Abstract
Background
Adverse childhood experiences (ACEs) are associated with increased risk of non-communicable diseases in adulthood, potentially mediated by chronic low-grade inflammation. Glycoprotein acetyls (GlycA) is a marker of chronic and cumulative inflammation. We investigated associations between ACEs and GlycA at different ages, in two generations of the population-based Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort.
Methods
ALSPAC offspring’s total ACE scores were generated for two age periods using prospectively collected data: 0-7y and 0-17y. GlycA was measured using high-resolution proton nuclear magnetic resonance at mean ages 8y, 18y, and 24y. Sample sizes ranged from: n=5116 (8y) to n=3085 (24y). ALSPAC mothers (n=4634) retrospectively reported ACEs experienced before age 18y and GlycA was assessed at mean age 49y. We used multivariable linear regression to estimate associations between ACEs (total ACE score and individual ACEs) and subsequent GlycA in both samples, adjusting for key confounders.
Results
Mean GlycA levels were similar in offspring and mothers and over time. In offspring, there was no evidence that ACEs (total score or individual ACE) were associated with GlycA at age 8y or 18y, or 24y after adjustment for maternal age at birth and parity, maternal marital status, household occupational social class, maternal education, maternal smoking, own ethnicity, sex, and age in months. In mothers, there was evidence of a positive association between the total ACE score and GlycA at age 49y (adjusted mean difference 0.007 mmol/L; 95%CI: 0.003, 0.01). Emotional neglect was the only individual ACE associated with higher GlycA after adjusting for confounders and other ACEs.
Conclusion
Results suggest the association between ACEs and GlycA may emerge in middle age. Future research should explore the extent to which inflammation in adulthood mediates well-documented associations between ACEs and adverse health outcomes in later life.
Adverse childhood experiences (ACEs) are associated with increased risk of non-communicable diseases in adulthood, potentially mediated by chronic low-grade inflammation. Glycoprotein acetyls (GlycA) is a marker of chronic and cumulative inflammation. We investigated associations between ACEs and GlycA at different ages, in two generations of the population-based Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort.
Methods
ALSPAC offspring’s total ACE scores were generated for two age periods using prospectively collected data: 0-7y and 0-17y. GlycA was measured using high-resolution proton nuclear magnetic resonance at mean ages 8y, 18y, and 24y. Sample sizes ranged from: n=5116 (8y) to n=3085 (24y). ALSPAC mothers (n=4634) retrospectively reported ACEs experienced before age 18y and GlycA was assessed at mean age 49y. We used multivariable linear regression to estimate associations between ACEs (total ACE score and individual ACEs) and subsequent GlycA in both samples, adjusting for key confounders.
Results
Mean GlycA levels were similar in offspring and mothers and over time. In offspring, there was no evidence that ACEs (total score or individual ACE) were associated with GlycA at age 8y or 18y, or 24y after adjustment for maternal age at birth and parity, maternal marital status, household occupational social class, maternal education, maternal smoking, own ethnicity, sex, and age in months. In mothers, there was evidence of a positive association between the total ACE score and GlycA at age 49y (adjusted mean difference 0.007 mmol/L; 95%CI: 0.003, 0.01). Emotional neglect was the only individual ACE associated with higher GlycA after adjusting for confounders and other ACEs.
Conclusion
Results suggest the association between ACEs and GlycA may emerge in middle age. Future research should explore the extent to which inflammation in adulthood mediates well-documented associations between ACEs and adverse health outcomes in later life.
| Original language | English |
|---|---|
| Pages (from-to) | 112-120 |
| Number of pages | 9 |
| Journal | Brain Behavior and Immunity |
| Volume | 100 |
| Early online date | 15 Nov 2021 |
| DOIs | |
| Publication status | Published - 28 Feb 2022 |
Bibliographical note
Funding Information:DB is supported by a National Health and Medical Research Council (Australia) Investigator Grant (GTN117574).
Funding Information:
ELA is funded by a Skills Development Fellowship from the UK Medical Research Council (MR/P014437/1).
Funding Information:
Research at Murdoch Children’s Research Institute is supported by the Victorian Government's Operational Infrastructure Support Program.
Funding Information:
RL was funded by the UK’s Economic and Social Research Council (grant code: ES/P010229/1).
Funding Information:
LDH is funded by a Career Development Award from the UK Medical Research Council (MR/M020894/1).
Funding Information:
The UK Medical Research Council and Wellcome (Grant ref: 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC. This publication is the work of the authors and DC will serve as guarantor for the contents of this paper. A comprehensive list of grants funding is available on the ALSPAC website ( http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf ).
Funding Information:
GMK acknowledges funding support from the Wellcome Trust (grant code: 201486/Z/16/Z), the MQ: Transforming Mental Health (grant code: MQDS17/40), the Medical Research Council UK (grant code: MC_PC_17213 and MR/S037675/1) and the BMA Foundation (J Moulton grant 2019).
Funding Information:
This work was supported in part by the GW4 BIOMED DTP (D.C., MR/N0137941/), awarded to the Universities of Bath, Bristol, Cardiff and Exeter from the Medical Research Council (MRC)/UKRI.
Keywords
- ALSPAC
- Adverse childhood experiences
- Biomarker
- Cohort study
- Glycoprotein acetyls
- Inflammation
ASJC Scopus subject areas
- Immunology
- Endocrine and Autonomic Systems
- Behavioral Neuroscience
