Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort study
Abstract Background Few studies have examined associations between maternal epigenetic age acceleration and adverse birth outcomes, and none have investigated paternal epigenetic age acceleration. Our objective was to assess the associations of parental (both maternal and paternal) epigenetic age ac...
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BMC
2024-11-01
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| Online Access: | https://doi.org/10.1186/s12916-024-03780-7 |
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| author | Maria C. Magnus Yunsung Lee Ellen Ø. Carlsen Lise A. Arge Astanand Jugessur Liv G. Kvalvik Nils-Halvdan Morken Cecilia H. Ramlau-Hansen Mikko Myrskylä Per Magnus Siri E. Håberg |
| author_facet | Maria C. Magnus Yunsung Lee Ellen Ø. Carlsen Lise A. Arge Astanand Jugessur Liv G. Kvalvik Nils-Halvdan Morken Cecilia H. Ramlau-Hansen Mikko Myrskylä Per Magnus Siri E. Håberg |
| author_sort | Maria C. Magnus |
| collection | DOAJ |
| description | Abstract Background Few studies have examined associations between maternal epigenetic age acceleration and adverse birth outcomes, and none have investigated paternal epigenetic age acceleration. Our objective was to assess the associations of parental (both maternal and paternal) epigenetic age acceleration in relation to birth outcomes. Methods Parental epigenetic age was estimated using seven established epigenetic clocks in 2198 mothers and 2193 fathers from the Norwegian Mother, Father, and Child Cohort Study (MoBa). Individual epigenetic age acceleration was then calculated as residuals from linear regressions of estimates from the epigenetic clocks on chronological age. Further, linear regression was used to analyze differences in continuous outcomes (gestational length and standardized birthweight), while logistic regression was used for binary outcomes (preterm birth, post-term birth, small-for-gestational age [SGA], large-for-gestational age [LGA], and pre-eclampsia), adjusting for chronological age, parity, educational level, smoking, and BMI. Results Increasing maternal, but not paternal, epigenetic age acceleration was associated with decreased gestational length for five out of six clocks, with adjusted estimates ranging from a mean 0.51-day decrease (95% CI − 1.00, − 0.02; p-value 0.043) for the Horvath clock to a 0.80-day decrease (95% CI − 1.29, − 0.31; p-value 0.002) for the Levine clock. An association with increasing maternal epigenetic age acceleration according to the DunedinPACE clock was also seen with greater standardized birthweight [mean difference 0.08 (95% CI 0.04, 0.12; p-value < 0.001]. These results were also reflected in an increased risk of spontaneous preterm birth and LGA. No associations were observed with post-term birth, SGA, or pre-eclampsia. Conclusions Maternal, but not paternal, epigenetic age acceleration is associated with shorter pregnancies and an increased risk of spontaneous preterm birth. This may suggest that women’s biological age acceleration, including factors such as metabolic and physiologic state, is an additional risk factor for preterm delivery, beyond chronological age. |
| format | Article |
| id | doaj-art-23d2907d1c7b437a98e407fa7f8ac55d |
| institution | Kabale University |
| issn | 1741-7015 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | BMC |
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| spelling | doaj-art-23d2907d1c7b437a98e407fa7f8ac55d2025-01-12T12:26:47ZengBMCBMC Medicine1741-70152024-11-0122111010.1186/s12916-024-03780-7Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort studyMaria C. Magnus0Yunsung Lee1Ellen Ø. Carlsen2Lise A. Arge3Astanand Jugessur4Liv G. Kvalvik5Nils-Halvdan Morken6Cecilia H. Ramlau-Hansen7Mikko Myrskylä8Per Magnus9Siri E. Håberg10Centre for Fertility and Health, Norwegian Institute of Public HealthCentre for Fertility and Health, Norwegian Institute of Public HealthCentre for Fertility and Health, Norwegian Institute of Public HealthCentre for Fertility and Health, Norwegian Institute of Public HealthCentre for Fertility and Health, Norwegian Institute of Public HealthDepartment of Global Public Health and Primary Care, University of BergenCentre for Fertility and Health, Norwegian Institute of Public HealthDepartment of Public Health, Research Unit for Epidemiology, Aarhus UniversityMax Planck Institute for Demographic ResearchCentre for Fertility and Health, Norwegian Institute of Public HealthCentre for Fertility and Health, Norwegian Institute of Public HealthAbstract Background Few studies have examined associations between maternal epigenetic age acceleration and adverse birth outcomes, and none have investigated paternal epigenetic age acceleration. Our objective was to assess the associations of parental (both maternal and paternal) epigenetic age acceleration in relation to birth outcomes. Methods Parental epigenetic age was estimated using seven established epigenetic clocks in 2198 mothers and 2193 fathers from the Norwegian Mother, Father, and Child Cohort Study (MoBa). Individual epigenetic age acceleration was then calculated as residuals from linear regressions of estimates from the epigenetic clocks on chronological age. Further, linear regression was used to analyze differences in continuous outcomes (gestational length and standardized birthweight), while logistic regression was used for binary outcomes (preterm birth, post-term birth, small-for-gestational age [SGA], large-for-gestational age [LGA], and pre-eclampsia), adjusting for chronological age, parity, educational level, smoking, and BMI. Results Increasing maternal, but not paternal, epigenetic age acceleration was associated with decreased gestational length for five out of six clocks, with adjusted estimates ranging from a mean 0.51-day decrease (95% CI − 1.00, − 0.02; p-value 0.043) for the Horvath clock to a 0.80-day decrease (95% CI − 1.29, − 0.31; p-value 0.002) for the Levine clock. An association with increasing maternal epigenetic age acceleration according to the DunedinPACE clock was also seen with greater standardized birthweight [mean difference 0.08 (95% CI 0.04, 0.12; p-value < 0.001]. These results were also reflected in an increased risk of spontaneous preterm birth and LGA. No associations were observed with post-term birth, SGA, or pre-eclampsia. Conclusions Maternal, but not paternal, epigenetic age acceleration is associated with shorter pregnancies and an increased risk of spontaneous preterm birth. This may suggest that women’s biological age acceleration, including factors such as metabolic and physiologic state, is an additional risk factor for preterm delivery, beyond chronological age.https://doi.org/10.1186/s12916-024-03780-7Epigenetic ageAdverse birth outcomesGestational ageBirthweightPre-eclampsia |
| spellingShingle | Maria C. Magnus Yunsung Lee Ellen Ø. Carlsen Lise A. Arge Astanand Jugessur Liv G. Kvalvik Nils-Halvdan Morken Cecilia H. Ramlau-Hansen Mikko Myrskylä Per Magnus Siri E. Håberg Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort study BMC Medicine Epigenetic age Adverse birth outcomes Gestational age Birthweight Pre-eclampsia |
| title | Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort study |
| title_full | Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort study |
| title_fullStr | Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort study |
| title_full_unstemmed | Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort study |
| title_short | Parental epigenetic age acceleration and risk of adverse birth outcomes: the Norwegian mother, father and child cohort study |
| title_sort | parental epigenetic age acceleration and risk of adverse birth outcomes the norwegian mother father and child cohort study |
| topic | Epigenetic age Adverse birth outcomes Gestational age Birthweight Pre-eclampsia |
| url | https://doi.org/10.1186/s12916-024-03780-7 |
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