Are Biological Consequences of Childhood Exposures Detectable in Telomere Length Decades Later?

儿童时期接触某些物质的生物学后果能否在数十年后通过端粒长度检测到?

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Abstract

Negative early-life exposures have been linked to a host of poor adult health outcomes, but are such early exposures associated with cellular senescence decades later? This study uses data from the Health and Retirement Study to examine the association between six childhood exposure domains (eg, socioeconomic disadvantage, risky parental behavior) and a biomarker of aging, telomere length, among 4,935 respondents. Telomere length is obtained from DNA of cells found in saliva and is measured as the telomere repeat copy number to single gene copy number ratio (T/S). Men who as children were exposed to risky parental behaviors or who reported risky adolescent behaviors have shorter telomeres (b = -0.031, p = .052; b = -0.041, p = .045, respectively); however, these relationships are attenuated after adjusting for adult risks and resources. Among women, parental substance abuse is associated with shorter telomeres even after adjusting for adult risks and resources (b = -0.041, p = .005). In addition, men and women whose mother lived at least until the age of 85 have longer telomeres than those without a long-lived mother (b = 0.021, p = .045; b = 0.032, p = .005, respectively). Taken together, the ways in which early-life exposures are associated with adult telomeres vary for men and women.

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