Childhood adversity and psychosis: Examining whether the association is due to genetic confounding using a monozygotic twin differences approach

Alemany, Silvia; Goldberg, Ximena; Winkel, Ruud van; Gastó, Cristòbal; Peralta, Víctor; Fañanás, Lourdes

doi:10.1016/j.eurpsy.2012.03.001

Cited by 51 publications

(49 citation statements)

References 46 publications

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“…This is consistent with an earlier adoption study reporting that severe institutional deprivation can cause inattention/overactivity symptoms (148) and with similar findings for other psychiatric conditions (190,191). Vulnerability for ADHD symptoms could result from alterations in neural pathways involved in working memory, executive and emotional control (152,153,192) following maltreatment.…”

Section: Can Environmental Risks Causally Contribute To Adhd?supporting

confidence: 80%

Environmental and Genetic Influences in Attention Deficit Hyperactivity Disorder (ADHD) and its Comorbidities

Capusan¹

2016

Linköping University Medical Dissertations

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Section: Can Environmental Risks Causally Contribute To Adhd?supporting

confidence: 80%

Environmental and Genetic Influences in Attention Deficit Hyperactivity Disorder (ADHD) and its Comorbidities

Capusan¹

2016

Linköping University Medical Dissertations

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“…While experimental studies on humans aimed at establishing causation are not an ethical option, there are recent findings from a study of monozygotic (MZ) twins that are relevant to this issue. Using the MZ twin differences approach, investigators obtained data on childhood adversity and subclinical “psychotic experiences” from both members of the twin pairs (Alemany et al, 2012). They found that within-pair twin differences in exposure to childhood adversity were significantly associated with corresponding differences in subclinical positive symptoms, suggesting that the relation between childhood adversity and symptoms is not solely attributable to genetically determined differences in vulnerability.…”

Section: Psychosocial Stress and The Prodromementioning

confidence: 99%

Stress and neurodevelopmental processes in the emergence of psychosis

et al. 2013

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The notion that stress plays a role in the etiology of psychotic disorders, especially schizophrenia, is longstanding. However, it is only in recent years that the potential neural mechanisms mediating this effect have come into sharper focus. The introduction of more sophisticated models of the interplay between psychosocial factors and brain function has expanded our opportunities for conceptualizing more detailed psychobiological models of stress in psychosis. Further, scientific advances in our understanding of adolescent brain development have shed light on a pivotal question that has challenged researchers; namely, why the first episode of psychosis typically occurs in late adolescence/young adulthood. In this paper, we begin by reviewing the evidence supporting associations between psychosocial stress and psychosis in diagnosed patients as well as individuals at clinical high risk for psychosis. We then discuss biological stress systems and examine changes that precede and follow psychosis onset. Next, research findings on structural and functional brain characteristics associated with psychosis are presented; these findings suggest that normal adolescent neuromaturational processes may go awry, thereby setting the stage for the emergence of psychotic syndromes. Finally, a model of neural mechanisms underlying the pathogenesis of psychosis is presented and directions for future research strategies are explored.

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“…All of these studies 7,19,20 reported strong and significant associations between childhood adversity and psychosis, even when controlling for genetic risk. These studies thus suggest that, even if we assume that genetic risk for psychosis increases the likelihood of exposure to CT, the actual exposure in itself further increases the risk for psychosis.…”

Section: Evidence For Associationmentioning

confidence: 99%

Childhood Trauma as a Cause of Psychosis: Linking Genes, Psychology, and Biology

et al. 2013

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Recent studies have provided robust evidence for an association between childhood trauma (CT) and psychosis. Meta-analyses have quantified the association, pointing to odds ratios in the order of around 3, and prospective studies have shown that reverse causation is unlikely to explain the association. However, more work is needed to address the possibility of a gene-environment correlation, that is, whether genetic risk for psychosis predicts exposure to CT. Nevertheless, multiple studies have convincingly shown that the association between CT and psychosis remains strong and significant when controlling for genetic risk, in agreement with a possible causal association. In addition, several studies have shown plausible psychological and neurobiological mechanisms linking adverse experiences to psychosis, including induction of social defeat and reduced self-value, sensitization of the mesolimbic dopamine system, changes in the stress and immune system, and concomitant changes in stress-related brain structures, such as the hippocampus and the amygdala, findings that should be integrated, however, in more complex models of vulnerability. It is currently unclear whether genetic vulnerability plays a role in conferring the mental consequences of adversity, and which genes are likely to be involved. The current, limited evidence points to genes that are not specifically involved in psychosis but more generally in regulating mood (serotonin transporter gene), neuroplasticity (brain-derived neurotrophic factor), and the stress-response system (FKBP5), in line with a general effect of CT on a range of mental disorders, rather than suggesting specificity for psychosis. W W W Traumatisme d'enfance comme cause de psychose : lier gènes, psychologie et biologieDes études récentes ont produit de solides données probantes de l'association entre un traumatisme d'enfance (TE) et la psychose. Des méta-analyses ont quantifié l'association, chiffrant les rapports de cotes de l'ordre de 3, et des études prospectives ont montré que la causalité inverse n'est pas susceptible d'expliquer l'association. Cependant, il faut plus de travaux pour étudier la possibilité d'une corrélation gène-environnement, c'est-à-dire, si le risque génétique de psychose prédit l'exposition au TE. Néanmoins, de nombreuses études ont démontré de façon convaincante que l'association entre TE et psychose demeure forte et significative lors d'un contrôle pour le risque génétique, ce qui concorde avec une possible association causale. En outre, plusieurs études ont démontré des mécanismes psychologiques et neurobiologiques plausibles qui lient les expériences indésirables à la psychose, notamment l'induction de la défaite sociale ou de l'estime de soi réduite, la sensibilisation du système de dopamine mésolimbique, les changements du système de stress et immunitaire, et les changements concomitants des structures cérébrales liées au stress, comme l'hippocampe et l'amygdale. Ces résultats devraient toutefois être intégrés à des modèles de vulnérabilité plus com...

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Childhood adversity and psychosis: Examining whether the association is due to genetic confounding using a monozygotic twin differences approach

Cited by 51 publications

References 46 publications

Environmental and Genetic Influences in Attention Deficit Hyperactivity Disorder (ADHD) and its Comorbidities

Environmental and Genetic Influences in Attention Deficit Hyperactivity Disorder (ADHD) and its Comorbidities

Stress and neurodevelopmental processes in the emergence of psychosis

Childhood Trauma as a Cause of Psychosis: Linking Genes, Psychology, and Biology

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