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Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence

  • Edward D. Barker (a1), Charlotte A. M. Cecil (a1), Esther Walton (a2), Lotte C. Houtepen (a2), Thomas G. O'Connor (a3), Andrea Danese (a1), Sara R. Jaffee (a4), Sarah K. G. Jensen (a5), Carmine Pariante (a1), Wendy McArdle (a2), Tom R. Gaunt (a2), Caroline L. Relton (a2) and Susanna Roberts (a1)...


In 785 mother–child (50% male) pairs from a longitudinal epidemiological birth cohort, we investigated associations between inflammation-related epigenetic polygenic risk scores (i-ePGS), environmental exposures, cognitive function, and child and adolescent internalizing and externalizing problems. We examined prenatal and postnatal effects. For externalizing problems, one prenatal effect was found: i-ePGS at birth associated with higher externalizing problems (ages 7–15) indirectly through lower cognitive function (age 7). For internalizing problems, we identified two effects. For a prenatal effect, i-ePGS at birth associated with higher internalizing symptoms via continuity in i-ePGS at age 7. For a postnatal effect, higher postnatal adversity exposure (birth through age 7) associated with higher internalizing problems (ages 7–15) via higher i-ePGS (age 7). Hence, externalizing problems were related mainly to prenatal effects involving lower cognitive function, whereas internalizing problems appeared related to both prenatal and postnatal effects. The present study supports a link between i-ePGS and child and adolescent mental health.

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Corresponding author

Address correspondence and reprint requests to: Edward D. Barker, Department of Psychology, King's College London, Institute of Psychiatry, Psychology and Neuroscience, De Crespigny Park, London, SE5 8AF UK; E-mail:


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We are extremely grateful to all the families who took part in this study, the midwives for their help in recruiting them, and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists, and nurses. With regard to the ALSPAC DNA methylation, we thank all involved, particularly the laboratory scientists and bioinformaticians who contributed considerable time and expertise to the data in this paper. The UK Medical Research Council and the Wellcome Trust (Grant102215/2/13/2) and the University of Bristol provide core support for ALSPAC. ARIES was funded by BBSRC Grants BBI025751/1 and BB/I025263/1. ARIES is maintained under the auspices of the MRC Integrative Epidemiology Unit at the University of Bristol (MC_UU_12013/2 and MC_UU_12013/8). This research was specifically supported by National Institute of Child and Human Development Grant R01HD068437 (to E.D.B.), Economic and Social Research Council Grants ES/R005516/1 (to E.D.B.) and ES/N001273/1 (to C.C.), and ESRC/BBSRC Grant ES/N000382/1 (to L.C.H.) for the Interpreting epigenetic signatures in studies of early life adversity project (Interstela Project).



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