Epidemiology of psychiatric disorder in childhood and adolescence

Author(s):  
E. Jane Costello ◽  
Adrian Angold

This chapter has covered a lot of ground; from the first stirrings of understanding about childhood psychiatric disorders to the possibility of using molecular genetics to identify gene–environment interactions that can generate psychiatric disorder. There are fuzzy boundaries between epidemiology and developmental psychopathology, life course epidemiology, genetic epidemiology, services research, and clinical psychiatry. It will be important to keep these boundaries pervious, to share a common language where possible, and to learn and use one another's methods.

1987 ◽  
Vol 151 (2) ◽  
pp. 179-184 ◽  
Author(s):  
I. M. Goodyer ◽  
I. Kolvin ◽  
Sonia Gatzanis

The timing and number of recent stressful life events occurring in the year before onset of emotional or behavioural disorder was examined in a consecutive sample of children. Overall, events increase the relative risk of psychiatric disorder by 3–6 times. Events occur throughout the 12 months, but tend to cluster in the 16 weeks nearest onset of symptoms. The number of events influences the onset of disorder: cases with multiple events are more likely to have an event within 16 weeks of onset; cases with single events are more likely to have the event 36–52 weeks before onset. Cases whose onset occurs within 4 weeks of an event may have experienced single or multiple events. The results support the concept of additivity of recent stressful events in some cases of emotional and behavioural disorders in childhood.


2015 ◽  
Vol 27 (2) ◽  
pp. 587-613 ◽  
Author(s):  
Luke W. Hyde

AbstractThe emerging field of neurogenetics seeks to model the complex pathways from gene to brain to behavior. This field has focused on imaging genetics techniques that examine how variability in common genetic polymorphisms predict differences in brain structure and function. These studies are informed by other complimentary techniques (e.g., animal models and multimodal imaging) and have recently begun to incorporate the environment through examination of Imaging Gene × Environment interactions. Though neurogenetics has the potential to inform our understanding of the development of psychopathology, there has been little integration between principles of neurogenetics and developmental psychopathology. The paper describes a neurogenetics and Imaging Gene × Environment approach and how these approaches have been usefully applied to the study of psychopathology. Six tenets of developmental psychopathology (the structure of phenotypes, the importance of exploring mechanisms, the conditional nature of risk, the complexity of multilevel pathways, the role of development, and the importance of who is studied) are identified, and how these principles can further neurogenetics applications to understanding the development of psychopathology is discussed. A major issue of this piece is how neurogenetics and current imaging and molecular genetics approaches can be incorporated into developmental psychopathology perspectives with a goal of providing models for better understanding pathways from among genes, environments, the brain, and behavior.


2021 ◽  
Vol 6 (3) ◽  
pp. 91-100
Author(s):  
Azizollah Mojahed ◽  
◽  
Behzad Rigi Kooteh ◽  
Mohammad Reza Mohammadi ◽  
Seyed Salman Alavi ◽  
...  

Background: Paying attention to psychiatric disorder in childhood and adolescence is critical. It causes the occurrence of mental disorders in adulthood. The present study aimed to explore the frequency of mental disorders among children and adolescents in Zahedan City, Iran. Materials & Methods: This was a descriptive and cross-sectional study. Individuals aged between 6 and 18 years were included in this investigation. In total, 1003 children and adolescents were selected by the random cluster sampling method. To collect the required information, in addition to demographic information, the Schedule for Affective Disorders and Schizophrenia (K-SADS-PL) for school-age Children-Present and Lifetime version was employed. The obtained data were analyzed using multivariate logistic regression method. Results: A total of 1003 children and adolescents participated in the study; of them, 489 (48.8%) and 514(51.2%) were males and females, respectively. The Mean±SD age of study participants was 11.96±3.99 years. Moreover, 86.8% of the study subjects were from urban areas and 13.2% from rural areas. The highest prevalence of psychiatric disorders concerned behavioral disorders (6.8%); anxiety disorders (6.7%); The lowest prevalence were related to post-traumatic stress disorder (0.2%) and autism (0.1%). The overall prevalence of psychiatric disorder among children and adolescence was 14.4%. Conclusion: This study found a high prevalence of psychiatric disorders similar to previous studies in the same age groups. The estimates played an important role in designing useful programs and interventions.


2016 ◽  
Author(s):  
Michel G. Nivard ◽  
Suzanne H. Gage ◽  
Jouke J. Hottenga ◽  
Catherina E.M. van Beijsterveldt ◽  
Abdel Abdellaoui ◽  
...  

AbstractVarious non-psychotic psychiatric disorders in childhood and adolescence can precede the onset of schizophrenia, but the nature of this relationship remains unclear. We investigated to what extent the association between schizophrenia and psychiatric disorders in childhood is explained by shared genetic risk factors.Polygenic risk scores (PRS), reflecting an individual’s genetic risk for schizophrenia, were constructed for participants in two birth cohorts (2,588 children from the Netherlands Twin Register (NTR) and 6,127 from the Avon Longitudinal Study of Parents And Children (ALSPAC)). The associations between schizophrenia PRS and measures of anxiety, depression, attention deficit hyperactivity disorder (ADHD), and oppositional defiant disorder/conduct disorder (ODD/CD) were estimated at age 7, 10, 12/13 and 15 years in the two cohorts. Results were then meta-analyzed, and age-effects and differences in the associations between disorders and PRS were formally tested in a meta-regression.The schizophrenia PRS was associated with childhood and adolescent psychopathology Where the association was weaker for ODD/CD at age 7. The associations increased with age this increase was steepest for ADHD and ODD/CD. The results are consistent with a common genetic etiology of schizophrenia and developmental psychopathology as well as with a stronger shared genetic etiology between schizophrenia and adolescent onset psychopathology.A multivariate meta-analysis of multiple and repeated observations enabled to optimally use the longitudinal data across diagnoses in order to provide knowledge on how childhood disorders develop into severe adult psychiatric disorders.


2019 ◽  
Vol 22 (4) ◽  
pp. 233-239 ◽  
Author(s):  
Nicole L. Schmidt ◽  
Rebecca J. Brooker ◽  
Ian C. Carroll ◽  
Jeffrey R. Gagne ◽  
Zhan Luo ◽  
...  

AbstractThe Wisconsin Twin Project comprises multiple longitudinal studies that span infancy to early adulthood. We summarize recent papers that show how twin designs with deep phenotyping, including biological measures, can inform questions about phenotypic structure, etiology, comorbidity, heterogeneity, and gene–environment interplay of temperamental constructs and mental and physical health conditions of children and adolescents. The general framework for investigations begins with rich characterization of early temperament and follows with study of experiences and exposures across childhood and adolescence. Many studies incorporate neuroimaging and hormone assays.


PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0258364
Author(s):  
Koki Sakurai ◽  
Taichi Itou ◽  
Makiko Morita ◽  
Emiko Kasahara ◽  
Tetsuji Moriyama ◽  
...  

Importin α1/KPNA1 is a member of the Importin α family widely present in the mammalian brain and has been characterized as a regulator of neuronal differentiation, synaptic functionality, and anxiety-like behavior. In humans, a de novo mutation of the KPNA1 (human Importin α5) gene has been linked with schizophrenia; however, the precise roles of KPNA1 in disorder-related behaviors are still unknown. Moreover, as recent studies have highlighted the importance of gene-environment interactions in the development of psychiatric disorders, we investigated the effects of Kpna1 deletion and social isolation stress, a paradigm that models social stress factors found in human patients, on psychiatric disorder-related behaviors in mice. Through assessment in a behavioral battery, we found that Kpna1 knockout resulted in the following behavioral phenotype: (1) decreased anxiety-like behavior in an elevated plus maze test, (2) short term memory deficits in novel object recognition test (3) impaired sensorimotor gating in a prepulse inhibition test. Importantly, exposure to social isolation stress resulted in additional behavioral abnormalities where isolated Kpna1 knockout mice exhibited: (1) impaired aversive learning and/or memory in the inhibitory avoidance test, as well as (2) increased depression-like behavior in the forced swim test. Furthermore, we investigated whether mice showed alterations in plasma levels of stress-associated signal molecules (corticosterone, cytokines, hormones, receptors), and found that Kpna1 knockout significantly altered levels of corticosterone and LIX (CXCL5). Moreover, significant decreases in the level of prolactin were found in all groups except for group-housed wild type mice. Our findings demonstrate that Kpna1 deletion can trigger widespread behavioral abnormalities associated with psychiatric disorders, some of which were further exacerbated by exposure to adolescent social isolation. The use of Kpna1 knockout mice as a model for psychiatric disorders may show promise for further investigation of gene-environment interactions involved in the pathogenesis of psychiatric disorders.


Author(s):  
Francis J. McMahon ◽  
Sevilla Detera-Wadleigh

Bipolar disorder represents one of the most highly heritable group of common psychiatric disorders, but the complex genetic basis of these disorders has only recently begun to reveal itself. This chapter reviews the genetic epidemiology, molecular genetics, and genetic modelling studies of bipolar disorder. The chapter concludes with a glimpse of anticipated developments of relevance to clinical care and anticipates some future research directions.


2004 ◽  
Vol 12 (1) ◽  
pp. 19-33 ◽  
Author(s):  
MICHAEL RUTTER

Quantitative genetics, using data from twin and adoptee studies, has shown substantial genetic influences on all forms of psychiatric disorder; however, with just a few exceptions, the evidence indicates that the disorders are multifactorial, with influences that are both genetic and environmental. In recent years, molecular genetics has begun to identify individual susceptibility genes; examples are given for schizophrenia, attention deficit/hyperactivity disorder, and Alzheimer's disease. Both quantitative and molecular genetics have shown the importance of gene-environment interplay with respect to the commoner disorders of emotions and behaviour. In particular, it has been found that genetic influences moderate people's vulnerability to environmental risks. Five main alternative routes by which genes indirectly (via their effects on proteins) lead to multifactorial psychiatric disorders are described. Four main research issues are highlighted: the fuller delineation of the mechanisms involved in nature–nurture interplay and its role in aetiology; determination of how genes play a role in the neural underpinning of psychiatric disorders; identification of the ways in which genes suggest a dissection of disorders; and an understanding of the role of risk dimensions and disorder dimensions.


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