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Extremely low birth weight babies grown up: Gene–environment interaction predicts internalizing problems in the third and fourth decades of life

Published online by Cambridge University Press:  15 July 2016

Ayelet Lahat
Affiliation:
McMaster University
Ryan J. van Lieshout
Affiliation:
McMaster University
Karen J. Mathewson
Affiliation:
McMaster University
James Mackillop
Affiliation:
McMaster University
Saroj Saigal
Affiliation:
McMaster University
Katherine M. Morrison
Affiliation:
McMaster University
Michael H. Boyle
Affiliation:
McMaster University
Louis A. Schmidt
Affiliation:
McMaster University
Corresponding
E-mail address:

Abstract

Extremely low birth weight (ELBW; <1000 g) infants have been exposed to stressful intrauterine and early postnatal environments. Even greater early adversity has been experienced by ELBW survivors who were also born small for gestational age (SGA; <10th percentile for GA) compared to those born appropriate for GA (AGA). ELBW survivors, particularly those born SGA, face increased risk for internalizing problems compared to normal BW (NBW; ≥2500 g) controls. Internalizing problems are related to allelic variations in the promoter region of the serotonin transporter linked polymorphic region gene (5-HTTLPR). We followed the oldest longitudinal cohort of ELBW survivors to adulthood. Participants provided buccal cells and reported on internalizing problems, using the Young Adult Self-Report when they were in their mid-20s (ELBW/SGA, N = 28; ELBW/AGA, N = 60; NBW, N = 81) and mid-30s (ELBW/SGA, N = 27; ELBW/AGA, N = 58; NBW, N = 76). The findings indicate that ELBW/SGAs carrying the 5-HTTLPR short allele reported increased internalizing problems, particularly depression, during the third and fourth decades of life. This is the first known report on gene–environment interactions predicting psychopathology among ELBW survivors. Our findings elucidate putative neurobiological pathways that underlie risk for psychopathology.

Type
Regular Articles
Copyright
Copyright © Cambridge University Press 2016 

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Footnotes

This research was supported by Canadian Institutes of Health Research Grants CIHR:TMH-103145 (to L.A.S) and CIHR:MOP42536 (to S.S.) and National Institute of Child Health and Human Development Grant NICHD:1-R01HD40219 (to S.S.). This research was also supported by a Social Sciences and Humanities Research Council Banting Post-Doctoral Fellowship (to A.L.) and the Peter Boris Chair in Addictions Research (to J.M.). We thank the study participants and their families for their continued participation in this work and Paz Fortier, Sue McKee, Vladimir Miskovic, Jordana Waxman, and Shirien Yunus for their help with data collection and data entry. We also thank Jane Foster for performing the genotyping.

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