Pilyoung Kim

Childhood Poverty and Health Cumulative Risk Exposure and Stress Dysregulation

A massive literature documents the inverse association between poverty or low socioeconomic status and health, but little is known about the mechanisms underlying this robust relation. We examined longitudinal relations between duration of poverty exposure since birth, cumulative risk exposure, and physiological stress in two hundred seven 13-year-olds. Chronic stress was assessed by basal blood pressure and overnight cortisol levels; stress regulation was assessed by cardiovascular reactivity to a standard acute stressor and recovery after exposure to this stressor. Cumulative risk exposure was measured by multiple physical (e.g., substandard housing) and social (e.g., family turmoil) risk factors. The greater the number of years spent living in poverty, the more elevated was overnight cortisol and the more dysregulated was the cardiovascular response (i.e., muted reactivity). Cardiovascular recovery was not affected by duration of poverty exposure. Unlike the duration of poverty exposure, concurrent poverty (i.e., during adolescence) did not affect these physiological stress outcomes. The effects of childhood poverty on stress dysregulation are largely explained by cumulative risk exposure accompanying childhood poverty.

Cumulative risk, maternal responsiveness, and allostatic load among young adolescents

The purpose of this study was to examine the impact of cumulative risk exposure in concert with maternal responsiveness on physiological indicators of chronic stress in children and youth. Middle-school children exposed to greater accumulated psychosocial (e.g., family turmoil, poverty) and physical (e.g., crowding, substandard housing) risk factors manifested higher levels of allostatic load, a physiological marker of cumulative wear and tear on the body caused by the mobilization of multiple, physiological response systems. This effect was longitudinal, residualizing allostatic load 3-4 years earlier when the youth were in elementary school. This effect, however, occurred only among adolescents with mothers low in responsiveness. Cumulative risk was also associated with dynamic cardiovascular processes in response to an acute stressor (mental arithmetic). Higher risk was associated with muted reactivity and slower, less efficient recovery in blood pressure. These dynamic cardiovascular effects occurred irrespective of maternal responsiveness.

Multiple risk exposure as a potential explanatory mechanism for the socioeconomic status–health gradient

The social patterning of disease and mortality provokes a search for explanation. One potential underlying explanation for socioeconomic status (SES) gradients in health is exposure to multiple risk factors. Income and class tend to sort individuals into different settings that are often accompanied by systematic differences in environmental quality. Housing and neighborhood quality, pollutants and toxins, crowding and congestion, and noise exposure all vary with SES. Persons lower in SES also experience more adverse interpersonal relationships with family members, friends, supervisors, and community members. Furthermore, exposure to these multiple risk factors is associated with worse health outcomes. Thus, the convergence of exposure to multiple physical and psychosocial risk factors accompanying disadvantage may account for a portion of SES gradients in health in both childhood and adulthood.

Effects of childhood poverty and chronic stress on emotion regulatory brain function in adulthood

Significance Childhood poverty has been linked to emotion dysregulation, which is further associated with negative physical and psychological health in adulthood. The current study provides evidence of prospective associations between childhood poverty and adult neural activity during effortful attempts to regulate negative emotion. Adults with lower family income at age 9 exhibited reduced ventrolateral and dorsolateral prefrontal cortex activity and failure to suppress amygdala activation at age 24. Chronic stressor exposure across childhood mediated the relations between family income at age 9 and prefrontal cortex activity. The concurrent adult income, on the other hand, was not associated with neural activity. The information on the developmental timing of poverty effects and neural mechanisms may inform early interventions aimed at reducing health disparities. Childhood poverty has pervasive negative physical and psychological health sequelae in adulthood. Exposure to chronic stressors may be one underlying mechanism for childhood poverty−health relations by influencing emotion regulatory systems. Animal work and human cross-sectional studies both suggest that chronic stressor exposure is associated with amygdala and prefrontal cortex regions important for emotion regulation. In this longitudinal functional magnetic resonance imaging study of 49 participants, we examined associations between childhood poverty at age 9 and adult neural circuitry activation during emotion regulation at age 24. To test developmental timing, concurrent, adult income was included as a covariate. Adults with lower family income at age 9 exhibited reduced ventrolateral and dorsolateral prefrontal cortex activity and failure to suppress amygdala activation during effortful regulation of negative emotion at age 24. In contrast to childhood income, concurrent adult income was not associated with neural activity during emotion regulation. Furthermore, chronic stressor exposure across childhood (at age 9, 13, and 17) mediated the relations between family income at age 9 and ventrolateral and dorsolateral prefrontal cortex activity at age 24. The findings demonstrate the significance of childhood chronic stress exposures in predicting neural outcomes during emotion regulation in adults who grew up in poverty.

Breastfeeding, brain activation to own infant cry, and maternal sensitivity

BACKGROUND Research points to the importance of breastfeeding for promoting close mother-infant contact and social-emotional development. Recent functional magnetic resonance imaging (fMRI) studies have identified brain regions related to maternal behaviors. However, little research has addressed the neurobiological mechanisms underlying the relationship between breastfeeding and maternal behavior in human mothers. We investigated the associations between breastfeeding, maternal brain response to own infant stimuli, and maternal sensitivity in the early postpartum. METHODS Seventeen biological mothers of healthy infants participated in two matched groups according to feeding method - exclusive breastfeeding and exclusive formula-feeding at 2-4 weeks postpartum. fMRI scanning was conducted in the first postpartum month to examine maternal brain activation in response to her own babys cry versus control baby-cry. Dyadic interactions between mothers and infants at 3-4 months postpartum were videotaped in the home and blindly coded for maternal sensitivity. RESULTS In the first postpartum month, breastfeeding mothers showed greater activations in the superior frontal gyrus, insula, precuneus, striatum, and amygdala while listening to their own baby-cry as compared to formula-feeding mothers. For both breastfeeding and formula-feeding mothers, greater activations in the right superior frontal gyrus and amygdala were associated with higher maternal sensitivity at 3-4 months postpartum. CONCLUSIONS Results suggest links between breastfeeding and greater response to infant cues in brain regions implicated in maternal-infant bonding and empathy during the early postpartum. Such brain activations may facilitate greater maternal sensitivity as infants enter their social world.

Approaching the biology of human parental attachment: brain imaging, oxytocin and coordinated assessments of mothers and fathers.

Brain networks that govern parental response to infant signals have been studied with imaging techniques over the last 15 years. The complex interaction of thoughts and behaviors required for sensitive parenting enables the formation of each individuals first social bonds and critically shapes development. This review concentrates on magnetic resonance imaging experiments which directly examine the brain systems involved in parental responses to infant cues. First, we introduce themes in the literature on parental brain circuits studied to date. Next, we present a thorough chronological review of state-of-the-art fMRI studies that probe the parental brain with a range of baby audio and visual stimuli. We also highlight the putative role of oxytocin and effects of psychopathology, as well as the most recent work on the paternal brain. Taken together, a new model emerges in which we propose that cortico-limbic networks interact to support parental brain responses to infants. These include circuitry for arousal/salience/motivation/reward, reflexive/instrumental caring, emotion response/regulation and integrative/complex cognitive processing. Maternal sensitivity and the quality of caregiving behavior are likely determined by the responsiveness of these circuits during early parent-infant experiences. The function of these circuits is modifiable by current and early-life experiences, hormonal and other factors. Severe deviation from the range of normal function in these systems is particularly associated with (maternal) mental illnesses - commonly, depression and anxiety, but also schizophrenia and bipolar disorder. Finally, we discuss the limits and extent to which brain imaging may broaden our understanding of the parental brain given our current model. Developments in the understanding of the parental brain may have profound implications for long-term outcomes in families across risk, resilience and possible interventions. This article is part of a Special Issue entitled Oxytocin and Social Behav.

Resilience after 9/11: Multimodal neuroimaging evidence for stress-related change in the healthy adult brain

Exposure to psychological trauma is common and predicts long-term physical and mental health problems, even in those who initially appear resilient. Here, we used multimodal neuroimaging in healthy adults who were at different distances from the World Trade Center on 9/11/01 to examine the neural mechanisms that may underlie this association. More than 3 years after 9/11/01, adults with closer proximity to the disaster had lower gray matter volume in amygdala, hippocampus, insula, anterior cingulate, and medial prefrontal cortex, with control for age, gender, and total gray matter volume. Further analysis showed a nonlinear (first-order quadratic) association between total number of traumas in lifetime and amygdala gray matter volume and function in the whole group. Post hoc analysis of subgroups with higher versus lower levels of lifetime trauma exposure revealed systematic associations between amygdala gray matter volume, amygdala functional reactivity, and anxiety that suggest a nonlinear trajectory in the neural response to accumulated trauma in healthy adults.

Childhood Poverty and Young Adults’ Allostatic Load: The Mediating Role of Childhood Cumulative Risk Exposure

Childhood poverty is linked to a host of physical and psychological disorders during childhood and later in life. In the study reported here, we showed that the proportion of childhood spent in poverty from birth to age 9 was linked to elevated allostatic load, a marker of chronic physiological stress, in 17-year-olds. Furthermore, this prospective longitudinal relationship was mediated by cumulative risk exposure at age 13. The greater the duration of early life spent in poverty, the greater the exposure to cumulative risk. This, in turn, leads to elevated allostatic load. Multiple psychological, biological, and neurological pathways likely account for the social patterning of psychological and physical disease.

Perceived quality of maternal care in childhood and structure and function of mothers' brain

Animal studies indicate that early maternal care has long-term effects on brain areas related to social attachment and parenting, whereas neglectful mothering is linked with heightened stress reactivity in the hippocampus across the lifespan. The present study explores the possibility, using magnetic resonance imaging, that perceived quality of maternal care in childhood is associated with brain structure and functional responses to salient infant stimuli among human mothers in the first postpartum month. Mothers who reported higher maternal care in childhood showed larger grey matter volumes in the superior and middle frontal gyri, orbital gyrus, superior temporal gyrus and fusiform gyrus. In response to infant cries, these mothers exhibited higher activations in the middle frontal gyrus, superior temporal gyrus and fusiform gyrus, whereas mothers reporting lower maternal care showed increased hippocampal activations. These findings suggest that maternal care in childhood may be associated with anatomy and functions in brain regions implicated in appropriate responsivity to infant stimuli in human mothers.

Neuroendocrinology of Parental Response to Baby‐Cry

This overview attempts to synthesise current understandings of the neuroendocrine basis of parenting. The parent–infant bond is central to the human condition, contributes to risks for mood and anxiety disorders, and provides the potential for resiliency and protection against the development of psychopathology. Animal models of parenting provide compelling evidence that biological mechanisms may be studied in humans. This has led to brain imaging and endocrine system studies of human parents using baby stimuli and concerted psychological and behavioural measures. Certain brain circuits and related hormonal systems, including subcortical regions for motivation (striatum, amygdala, hypothalamus and hippocampus) and cortical regions for social cognition (anterior cingulate, insula, medial frontal and orbitofrontal cortices), appear to be involved. These brain circuits work with a range of endocrine systems to manage stress and motivate appropriate parental caring behaviour with a flexibility appropriate to the environment. Work in this field promises to link evolving models of parental brain performance with resilience, risk and treatment toward mother–infant mental health.