Prenatal and childhood adversity and inflammation in children: A population-based longitudinal study
Eirini Flouri1, Marta Francesconi1, Emily Midouhas1
1Department of Psychology and Human Development, UCL Institute of Education, University College London, UK.
Insights
Childhood stress, not prenatal stress, is linked to higher inflammation in girls. The number and increase of stressful events in childhood are associated with elevated interleukin-6 (IL-6) levels in females, highlighting gender-specific effects.
Area of Science:
- Child Health
- Psychoneuroimmunology
- Developmental Psychology
Background:
- Childhood stressful life events are linked to inflammation.
- Prenatal development exposures also correlate with childhood inflammation.
- The joint effect and interaction of these exposures remain understudied.
Purpose of the Study:
- To investigate the relationship between prenatal and childhood stressful events and inflammatory markers (CRP and IL-6) at age 9.
- To explore the interaction effect of these exposures on inflammation.
- To examine gender-specific associations.
Main Methods:
- Utilized data from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (n=3,915).
- Employed latent growth curve modeling for childhood event trajectories.
- Applied linear regression, controlling for confounders and stratifying by gender.
Main Results:
- Childhood stressful events (number and increase) were associated with higher IL-6 levels in girls, independent of prenatal events.
- Prenatal events did not show an association with inflammatory markers when childhood events were controlled.
- No synergistic effects between prenatal and childhood events were observed.
Conclusions:
- Adverse childhood life events, but not prenatal events, are independently associated with elevated inflammatory markers in girls.
- The findings suggest a gender-specific impact of childhood stress on inflammation.
- Further research into this gender specificity is warranted.
Background:
Stressful life events experienced during childhood and early prenatal development have been associated with inflammation during childhood. However, no study has considered these two exposures jointly, or has investigated the effect of their interaction.
Methods:
In the Avon Longitudinal Study of Parents and Children, a general-population birth cohort, we explored if inflammatory markers [serum C-reactive protein (CRP) and interleukin 6 (IL-6)] at age 9 years were related to early prenatal events (at 18 weeks pregnancy), childhood events (measured on seven occasions at ages 0-9 years) and their interaction (n = 3,915). Latent growth curve modelling estimated trajectories of childhood events, and linear regression explored associations of prenatal and childhood events with inflammatory markers. Models controlled for ethnicity, socioeconomic status and body mass index, were stratified by gender and considered both unweighted and weighted (by impact) event exposures.
Results:
Even after adjustment for confounders and prenatal events, both the intercept and the slope of number of childhood events were associated with IL-6, but only in females. The significant effect of the slope held for both weighted (by impact) and unweighted event specifications. Prenatal events were not associated with either inflammatory marker when childhood events were controlled. There was no evidence for synergistic effects of prenatal and childhood events.
Conclusion:
Independently of prenatal adverse life events, the number and increase in number of adverse life events experienced in childhood were associated positively with plasma levels of inflammatory markers, such as IL-6, in girls. This gender specificity warrants further research.
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