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Extremely low birth weight influences the relationship between stress and telomere length in adulthood

Published online by Cambridge University Press:  29 May 2020

Calan D. Savoy
Affiliation:
Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON L8S 4L8, Canada
Louis A. Schmidt
Affiliation:
Department of Psychology, Neuroscience and Behaviour, McMaster University, Hamilton, ON L8S 4L8, Canada
Patrick O. McGowan
Affiliation:
Department of Biological Sciences, University of Toronto Scarborough, Toronto, ON M1C 1A4, Canada
Saroj Saigal
Affiliation:
Department of Pediatrics, McMaster University, Hamilton, ON L8S 4L8, Canada
Ryan J. Van Lieshout
Affiliation:
Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON L8S 4L8, Canada
Corresponding
E-mail address:

Abstract

This study examined the link between two biological markers of stress vulnerability at 22–26 years of age and telomere length at 30–35 among extremely low birth weight (ELBW; <1000 g) survivors and normal birth weight (NBW; >2500 g) control participants. Sixteen ELBW and 22 NBW participants provided baseline afternoon salivary cortisol samples and resting frontal electroencephalogram (EEG) alpha asymmetry data at 22–26 years. Buccal cells were assayed for telomere length at 30–35 years. Analyses controlled for sex, postnatal steroid exposure, childhood socioeconomic status, time of cortisol sample collection, and body mass index at 22–26 years. Salivary cortisol and frontal asymmetry at age 22–26 independently predicted telomere length at age 30–35, such that relatively higher cortisol and greater relative right frontal asymmetry at rest predicted telomere shortening among NBW controls, but not among ELBW survivors. However, similar associations were not noted in ELBW survivors, suggesting that ELBW survivors may have different mechanisms of stress coping as a result of their early-life exposures. These findings offer preliminary evidence in support of the role of stress in the genesis of cellular senescence at least among those born at NBW, but that these links may differ in those born preterm.

Type
Original Article
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2020

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