The Relationship of Prenatal Alcohol Exposure and the Postnatal Environment to Child Depressive Symptoms

UCLA Neuropsychiatric Institute & Hospital, 760 Westwood Plaza, Room 68-265 A, Los Angeles, California 90024, USA.
Journal of Pediatric Psychology (Impact Factor: 2.91). 11/2005; 31(1):50-64. DOI: 10.1093/jpepsy/jsj021
Source: PubMed


This study examined the association between prenatal alcohol exposure and child depressive symptoms, and the mediating effects of maternal and child characteristics.
Participants were 42 children aged 4-5 years and their biological mothers. Prenatal alcohol consumption was assessed by self-report of maximum drinks per drinking occasion. The Pictorial Depression Scale (PDS) measured child depressive symptoms. Mother-child interactions were assessed using the family interaction puzzle task.
Structural equation modeling indicated that prenatal alcohol exposure was associated with more negative child affect. In turn, mothers of more negative children were less emotionally connected to their children, and those children had higher levels of depressive symptomatology. Results could not be explained by current maternal drinking patterns or maternal depression.
Study findings highlight the importance of examining prenatal alcohol exposure as a risk factor in the prediction of childhood-onset depression and the environmental mechanisms that may mediate that relationship.

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    • "Although several studies support the FKBP51:FKBP52 ratio model for the control of GR complex formation, subcellular localization and action, it is likely that there also are cell/tissue-specific mechanisms that contribute to the control of GR signaling [40]. It is interesting to note that alterations in FKBP51 levels have been implicated in psychiatric disorders, including depression [41], which have a higher incidence in FASD populations [42]. "
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    ABSTRACT: Prenatal alcohol exposure (PAE) has been shown to impair learning, memory and executive functioning in children. Perseveration, or the failure to respond adaptively to changing contingencies, is a hallmark on neurobehavioral assessment tasks for human fetal alcohol spectrum disorder (FASD). Adaptive responding is predominantly a product of the medial prefrontal cortex (mPFC) and is regulated by corticosteroids. In our mouse model of PAE we recently reported deficits in hippocampal formation-dependent learning and memory and a dysregulation of hippocampal formation glucocorticoid receptor (GR) subcellular distribution. Here, we examined the effect of PAE on frontal cortical-dependent behavior, as well as mPFC GR subcellular distribution and the levels of regulators of intracellular GR transport. PAE mice displayed significantly reduced response flexibility in a Y-maze reversal learning task. While the levels of total nuclear GR were reduced in PAE mPFC, levels of GR phosphorylated at serines 203, 211 and 226 were not significantly changed. Cytosolic, but not nuclear, MR levels were elevated in the PAE mPFC. The levels of critical GR trafficking proteins, FKBP51, Hsp90, cyclophilin 40, dynamitin and dynein intermediate chain, were altered in PAE mice, in favor of the exclusion of GR from the nucleus, indicating dysregulation of GR trafficking. Our findings suggest that there may be a link between a deficit in GR nuclear localization and frontal cortical learning deficits in prenatal alcohol-exposed mice.
    PLoS ONE 04/2014; 9(4):e96200. DOI:10.1371/journal.pone.0096200 · 3.23 Impact Factor
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    • "Thus, stress hyperresponsivity and HPA dysregulation may be a crucial factor mediating the increased vulnerability of these individuals to develop later psychopathologies (5, 31, 32). An aggravating factor to this already unfavorable situation is that individuals prenatally exposed to alcohol are, in general, at a higher risk of encountering a more stressful environment throughout the lifespan (12, 13, 33). "
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    ABSTRACT: Individuals exposed to alcohol during gestation show higher rates of psychopathologies. The hyperresponsivity to stress induced by prenatal alcohol exposure (PAE) may be related to this increased rate of psychopathologies, especially because this population is more likely to be exposed to stressful environments throughout life. However, alcohol-induced changes in the overlapping neurocircuitries that underlie stress and the expression of psychopathologies are not fully understood. Here, we performed a comprehensive analysis of the neural activity within central areas known to play key roles in both emotional and stress regulation. Adult male and female offspring from PAE, pair-fed, and ad libitum-fed control conditions were exposed to chronic mild stress (CMS). Following CMS, the neural activity (c-fos mRNA) of the amygdala, ventral hippocampal formation, medial prefrontal cortex (mPFC), and paraventricular nucleus of hypothalamus (PVN) was assessed in response to an acute stress (elevated plus maze). Our results demonstrate that, overall, PAE decreased neural activity within the amygdala and hippocampal formation in males and increased neural activity within the amygdala and mPFC in females. CMS reduced neural activity within the mPFC and PVN in PAE males, but reduced activity in all areas analyzed in control males. By contrast, CMS reduced neural activity in the mPFC in PAE females and had no effects in control females. Furthermore, the constrained principal component analysis revealed that these patterns of neural activity resulted in differential activation of the functional neural networks in males compared to females, indicating sexually dimorphic effects of PAE and CMS. Importantly, the altered networks of brain activation in PAE animals may underlie the hyperresponsivity to stress and increased psychopathologies observed among individuals prenatally exposed to alcohol.
    Frontiers in Endocrinology 02/2014; 5:5. DOI:10.3389/fendo.2014.00005
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    • "Some studies have identified a dose-response effect between prenatal alcohol exposure and behavioral problems taking together both the effects of environmental factors and prenatal alcohol exposure when evaluating the association with behavioral difficulties and psychiatric disorders in affected children (Hill et al., 2000; O'Connor and Paley, 2006; Guerri et al., 2009; Rodriguez et al., 2009). A recent observational cohort study including 592 adolescents observed that those exposed to an average of one or more drinks of alcohol per day in the first trimester of pregnancy were three times more likely to meet criteria for a lifetime diagnosis of conduct disorders than were adolescents whose mothers drank less than that amount or abstained (Larkby et al., 2011). "
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    ABSTRACT: Prenatal alcohol exposure can have serious and permanent adverse effects. The developing brain is the most vulnerable organ to the insults of prenatal alcohol exposure. A behavioral phenotype of prenatal alcohol exposure including conduct disorders is also described. This study on a sample of Brazilian adolescents convicted for criminal behavior aimed to evaluate possible clinical features of Fetal Alcohol Syndrome (FAS). These were compared to a control group of school adolescents, as well as tested for other environmental risk factors for antisocial behavior. A sample of 262 institutionalized male adolescents due to criminal behavior and 154 male students aged between 13 and 21 years comprised the study population. Maternal use of alcohol was admitted by 48.8% of the mothers of institutionalized adolescents and by 39.9% of the school students. In this sample of adolescents we could not identify individual cases with a clear diagnosis of FAS, but signs suggestive of FASD were more common in the institutionalized adolescents. Social factors like domestic and family violence were frequent in the risk group, this also being associated to maternal drinking during pregnancy. The inference is that in our sample, criminal behavior is more related to complex interactions between environmental and social issues including prenatal alcohol exposure.
    Genetics and Molecular Biology 12/2012; 35(4 (suppl)):960-5. DOI:10.1590/S1415-47572012000600011 · 1.20 Impact Factor
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