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.
Highlights
Eating disorders (ED) are chronic psychiatric disorders, common amongst women of reproductive age
Cord blood of offspring of women with active ED had the lowest methylation level (49.1%; 95% confidence intervals 50.5–47.7%); offspring of controls had the highest global methylation levels (52.4%; 95% CI 53.0–51.0%)
The offspring of women with past ED had a lower global methylation level compared to those of controls (49.2%; 95% CI 50.7– 47.7.0%) and slightly higher than the active ED group
Summary
Eating disorders (ED) are chronic psychiatric disorders, common amongst women of reproductive age. ED in pregnancy are associated with poor nutrition and abnormal intrauterine growth. 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. Maternal ED, both active—during pregnancy—and past, have been shown to affect child eating, growth, psychopathology and development [4,5,6,7,8]. Increasing evidence has highlighted the effect of maternal nutrition in pregnancy on epigenetic modifications, in particular DNA methylation, both in animals and. Low micronutrient (methyl donors) and protein intake, as well as low maternal pre-pregnancy BMI, have been prospectively associated with lower global methylation levels and hypomethylation at specific sites [14, 16]
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