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Mitchell finds children who lose fathers suffer at cellular level

Seefeldt says hard work alone won't allow poor to reach middle-class status in America

Shaefer says proposed plan to cover tax cuts would hurt a lot of struggling Americans

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Neal Krause wins GSA's Robert Kleemeier Award

MiCDA Research Fellowship - applications due July 21, 2017

U-M awarded $58 million to develop ideas for preventing and treating health problems

Bailey, Eisenberg , and Fomby promoted at PSC

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Telomeres

Children's telomere length and social disadvantage

4/18/2014 feature story

Colter Mitchell and colleagues found that 9-year olds growing up in highly disadvantaged environments had shorter telomeres than their highly advantaged counterparts, with genetic sensitivity having a moderating effect.

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Colter Mitchell

Publication Information:

Mitchell, Colter, John Hobcraft, Sara McLanahan, Susan Rutherford Siegel, Arthur Berg, Jeanne Brooks-Gunn, Irwin Garfinkel, and Daniel Notterman. 2014. "Social disadvantage, genetic sensitivity, and children’s telomere length." Proceedings of the National Academy of Sciences of the United States of America, 111(16): 5944-5949. PMCID: PMC4000782.

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. Using data from 40, 9-year-old boys participating in the Fragile Families and Child Wellbeing Study, we show that those who grow up in highly disadvantaged environments have shorter telomeres than boys who grow up in highly advantaged environments. We also find that the association between the social environment and TL is moderated by genetic variation within the serotonin and dopamine pathways. Boys with the highest genetic sensitivity scores had the shortest TL when exposed to disadvantaged environments and the longest TL when exposed to advantaged environments. To our knowledge, this report is the first to document a gene–social environment interaction for TL, a biomarker of stress exposure.

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