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Growing up or growing old? Cellular aging linked with testosterone reactivity to stress in youth.
Published: 07/23/2014, The American journal of the medical sciences
Background
Given the established relation between testosterone and aging in older adults, we tested whether buccal telomere length (TL), an established cellular biomarker of aging, was associated with testosterone levels in youth.
Methods
Children, mean age 10.2 years, were recruited from the greater New Orleans area, and salivary testosterone was measured diurnally and during an acute stressor. Buccal TL was measured using monochrome multiplex quantitative real-time polymerase chain reaction. Testosterone and TL data were available on 77 individuals. The association between buccal TL and testosterone was tested using multivariate generalized estimating equations to account for clustering of children within families.
Results
Greater peak testosterone levels (β = -0.87, P < 0.01) and slower recovery (β = -0.56, P < 0.01) and reactivity (β = -1.22, P < 0.01) following a social stressor were significantly associated with shorter buccal TL after controlling for parental age at conception, child age, sex, sociodemographic factors and puberty. No association was initially present between diurnal measurements of testosterone or morning basal testosterone levels and buccal TL. Sex significantly moderated the relation between testosterone reactivity and buccal TL.
Conclusions
The association between testosterone and buccal TL supports gonadal maturation as a developmentally sensitive biomarker of aging within youth. As stress levels of testosterone were significantly associated with buccal TL, these findings are consistent with the growing literature linking stress exposure and accelerated maturation. The lack of association of diurnal testosterone or morning basal levels with buccal TL bolsters the notion of a shared stress-related maturational mechanism between cellular stress and the hypothalamic pituitary gonadal axis. These data provide novel evidence supporting the interaction of aging, physiologic stress and cellular processes as an underlying mechanism linking negative health outcomes and early life stress.
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