongly related to physiology.
ECONOMIC-MARGINALIZATION IS RELATED TO HEIGHTENED FEEDBACK LEARNING: THE ROLE OF STRESS-EXPOSURE AND REWARD NEUROBIOLOGY
J.L. Hanson1 (Primary Presenter)
1University of Pittsburgh
While child poverty can be viewed as detrimental, the developmental impacts of poverty may be better conceptualized as learning-based, contextual adaptations. Economically-marginalized environments may have different amounts of stress, and youth may become sensitized to and learn from specific types of positive and negative experiences in these contexts. Here, grounded in these ideas, we investigate the influence of poverty on learning processes and underlying neurobiology in a sample of youth from across the socioeconomic status spectrum (n=77; ages 12-17). Using a well-validated probabilistic learning task and computational modeling, we first found that poverty (operationalized by census-tract based economic indicators) was related to heightened learning for negative feedback (β=-0.451, p<0.005). We, next, focused on the structural connectivity of the corticostriatal circuit, a brain network critical to learning, motivation, and decision-making that includes the ventral striatum and different prefrontal subregions. We found that accumbofrontal pathways, critical white matter connecting the corticostriatal circuit, were related to poverty, with lower quantitative anisotropy relating to economic marginalization (β=0.361, p=0.009). Interestingly, these white matter differences statistically explained associations between poverty and heightened feedback learning (z=1.95, p=.05). Related to ideas of learning-based, contextual adaptations, we further investigated the role of stress exposure in these relations and only found these associations in high-stress exposed, economically-marginalized youth. Similar relations were not seen for learning from positive feedback. We ground and unpack our results in recent dimensional models of stress exposure noting that heightened sensitivity to negative feedback may be advantageous and adaptive in high stress contexts.
COMMUNITY VIOLENCE EXPOSURE AND PRO-INFLAMMATORY MONOCYTES DURING ADOLESCENCE
E.D. Finegood, (Primary Presenter), R. Weissman-Tsukamoto, L. Hoffer, E. Chen, & G. Miller
1Northwestern University, Evanston, IL
Community violence exposure is associated with physical health problems, but little is known about the biological processes involved. One possible mechanism may be stress-related increases in innate immune activity that promote systemic inflammation. Prior work from our laboratory has demonstrated that adolescents (8th graders) exposed to community violence evidence heightened numbers of circulating classical monocytes (CD14++CD16-), a pro-inflammatory leukocyte that is sensitive to stress exposure. In this follow-up analysis of Chicago-residing adolescents (n= 167) in 10th grade, we tested whether change in community violence exposure from 8th to 10th grade predicted classical monocyte counts at 10th grade. We utilized publicly available violent crime data in Chicago to calculate the sum of homicides within 1 mile of where youth lived in the six months prior to 8th and 10th grade laboratory visits and computed a delta score. Youth provided a fasting morning blood sample from which populations of classical monocytes were enumerated by flow cytometry. The association between change in homicide exposure from 8th to 10th grade and classical monocytes at 10th grade depended on youths’ homicide exposure in 8th grade (βHomicdesT1_X_ΔhomicidesT1T2=-0.35, p=0.007). Among those exposed to no homicides at 8th grade, an increase in homicide exposure was positively associated with monocytes in 10th grade (β=.24, p=.03). Among those exposed to a comparatively high number of homicides in 8th grade (+1SD from mean), there was no association (β=.09, p = .28). Results provide further evidence that pro-inflammatory monocytes may be sensitive to contextual stressors, and in particular, to community violence exposure.