Maternal eating disorders affect offspring cord blood DNA methylation: a prospective study

Abstract

BackgroundEating disorders (ED) are chronic psychiatric disorders, common amongst women of reproductive age. ED in pregnancy are associated with poor nutrition and abnormal intrauterine growth. Increasing evidence also shows offspring of women with ED have adverse developmental and birth outcomes. We sought to carry out the first study investigating DNA methylation in offspring of women with ED. We compared cord blood DNA methylation in offspring of women with active ED (n = 21), past ED (n = 43) and age- and social class-matched controls (n = 126) as part of the Avon Longitudinal Study of Parents and Children.ResultsOffspring of women with both active and past ED had lower whole-genome methylation compared to controls (active ED 49.1% (95% confidence intervals 50.5–47.7%), past ED 49.2% (95% CI 50.7–47.7.0%), controls 52.4% (95% CI 53.0%–51.0%)). Amongst offspring of ED women, those born to women with restrictive-type and purging-type ED had lower methylation levels compared to those of controls. Offspring of women with an active restrictive ED in pregnancy had lower whole-genome methylation compared to offspring of women with past restrictive ED. We observed decreased methylation at the DHCR24 locus in offspring of women with active pregnancy ED (effect size (ES) = − 0.124, p = 6.94 × 10−8) and increased methylation at the LGALS2 locus in offspring of women with past ED (ES = 0.07, p = 3.74 × 10−7) compared to controls.ConclusionsMaternal active and past ED are associated with differences in offspring whole-genome methylation. Our results show altered DNA methylation in loci relevant to metabolism; these might be biomarkers of disrupted metabolic pathways in offspring of ED mothers. Further work is needed to examine potential mechanisms and functional outcomes of the observed methylation patterns.Electronic supplementary materialThe online version of this article (10.1186/s13148-017-0418-3) contains supplementary material, which is available to authorized users.

Eating Disorders During Gestation: Implications for Mother's Health, Fetal Outcomes, and Epigenetic Changes

“…A recent study performed in 21 active ED, 43 past ED and 126 controls concluded that offspring of women with an active restrictive ED during pregnancy showed lower global methylation pattern in their genome compared to offspring of women with past restrictive ED. This study also demonstrated a decreased methylation at the DHCR24 locus in offspring of women with active ED during pregnancy and an increased methylation at the LGALS2 locus in offspring of women with past ED compared to controls (149).…”

Outcomes for infants whose mothers had an eating disorder in the perinatal period: A systematic review of the evidence

“…Studies are high quality unless otherwise identified, for ease of reading. Some studies did not differentiate between eating disorder diagnosis, instead just reporting outcomes for eating disorders as a combined group (Bansil et al, 2008; Barona et al, 2017; Conti et al, 1998; Easter et al, 2017; Franko et al, 2001; Kazmi et al, 2017; Martini et al, 2019; Squires et al, 2014). Results for these studies are presented using the phrases “any/unspecified eating disorder.” Twelve of the studies reported data from three longitudinal cohort studies, the Norwegian Mother and Child Cohort Study (Bulik et al, 2008; Bulik et al, 2009; Perrin et al, 2015; Torgersen et al, 2010; Torgersen et al, 2015; Watson et al, 2017; Zerwas et al, 2012), the Avon Longitudinal Study of Parents and Children (Kazmi et al, 2017; Micali et al, 2011), and the Nutrition and Stress in Pregnancy Study (Barona et al, 2017; Easter et al, 2017; Martini et al, 2019).…”

“…Some studies did not differentiate between eating disorder diagnosis, instead just reporting outcomes for eating disorders as a combined group (Bansil et al, 2008; Barona et al, 2017; Conti et al, 1998; Easter et al, 2017; Franko et al, 2001; Kazmi et al, 2017; Martini et al, 2019; Squires et al, 2014). Results for these studies are presented using the phrases “any/unspecified eating disorder.” Twelve of the studies reported data from three longitudinal cohort studies, the Norwegian Mother and Child Cohort Study (Bulik et al, 2008; Bulik et al, 2009; Perrin et al, 2015; Torgersen et al, 2010; Torgersen et al, 2015; Watson et al, 2017; Zerwas et al, 2012), the Avon Longitudinal Study of Parents and Children (Kazmi et al, 2017; Micali et al, 2011), and the Nutrition and Stress in Pregnancy Study (Barona et al, 2017; Easter et al, 2017; Martini et al, 2019). Most of the studies from these three cohorts reported separate infant outcomes, although five infant outcomes were each assessed by more than one study from the same longitudinal cohort—prematurity (Bulik et al, 2009; Torgersen et al, 2010), LBW (Bulik et al, 2009; Torgersen et al, 2010), SGA (Bulik et al, 2009; Torgersen et al, 2010; Watson et al, 2017), LGA (Bulik et al, 2009; Watson et al, 2017) and proportion of breastfeeding (Torgersen et al, 2010; Torgersen et al, 2015).…”

Eating Disorders, Heredity and Environmental Activation: Getting Epigenetic Concepts into Practice

“…Interestingly, children who had higher methylation levels at age 13 concurrently had a lower BMI and lower central adiposity [41]. Investigating possible epigenetic effects of maternal EDs upon their offspring, Kazmi and colleagues [42] measured genome-wide methylation of cord blood DNA in 21 babies of women with active AN, 43 with a past AN, and 126 normal-eater controls. Infants of women with AN had lower global methylation levels than did controls.…”