Early adversity and the prospective prediction of depressive and anxiety disorders in adolescents

Department of Psychology, University of California, Los Angeles, California 90095, USA.
Journal of Abnormal Child Psychology (Impact Factor: 3.09). 03/2005; 33(1):13-24. DOI: 10.1007/s10802-005-0930-3
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ABSTRACT The current study was a prospective exploration of the specificity of early childhood adversities as predictors of anxiety and depressive disorders in adolescents. Participants were 816 adolescents (414 males, 402 females) with diagnostic information collected at age 15; information on early adversities had been collected from the mothers during pregnancy, at birth, age 6 months, and age 5 years for a related study. Adolescents with "pure" anxiety disorders were compared with adolescents with "pure" depressive disorders (major depressive disorder, dysthymia), and these groups were compared to never-ill controls. Analyses controlled for gender and maternal depression and anxiety disorders. Results indicated that adolescents with anxiety disorders were more likely than depressed youth to have been exposed to various early stressors, such as maternal prenatal stress, multiple maternal partner changes, and more total adversities, whereas few early childhood variables predicted depressive disorders. Even when current family stressors at age 15 were controlled, early adversity variables again significantly predicted anxiety disorders. Results suggest that anxiety disorders may be more strongly related to early stress exposure, while depressive disorders may be related to more proximal stressors or to early stressors not assessed in the current study.

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Available from: Patricia A Brennan, Aug 23, 2015
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    • "In humans, for example, retrospective studies and, more recently, prospective studies, document the increased occurrence of emotional problems in children and adolescents whose mothers experienced emotional stress during pregnancy (Talge et al., 2007). Exposure to various types of stressors in utero, such as obstetric complications, psychological stress, natural disasters or intra-uterine infections, has also been associated with an increased risk of developing anxiety, depressive states, schizophrenia, ADHD, autism and substance abuse (Melichar et al., 2001; Koenig et al., 2002; Ben Amor et al., 2005; Phillips et al., 2005; Szpir, 2006; Khashan et al., 2008; Weinstock, 2011). These commonest brain disorders typically exhibit a neurodevelopment component and a sex bias, as well as an involvement of midbrain dopaminergic circuitry. "
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    ABSTRACT: The knowledge that diverse populations of dopaminergic neurons within the ventral tegmental area (VTA) can be distinguished in terms of their molecular, electrophysiological and functional properties, as well as their differential projections to cortical and subcortical regions has significance for key brain functions, such as the regulation of motivation, working memory and sensorimotor control. Almost without exception, this understanding has evolved from landmark studies performed in the male sex. However, converging evidence from both clinical and pre-clinical studies illustrates that the structure and functioning of the VTA dopaminergic systems are intrinsically different in males and females. This may be driven by sex differences in the hormonal environment during adulthood ('activational' effects) and development (perinatal and/or pubertal 'organizational' effects), as well as genetic factors, especially the SRY gene on the Y chromosome in males, which is expressed in a sub-population of adult midbrain dopaminergic neurons. Stress and stress hormones, especially glucocorticoids, are important factors which interact with the VTA dopaminergic systems in order to achieve behavioral adaptation and enable the individual to cope with environmental change. Here, also, there is male/female diversity not only during adulthood, but also in early life when neurobiological programing by stress or glucocorticoid exposure differentially impacts dopaminergic developmental trajectories in male and female brains. This may have enduring consequences for individual resilience or susceptibility to pathophysiological change induced by stressors in later life, with potential translational significance for sex bias commonly found in disorders involving dysfunction of the mesocorticolimbic dopaminergic systems. These findings highlight the urgent need for a better understanding of the sexual dimorphism in the VTA if we are to improve strategies for the prevention and treatment of debilitating conditions which differentially affect men and women in their prevalence and nature, including schizophrenia, attention/deficit hyperactivity disorder, autism spectrum disorders, anxiety, depression and addiction.
    Neuroscience 06/2014; 282. DOI:10.1016/j.neuroscience.2014.05.033 · 3.33 Impact Factor
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    • "This issue is critical for understanding how stress confers risk for developing psychopathology, as epidemiological studies reveal that individuals who consider stressful experiences to be uncontrollable and overwhelming are substantially more likely to develop psychiatric symptoms following stress exposure (Kendler et al., 1993, 2004; Kessler, 1997). This is particularly true for symptoms related to impaired reward-reward processing, such as anhedonic symptoms in depression and schizophrenia (Kuiper et al., 1986; Docherty, 1996; Myin-Germeys et al., 2001; Hammen, 2005; Myin-Germeys et al., 2005; Phillips et al., 2005; Rao et al., 2009). Highlighting the importance of this distinction, rodent models suggest that uncontrollable stressors produce a unique pattern of neurobiological changes, particularly in the mPFC (Cabib and Puglisi-Allegra, 1994, 2011; Bland et al., 2003; Amat et al., 2005; Maier and Watkins, 2010). "
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    ABSTRACT: Stress is a significant risk factor for the development of psychopathology, particularly symptoms related to reward processing. Importantly, individuals display marked variation in how they perceive and cope with stressful events, and such differences are strongly linked to risk for developing psychiatric symptoms following stress exposure. However, many questions remain regarding the neural architecture that underlies inter-subject variability in perceptions of stressors. Using functional magnetic resonance imaging (fMRI) during a Monetary Incentive Delay (MID) paradigm, we examined the effects of self-reported perceived stress levels on neural activity during reward anticipation and feedback in a sample of healthy individuals. We found that subjects reporting more uncontrollable and overwhelming stressors displayed blunted neural responses in medial prefrontal cortex (mPFC) following feedback related to monetary gains as well monetary losses. This is consistent with preclinical models that implicate the mPFC as a key site of vulnerability to the noxious effects of uncontrollable stressors. Our data help translate these findings to humans, and elucidate some of the neural mechanisms that may underlie stress-linked risk for developing reward-related psychiatric symptoms.
    Frontiers in Human Neuroscience 05/2013; 7:180. DOI:10.3389/fnhum.2013.00180 · 2.90 Impact Factor
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    • "It is now well established in animal models (see Weinstock, 2001, 2005), and increasingly in humans, that stress experienced by the mother during pregnancy is associated with increased risk for many adverse long-term effects on the child (Talge et al., 2007; O'Donnell et al., 2009; Glover, 2011). These can include an increased risk of anxiety (Phillips et al., 2005), ADHD (Motlagh et al., 2010), conduct problems (Barker and Maughan, 2009), and cognitive deficits (Bergman et al., 2010; Davis and Sandman, 2010). A wide range of stressors have been found in different studies to be associated with altered child outcome, ranging from daily hassles (Huizink et al., 2003), symptoms of anxiety (O'Connor et al., 2003, 2005) or depression (Davis et al., 2007), life events (Bergman et al., 2007, 2010) and natural disasters (King and Laplante, 2005; King et al., 2009). "
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    ABSTRACT: Raised maternal anxiety during pregnancy is associated with increased risk of adverse neurodevelopmental outcomes for her child. The mechanisms underlying this are not known but animal studies suggest prenatal stress may alter the function of the placenta. Here we determined whether maternal prenatal anxiety was associated with a downregulation of placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), the enzyme which metabolises cortisol. We recruited mothers the day before delivery by elective caesarean, and gave them the Spielberger Trait and State anxiety and Edinburgh Depression self-rating scales. Placentae were collected and aliquots stored for later analysis. Prenatal Trait anxiety was negatively correlated with placental 11β-HSD2 mRNA expression (r=-0.40, p<0.01, n=56). Results were similar with male and female fetuses (r=-0.39, p=0.04, n=28; r=-0.40, p=0.03, n=28) respectively. Results were also significant with State anxiety (r=-0.27, p=0.05, n=56) but somewhat weaker for depression (r=-0.20, p=0.13, n=56). Preliminary analyses on a subset of cases (n=25) suggested parallel results for enzyme activity. These findings provide evidence for an association between prenatal maternal mood and downregulation of placental 11β-HSD2. Results are consistent with raised maternal anxiety being associated with increased fetal exposure to maternal cortisol, and support the hypothesis that this may be one mechanism underlying fetal programming by prenatal stress.
    Psychoneuroendocrinology 10/2011; 37(6):818-26. DOI:10.1016/j.psyneuen.2011.09.014 · 5.59 Impact Factor
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