<?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%">Mitchell, Colter</style></author><author><style face="normal" font="default" size="100%">Hobcraft, John</style></author><author><style face="normal" font="default" size="100%">McLanahan, Sara S</style></author><author><style face="normal" font="default" size="100%">Siegel, Susan Rutherford</style></author><author><style face="normal" font="default" size="100%">Berg, Arthur</style></author><author><style face="normal" font="default" size="100%">Brooks-Gunn, Jeanne</style></author><author><style face="normal" font="default" size="100%">Garfinkel, Irwin</style></author><author><style face="normal" font="default" size="100%">Notterman, Daniel</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Social disadvantage, genetic sensitivity, and children's telomere length.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Proc. Natl. Acad. Sci. U.S.A.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Dopamine</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene-Environment Interaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Regression Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Serotonin</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Social Environment</style></keyword><keyword><style  face="normal" font="default" size="100%">Telomere Homeostasis</style></keyword><keyword><style  face="normal" font="default" size="100%">Vulnerable Populations</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Apr 22</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">111</style></volume><pages><style face="normal" font="default" size="100%">5944-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Disadvantaged social environments are associated with adverse health outcomes. This has been attributed, in part, to chronic stress. Telomere length (TL) has been used as a biomarker of chronic stress: TL is shorter in adults in a variety of contexts, including disadvantaged social standing and depression. We use data from 40, 9-y-old boys participating in the Fragile Families and Child Wellbeing Study to extend this observation to African American children. We report that exposure to disadvantaged environments is associated with reduced TL by age 9 y. We document significant associations between low income, low maternal education, unstable family structure, and harsh parenting and TL. These effects were moderated by genetic variants in serotonergic and dopaminergic pathways. Consistent with the differential susceptibility hypothesis, subjects with the highest genetic sensitivity scores had the shortest TL when exposed to disadvantaged social environments and the longest TL when exposed to advantaged environments.&lt;/p&gt;
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