Supplementary information files for The relationship of childhood adversity with diurnal cortisol patterns and C-reactive protein at 60-64 years of age in the 1946 National Survey of Health and Development
datasetposted on 2021-07-20, 08:53 authored by Ellie RobsonEllie Robson, Tom Norris, Mark Hamer, Silvia CostaSilvia Costa, Rebecca Hardy, Will JohnsonWill Johnson
Supplementary files for article The relationship of childhood adversity with diurnal cortisol patterns and C-reactive protein at 60-64 years of age in the 1946 National Survey of Health and Development.
Early life adversity is increasingly prevalent and associated with greater morbidity and mortality. It is hypothesised that the link between psychosocial early life adversity and poor health in adulthood is due to abnormal hypothalamic-pituitary-adrenal (HPA) axis functioning (often measured as cortisol patterning) and inflammation (often measured via c-reactive protein (CRP)). This study aimed to investigate the relationship between early life psychosocial adversity and cortisol patterning and CRP at 60-64 years of age.
The MRC National Survey of Health and Development (NSHD) was used. The analytic “cortisol sample” included 843 individuals and the “CRP sample” included 1,150 individuals. Data on adversity experienced between ages 0-15 years were utilised to compose a cumulative childhood psychosocial early life adversity (ELA) score (0, 1, 2, 3+). CRP and salivary cortisol (waking, 30 min after waking, and evening) were collected at 60-64 years. Associations between the psychosocial ELA score and cortisol outcomes (cortisol awakening response (CAR), diurnal slope (DS), and evening and morning cortisol) were assessed using general linear regression. Tobit regression was used to assess the association between psychosocial ELA score and CRP. Adjustments were made for age at follow-up, sex, childhood maternal education, childhood paternal social class, childhood housing tenure, and birth weight. After testing for sex by ELA score interactions, analyses were repeated stratified by sex for the CRP sample.
In fully adjusted models, individuals who experienced the highest level of childhood psychosocial adversity (3+) had a 24.63 (-41.49, -7.76) % lower waking cortisol and a 7.30 (1.49, 13.12) % lower decline in cortisol across the day compared to those with a psychosocial ELA score of zero. In females, the highest level of childhood psychosocial adversity, compared to the lowest, was associated with 32.61 (2.98, 62.25) % higher CRP at 60-64 years, which attenuated to 20.38 % (-9.38, 50.14) upon adjustment for measures of early life socioeconomic position. Conversely, the association between childhood psychosocial adversity and CRP in males was null.
Our results suggest that high-levels of psychosocial adversity in childhood might result in a lower morning cortisol and flatter DS in mid-to-late-adulthood. The finding that adversity was related to higher CRP in females but not males requires replication and further investigation.
UK Medical Research Council (MRC) New Investigator Research Grant (MR/P023347/1)
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