scholarly journals 1173The impact of adverse and positive experiences on inflammatory outcomes in Australian and UK children

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Shuaijun Guo ◽  
Dawid Gondek ◽  
Meredith O’Connor ◽  
Stephanie Cahill ◽  
Marnie Downes ◽  
...  

Abstract Background Inflammation is one of key mechanisms linking childhood experiences to later chronic disease risk. Childhood adversity is associated with inflammation, but little is known about positive experiences. We examine how adverse and positive experiences are associated with inflammatory markers in late childhood, and whether they have an interaction effect. Methods Data sources: Longitudinal Study of Australian Children (LSAC; N = 1237) and Avon Longitudinal Study of Parents and Children (ALSPAC; N = 3488). Exposures: Adverse and positive experiences assessed from 0 to 11 (LSAC) and 0-14 years (ALSPAC). Adversity indicators included parent legal problems, family violence, mental illness, substance abuse, harsh parenting, parental divorce, neighbourhood violence, family member death, and bullying victimization. Positive experiences included positive parenting practice, trusting and supportive relationships, supportive neighbourhood and home learning environments, social engagement and enjoyment. Outcomes: Inflammation quantified by high-sensitivity C-reactive protein (hsCRP) and glycoprotein acetyls (GlycA). Analyses: Linear regression was used to estimate relative change in inflammatory markers, adjusted for sociodemographics. Outcomes were log-transformed. Results Exposure to adversity was associated with higher levels of inflammation (e.g., CRP: β = 8.8%, 95% CI= -16.5% to 34.2% in LSAC), whereas exposure to positive experiences was associated with lower levels (e.g., CRP: β=-18.9%, 95% CI= -45.8% to 7.9% in LSAC), after adjusting for sociodemographics. There was no interaction effect of adverse and positive experiences on inflammation. Conclusions Adverse and positive experiences have independent and small effects on children’s inflammation across two cohorts. Key messages Positive experiences are critical to inform interventions to improve inflammatory outcomes for children who face adversity.

2018 ◽  
Vol 3 ◽  
pp. 106 ◽  
Author(s):  
Lotte C. Houtepen ◽  
Jon Heron ◽  
Matthew J. Suderman ◽  
Kate Tilling ◽  
Laura D. Howe

Background: Exposure to adverse childhood experiences (ACEs) is a risk factor for poor later life health. Here, we describe the ACE variables measured in the children of the Avon Longitudinal Study of Parents and Children (ALSPAC) study, and a method used to derive summary measures and deal with missing data in them.    Methods: The ALSPAC data catalogue (59 608 variables) was searched in September 2017 for measures on adversity exposure between birth and 18 years. 6140 adversity questions were then screened for conforming to our ACE definitions and suitability for dichotomisation. This screening identified 541 questions on ten ‘classic’ ACEs (sexual, physical or emotional abuse, emotional neglect, substance abuse by the parents, parental mental illness or suicide attempt, violence between parents, parental separation, bullying and parental criminal conviction) and nine additional ACEs (bond between parent and child, satisfaction with neighbourhood, social support for the parent, social support for the child, physical illness of a parent, physical illness of the child, financial difficulties, low social class and violence between child and partner). These were used to derive a binary construct for exposure to each ACE. Finally, as cumulative measures of childhood adversity, different combinations of the 19 ACE constructs were summed to give total adversity scores. An appropriate strategy for multiple imputation was developed to deal with the complex patterns of missing data. Results: The ACE constructs and ACE-scores for exposure between birth and 16 years had prevalence estimates that were comparable to previous reports (for instance 4% sexual abuse, 18% physical abuse, 25% bullied, 32% parental separation). Conclusions: ACE constructs, derived using a pragmatic approach to handle the high dimensional ALSPAC data, can be used in future analyses on childhood adversity in ALSPAC children.


2019 ◽  
Vol 36 (7) ◽  
pp. 596-606 ◽  
Author(s):  
Melissa Tracy ◽  
Madeleine Salo ◽  
Natalie Slopen ◽  
Tomoko Udo ◽  
Allison A. Appleton

2020 ◽  
Vol 122 ◽  
pp. 104914
Author(s):  
Rebecca E Lacey ◽  
Mel Bartley ◽  
Michelle Kelly-Irving ◽  
Leonardo Bevilacqua ◽  
Eleonora Iob ◽  
...  

2021 ◽  
pp. 1-11
Author(s):  
Leslie Atkinson ◽  
Divya Joshi ◽  
Parminder Raina ◽  
Lauren E. Griffith ◽  
Harriet MacMillan ◽  
...  

Abstract Background Adverse childhood experiences (ACEs) are associated with multimorbidity in adulthood. This link may be mediated by psychosocial and biological factors, but evidence is lacking. The current study evaluates this mediation model. Method We analyzed data from the Canadian Longitudinal Study of Aging (N = 27 170 community participants). Participants were 45–85 years at recruitment, when allostatic load and social engagement data were collected, and 3 years older at follow-up, when ACEs and multimorbidity data were collected. Structural equation modeling was used to test for mediation in the overall sample, and in sex- and age-stratified subsamples, all analyses adjusted for concurrent lifestyle confounds. Results In the overall sample, ACEs were associated with multimorbidity, directly, β = 0.12 (95% confidence interval 0.11–0.13) and indirectly. Regarding indirect associations, ACEs were related to social engagement, β = −0.14 (−0.16 to −0.12) and social engagement was related to multimorbidity, β = −0.10 (−0.12 to −0.08). ACEs were related to allostatic load, β = 0.04 (0.03–0.05) and allostatic load was related to multimorbidity, β = 0.16 (0.15–0.17). The model was significant for males and females and across age cohorts, with qualifications in the oldest stratum (age 75–85). Conclusions ACEs are related to multimorbidity, directly and via social engagement and allostatic load. This is the first study to show mediated pathways between early adversity and multimorbidity in adulthood. It provides a platform for understanding multimorbidity as a lifespan dynamic informing the co-occurrence of the varied disease processes represented in multimorbidity.


Author(s):  
Riikka E. Taskinen ◽  
Sari Hantunen ◽  
Tomi-Pekka Tuomainen ◽  
Jyrki K. Virtanen

Abstract Background/objectives Epidemiological studies suggest that whole grain intake has inverse associations with low-grade inflammation, but findings regarding refined grains are inconclusive. Our objective was to investigate whether consumption of whole or refined grains is associated with serum high sensitivity CRP (hs-CRP). Subjects/methods The study included 756 generally healthy men and women aged 53–73 years from the Kuopio Ischaemic Heart Disease Risk Factory Study, examined in 1999–2001. Dietary intakes were assessed using 4-day food records. ANCOVA and linear regression were used for analyses. Results The mean intake of whole and refined grains was 136 g/day (SD 80) and 84 g/day (SD 46), respectively. Higher whole grain intake was associated with lower hs-CRP concentration and higher refined grain intake with higher concentration after adjustment for lifestyle and dietary factors. Each 50 g/d higher whole grain intake was associated with 0.12 mg/L (95% Cl 0.02–0.21 mg/L) lower hs-CRP concentration and each 50 g/d higher refined grain intake with 0.23 mg/L (95% Cl 0.08–0.38) higher concentration. Adjustment for fibre from grains attenuated the associations especially with whole grains. There were no statistically significant interactions according to gender or BMI (P for interactions >0.065). Conclusions The results of this study suggest that higher intake of whole grains is associated with lower concentrations of hs-CRP and higher intake of refined grains is associated with higher concentrations. However, especially the association with whole grain intake was attenuated after adjusting for fibre intake from grains, suggesting that cereal fibre may partly explain the association.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yingxin Chen ◽  
Susan Hodgson ◽  
John Gulliver ◽  
Raquel Granell ◽  
A. John Henderson ◽  
...  

Abstract Background Evidence suggests that exposure to particulate matter with aerodynamic diameter less than 10 μm (PM10) is associated with reduced birth weight, but information is limited on the sources of PM10 and exposure misclassification from assigning exposures to place of residence at birth. Methods Trimester and source-specific PM10 exposures (PM10 from road source, local non-road source, and total source) in pregnancy were estimated using dispersion models and a full maternal residential history for 12,020 births from the Avon longitudinal study of parents and children (ALSPAC) cohort in 1990–1992 in the Bristol area. Information on birth outcomes were obtained from birth records. Maternal sociodemographic and lifestyle factors were obtained from questionnaires. We used linear regression models for continuous outcomes (birth weight, head circumference (HC), and birth length (BL) and logistic regression models for binary outcomes (preterm birth (PTB), term low birth weight (TLBW) and small for gestational age (SGA)). Sensitivity analysis was performed using multiple imputation for missing covariate data. Results After adjustment, interquartile range increases in source specific PM10 from traffic were associated with 17 to 18% increased odds of TLBW in all pregnancy periods. We also found odds of TLBW increased by 40% (OR: 1.40, 95%CI: 1.12, 1.75) and odds of SGA increased by 18% (OR: 1.18, 95%CI: 1.05, 1.32) per IQR (6.54 μg/m3) increase of total PM10 exposure in the third trimester. Conclusion This study adds to evidence that maternal PM10 exposures affect birth weight, with particular concern in relation to exposures to PM10 from road transport sources; results for total PM10 suggest greatest effect in the third trimester. Effect size estimates relate to exposures in the 1990s and are higher than those for recent studies – this may relate to reduced exposure misclassification through use of full residential history information, changes in air pollution toxicity over time and/or residual confounding.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Darina Czamara ◽  
Elleke Tissink ◽  
Johanna Tuhkanen ◽  
Jade Martins ◽  
Yvonne Awaloff ◽  
...  

AbstractLasting effects of adversity, such as exposure to childhood adversity (CA) on disease risk, may be embedded via epigenetic mechanisms but findings from human studies investigating the main effects of such exposure on epigenetic measures, including DNA methylation (DNAm), are inconsistent. Studies in perinatal tissues indicate that variability of DNAm at birth is best explained by the joint effects of genotype and prenatal environment. Here, we extend these analyses to postnatal stressors. We investigated the contribution of CA, cis genotype (G), and their additive (G + CA) and interactive (G × CA) effects to DNAm variability in blood or saliva from five independent cohorts with a total sample size of 1074 ranging in age from childhood to late adulthood. Of these, 541 were exposed to CA, which was assessed retrospectively using self-reports or verified through social services and registries. For the majority of sites (over 50%) in the adult cohorts, variability in DNAm was best explained by G + CA or G × CA but almost never by CA alone. Across ages and tissues, 1672 DNAm sites showed consistency of the best model in all five cohorts, with G × CA interactions explaining most variance. The consistent G × CA sites mapped to genes enriched in brain-specific transcripts and Gene Ontology terms related to development and synaptic function. Interaction of CA with genotypes showed the strongest contribution to DNAm variability, with stable effects across cohorts in functionally relevant genes. This underscores the importance of including genotype in studies investigating the impact of environmental factors on epigenetic marks.


Author(s):  
Ieuan Evans ◽  
Jon Heron ◽  
Joseph Murray ◽  
Matthew Hickman ◽  
Gemma Hammerton

Experimental studies support the conventional belief that people behave more aggressively whilst under the influence of alcohol. To examine how these experimental findings manifest in real life situations, this study uses a method for estimating evidence for causality with observational data—‘situational decomposition’ to examine the association between alcohol consumption and crime in young adults from the Avon Longitudinal Study of Parents and Children. Self-report questionnaires were completed at age 24 years to assess typical alcohol consumption and frequency, participation in fighting, shoplifting and vandalism in the previous year, and whether these crimes were committed under the influence of alcohol. Situational decomposition compares the strength of two associations, (1) the total association between alcohol consumption and crime (sober or intoxicated) versus (2) the association between alcohol consumption and crime committed while sober. There was an association between typical alcohol consumption and total crime for fighting [OR (95% CI): 1.47 (1.29, 1.67)], shoplifting [OR (95% CI): 1.25 (1.12, 1.40)], and vandalism [OR (95% CI): 1.33 (1.12, 1.57)]. The associations for both fighting and shoplifting had a small causal component (with the association for sober crime slightly smaller than the association for total crime). However, the association for vandalism had a larger causal component.


Sign in / Sign up

Export Citation Format

Share Document