<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sciberras, E.</style></author><author><style face="normal" font="default" size="100%">Mulraney, M.</style></author><author><style face="normal" font="default" size="100%">Silva, D.</style></author><author><style face="normal" font="default" size="100%">Coghill, D.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Prenatal Risk Factors and the Etiology of ADHD-Review of Existing Evidence</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Psychiatry Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Current psychiatry reports</style></alt-title><short-title><style face="normal" font="default" size="100%">Current psychiatry reportsCurrent psychiatry reports</style></short-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">*Gene-Environment Interaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Adhd</style></keyword><keyword><style  face="normal" font="default" size="100%">Attention Deficit Disorder with Hyperactivity/epidemiology/*etiology/genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Causality</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Cross-Sectional Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental</style></keyword><keyword><style  face="normal" font="default" size="100%">Etiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Low Birth Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Premature, Diseases/diagnosis/epidemiology/etiology/genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Prenatal</style></keyword><keyword><style  face="normal" font="default" size="100%">Prenatal Exposure Delayed Effects/*diagnosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Research Design</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Statistics as Topic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">1</style></number><edition><style face="normal" font="default" size="100%">2017/01/17</style></edition><volume><style face="normal" font="default" size="100%">19</style></volume><pages><style face="normal" font="default" size="100%">1</style></pages><isbn><style face="normal" font="default" size="100%">1523-3812</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">While it is well accepted that attention-deficit/hyperactivity disorder (ADHD) is a highly heritable disorder, not all of the risk is genetic. It is estimated that between 10 and 40% of the variance associated with ADHD is likely to be accounted for by environmental factors. There is considerable interest in the role that the prenatal environment might play in the development of ADHD with previous reviews concluding that despite demonstration of associations between prenatal risk factors (e.g. prematurity, maternal smoking during pregnancy) and ADHD, there remains insufficient evidence to support a definite causal relationship. This article provides an update of research investigating the relationship between prenatal risk factors and ADHD published over the past 3 years. Recently, several epidemiological and data linkage studies have made substantial contributions to our understanding of this relationship. In particular, these studies have started to account for some of the genetic and familial confounds that, when taken into account, throw several established findings into doubt. None of the proposed prenatal risk factors can be confirmed as causal for ADHD, and the stronger the study design, the less likely it is to support an association. We need a new benchmark for studies investigating the etiology of ADHD whereby there is an expectation not only that data will be collected prospectively but also that the design allows the broad range of genetic and familial factors to be accounted for.</style></abstract><accession-num><style face="normal" font="default" size="100%">28091799</style></accession-num><notes><style face="normal" font="default" size="100%">1535-1645&lt;br/&gt;Sciberras, Emma&lt;br/&gt;Mulraney, Melissa&lt;br/&gt;Silva, Desiree&lt;br/&gt;Coghill, David&lt;br/&gt;Journal Article&lt;br/&gt;Review&lt;br/&gt;United States&lt;br/&gt;Curr Psychiatry Rep. 2017 Jan;19(1):1. doi: 10.1007/s11920-017-0753-2.</style></notes><auth-address><style face="normal" font="default" size="100%">Deakin University, Melbourne, VIC, Australia.&lt;br/&gt;Murdoch Childrens Research Institute, Parkville, VIC, Australia.&lt;br/&gt;The Royal Children's Hospital, Level 2 East, 50 Flemington Road, Parkville, 3052, Victoria, Australia.&lt;br/&gt;School of Paediatrics and Child Health, University of Western, Perth, Australia.&lt;br/&gt;Murdoch Childrens Research Institute, Parkville, VIC, Australia. david.coghill@unimelb.edu.au.&lt;br/&gt;The Royal Children's Hospital, Level 2 East, 50 Flemington Road, Parkville, 3052, Victoria, Australia. david.coghill@unimelb.edu.au.&lt;br/&gt;Departments of Paediatrics and Psychiatry, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Australia. david.coghill@unimelb.edu.au.</style></auth-address><remote-database-provider><style face="normal" font="default" size="100%">NLM</style></remote-database-provider></record></records></xml>