Neuropsychopharmacology. 2015 Mar;40(4):996-1004.
The long-term impact of early life poverty on orbitofrontal cortex volume in adulthood: results from a prospective study over 25 years.
- 1Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany.
- 2Department of Biostatistics, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany.
- 31] Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany  Department of Neuroimaging, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany.
- 4Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany.
- 5Department of Psychology, University of Potsdam, Potsdam OT Golm, Germany.
- 61] Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany  Department of Child and Adolescent Psychiatry, University of Zurich, Zurich, Switzerland.
- 71] Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany  Department of Psychology, University of Potsdam, Potsdam OT Golm, Germany.
Converging evidence has highlighted the association between poverty and conduct disorder (CD) without specifying neurobiological pathways. Neuroimaging research has emphasized structural and functional alterations in the orbitofrontal cortex (OFC) as one key mechanism underlying this disorder. The present study aimed to clarify the long-term influence of early poverty on OFC volume and its association with CD symptoms in healthy participants of an epidemiological cohort study followed since birth. At age 25 years, voxel-based morphometry was applied to study brain volume differences. Poverty (0=non-exposed (N=134), 1=exposed (N=33)) and smoking during pregnancy were determined using a standardized parent interview, and information on maternal responsiveness was derived from videotaped mother-infant interactions at the age of 3 months. CD symptoms were assessed by diagnostic interview from 8 to 19 years of age. Information on life stress was acquired at each assessment and childhood maltreatment was measured using retrospective self-report at the age of 23 years. Analyses were adjusted for sex, parental psychopathology and delinquency, obstetric adversity, parental education, and current poverty. Individuals exposed to early life poverty exhibited a lower OFC volume. Moreover, we replicated previous findings of increased CD symptoms as a consequence of childhood poverty. This effect proved statistically mediated by OFC volume and exposure to life stress and smoking during pregnancy, but not by childhood maltreatment and maternal responsiveness. These findings underline the importance of studying the impact of early life adversity on brain alterations and highlight the need for programs to decrease income-related disparities.
A variety of studies have demonstrated that environmental adversity confers risk for later psychopathology, both internalizing and externalizing disorders (Holz, Laucht, & Meyer-Lindenberg, 2015). In this line, poverty has been outlined as comprising an environmental factor which increases the risk of conduct disorder (CD). So far, however, the mechanisms behind this association remain unclear. Moreover, research is lacking which provides a link between early adversity, morphometric brain changes, and psychopathology. In the study presented below, we tried to answer this question by examining whether socioeconomic disadvantage, i.e., early life poverty, may converge in neural alterations leading to a compromised brain structure related to CD.
Figure 1. Assessment waves through lifetime. Participation rates are indicated in italics on the top of each assessment.
We concentrated on the impact of early life poverty on the orbitofrontal cortex (OFC), which is amongst others related to control processes of affective processing and has been identified as a key region compromised in CD. The study was performed in the framework of the Mannheim Study of Children at Risk, which is an epidemiological cohort study conducted over 30 years since birth (Laucht, Esser, & Schmidt, 1997) (Figure 1). Given the prospective design with continuous psychopathological and ecological assessments, the study is predestined to examine the long-term effects of early life adversities. Early risk of poverty was determined in 167 young adults (67 males) (non-exposed: N=134, exposed: N=33) and CD symptoms were assessed using standardized psychiatric interviews during childhood and adolescence. To assess volume differences in the OFC, voxel-based morphometry data were acquired during early adulthood. When investigating the long-term vestiges of such early risk factors, it is essential to ensure that the analyzed associations could not be attributed to confounding factors, which are likely to coincide with early life poverty. As such, it has been demonstrated that poverty is associated with a wide range of related risks including parental psychopathology, lower parental education, obstetric adversity, as well as substance abuse in the offspring. While the former were all assessed shortly after birth, the latter comprised lifetime sum scores of alcohol, nicotine and cannabis abuse in the offspring. In addition, to rule out that current poverty accounts for the effects, analyses were also controlled for this confounder. Our results revealed that early life poverty is associated with more CD symptoms as well as a decreased OFC volume. Further, given that poverty is a distal risk factor, we examined whether other more proximal measures are likely to mediate the association. One of the behavioral correlates investigated refers to the amount of life stress encountered by the offspring, which was measured at each assessment by a semi-structured interview. A second related risk factor is smoking during pregnancy with increased rates being observed in mothers living in poverty. Our findings showed three different pathways by which poverty may exert its effects on CD. First, from a neurobiological perspective, poverty was related to a decreased volume in the OFC, which, in turn, was associated with more CD symptoms. Second, on a behavioral level, we identified a higher level of smoking during pregnancy and stressful life events encountered by the offspring as two possible trajectories mediating the relationship between poverty and CD (Figure 2). In conclusion, the findings presented here highlight the detrimental impact of exposure to adversity in the early postnatal period and during childhood on brain structure related to externalizing psychopathology. Given that 20% of children in the Western population is currently at risk of poverty, we strongly encourage the need for programs aimed at decreasing income-related disparities in young families and the implementation of preventive health care programs during childhood in high-risk groups.
Figure 2. Mediation of the relationship between poverty and conduct disorder by volume in the orbitofrontal cortex (top), smoking during pregnancy (middle) and stressful life events (bottom).
Holz, N. E., Laucht, M., & Meyer-Lindenberg, A. (2015). Recent advances in understanding the neurobiology of childhood socioeconomic disadvantage. Curr Opin Psychiatry, 28(5), 365-370. doi:10.1097/YCO.0000000000000178
Laucht, M., Esser, G., & Schmidt, M. H. (1997). Developmental outcome of infants born with biological and psychosocial risks. Journal of Child Psychology and Psychiatry and Allied Disciplines, 38(7), 843-853.