A Critique of the Adverse Childhood Experiences Framework in Epidemiology and Public Health: Uses and Misuses

International audienceAdverse childhood experiences (ACEs) have emerged as a major research theme. They make reference to an array of potentially harmful exposures occurring from birth to eighteen years of age and may be involved in the construction of health inequalities over the lifecourse. As with many simplified concepts, ACEs present limitations. They include diverse types of exposures, are often considered cumulatively, can be identified using prospective and retrospective approaches, and their multidimensional nature may lead to greater measurement error. From a public health perspective, ACEs are useful for describing the need to act upon complex social environments to prevent health inequalities at a population level. As the ACEs concept becomes popular in the context of policy interventions, concerns have emerged. As a probabilistic and population-level tool, it is not adapted to diagnose individual-level vulnerabilities, an approach which could ultimately exacerbate inequalities. Here, we present a critique of the ACEs framework, discussing its strengths and limits

Big Data and the Study of Social Inequalities in Health: Expectations and Issues

Understanding the construction of the social gradient in health is a major challenge in the field of social epidemiology, a branch of epidemiology that seeks to understand how society and its different forms of organization influence health at a population level. Attempting to answer these questions involves large datasets of varied heterogeneous data suggesting that Big Data approaches could be then particularly relevant to the study of social inequalities in health. Nevertheless, real challenges have to be addressed in order to make the best use of the development of Big Data in health for the benefit of all. The main purpose of this perspective is to discuss some of these challenges, in particular: (i) the perimeter and the particularity of Big Data in health, which must be broader than a vision centerd solely on care, the individual and his or her biological characteristics; (ii) the need for clarification regarding the notion of data, the validity of data and the question of causal inference for various actors involved in health, such data as researchers, health professionals and the civilian population; (iii) the need for regulation and control of data and their uses by public authorities for the common good and the fight against social inequalities in health. To face these issues, it seems essential to integrate different approaches into a close dialog, integrating methodological, societal, and ethical issues. This question cannot escape an interdisciplinary approach, including users or patients

Adverse childhood experiences and adult mood problems: evidence from a five-decade prospective birth cohort

Background Retrospectively recalled adverse childhood experiences (ACEs) are associated with adult mood problems, but evidence from prospective population cohorts is limited. The aims of this study were to test links between prospectively ascertained ACEs and adult mood problems up to age 50, to examine the role of child mental health in accounting for observed associations, and to test gender differences in associations. Methods The National Child Development Study is a UK population cohort of children born in 1958. ACEs were defined using parent or teacher reports of family adversity (parental separation, child taken into care, parental neglect, family mental health service use, alcoholism and criminality) at ages 7–16. Children with no known (n = 9168), single (n = 2488) and multiple (n = 897) ACEs were identified in childhood. Adult mood problems were assessed using the Malaise inventory at ages 23, 33, 42 and 50 years. Associations were examined separately for males and females. Results Experiencing single or multiple ACEs was associated with increased rates of adult mood problems after adjustment for childhood psychopathology and confounders at birth [2+ v. 0 ACEs – men: age 23: odds ratio (OR) 2.36 (95% confidence interval (CI) 1.7–3.3); age 33: OR 2.40 (1.7–3.4); age 42: OR 1.85 (1.4–2.4); age 50: OR 2.63 (2.0–3.5); women: age 23: OR 2.00 (95% CI 1.5–2.6); age 33: OR 1.81 (1.3–2.5); age 42: OR 1.59 (1.2–2.1); age 50: OR 1.32 (1.0–1.7)]. Conclusions Children exposed to ACEs are at elevated risk for adult mood problems and a priority for early prevention irrespective of the presence of psychopathology in childhood

Adverse childhood experiences and early life inflammation in the Avon Longitudinal Study of Parents and Children

BACKGROUND: Adverse childhood experiences (ACEs) have been associated with poorer health across the life course. Previous studies have used cumulative risk scores (ACE scores) or individual ACEs but these two approaches have important shortcomings. ACE scores assume that each adversity is equally important for the outcome of interest and the single adversity approach assumes that ACEs do not co-occur. Latent class analysis (LCA) is an alternative approach to operationalising ACEs data, identifying groups of people co-reporting similar ACEs. Here we apply these three approaches for ACEs operationalisation with inflammation in childhood with the aim of identifying particular ACEs or ACE combinations that are particularly associated with higher inflammation in early life. METHODS: Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) we compare ACE scores, single adversities and LCA-derived ACE clusters in their relationships with Interleukin-6 at age 9 (n = 4935) and C-Reactive Protein (CRP) at age 9 (n = 4887). ACEs included were parental separation/divorce, parental alcohol problems, parental mental health problems, parental offending, inter-parental violence, parental drug misuse, and physical, emotional and sexual abuse. RESULTS: Two thirds of the sample reported at least one ACE. Mother’s mental health problems was the most frequently reported ACE (32.3 %). LCA identified four ACE classes – ‘Low ACEs’ (81.1 %), ‘Maternal mental health problems’ (10.3 %), ‘Maternal mental health problems and physical abuse’ (6.3 %) and ‘Parental conflict, mental health problems and emotional abuse’ (2.4 %). Parental separation/divorce was associated with higher IL-6. Parental alcohol problems, paternal mental health problems, parental convictions and emotional abuse were associated with lower levels of IL-6. Associations for paternal mental health problems and emotional abuse were only observed for boys. ACE score and LCA-derived ACE classes were not associated with differences in IL-6. Girls in the ‘Maternal mental health problems’ cluster had lower CRP levels. CONCLUSIONS: Specific adversities and adversity combinations are important for differences in childhood inflammation. Some associations were only observed for girls or boys

Epigenetic modification of cytosines fine tunes the stability of i-motif DNA

i-Motifs are widely used in nanotechnology, play a part in gene regulation and have been detected in human nuclei. As these structures are composed of cytosine, they are potential sites for epigenetic modification. In addition to 5-methyl- and 5-hydroxymethylcytosine modifications, recent evidence has suggested biological roles for 5-formylcytosine and 5-carboxylcytosine. Herein the human telomeric i-motif sequence was used to examine how these four epigenetic modifications alter the thermal and pH stability of i-motifs. Changes in melting temperature and transitional pH depended on both the type of modification and its position within the i-motif forming sequence. The cytosines most sensitive to modification were next to the first and third loops within the structure. Using previously described i-motif forming sequences, we screened the MCF-7 and MCF-10A methylomes to map 5-methylcytosine and found the majority of sequences were differentially methylated in MCF7 (cancerous) and MCF10A (non-cancerous) cell lines. Furthermore, i-motif forming sequences stable at neutral pH were significantly more likely to be epigenetically modified than traditional acidic i-motif forming sequences. This work has implications not only in the epigenetic regulation of DNA, but also allows discreet tunability of i-motif stability for nanotechnological applications

Neighbourhood socioeconomic deprivation and allostatic load : a multi-cohort study

Living in deprived neighbourhoods may have biological consequences, but few studies have assessed this empirically. We examined the association between neighbourhood deprivation and allostatic load, a biological marker of wear and tear, taking into account individual's socioeconomic position. We analysed data from three cohort studies (CoLaus-Switzerland; EPIPorto-Portugal; Whitehall II-UK) comprising 16,364 participants. We defined allostatic load using ten biomarkers of dysregulated metabolic, cardiovascular, and inflammatory systems (body mass index; waist circumference; total, high and low density lipoprotein cholesterol; trig lycerides; glucose; systolic and diastolic blood pressure; C-reactive protein). Mixed Poisson regression models were fitted to examine associations with neighbourhood deprivation (in quintiles, Q1-least deprived as reference). After adjustment for confounding variables, participants living in the most deprived quintile had 1.13 times higher allostatic load than those living in the least deprived quintile (Relative Risk, RR, for Q2 RR = 1.06, 95%CI 1.03-1.09; Q3 = 1.06, 1.03-1.10; Q4 = 1.09, 1.06-1.12; Q5 = 1.13, 1.09-1.16). This association was partially modified by individual's socioeconomic position, such that the relative risk was higher in participants with low socioeconomic position (Q5 vs Q11.16, 1.11-1.22) than those with high socioeconomic position (Q5 vs Q1 1.07, 1.11-1.13). Neighbourhood deprivation is associated with biological wear and tear, suggesting that neighbourhood-level interventions may yield health gains.Peer reviewe

Association of neighbourhood disadvantage and individual socioeconomic position with all-cause mortality: a longitudinal multicohort analysis

BACKGROUND: Few studies have examined the interactions between individual socioeconomic position and neighbourhood deprivation and the findings so far are heterogeneous. Using a large sample of diverse cohorts, we investigated the interaction effect of neighbourhood socioeconomic deprivation and individual socioeconomic position, assessed using education, on mortality. METHODS: We did a longitudinal multicohort analysis that included six cohort studies participating in the European LIFEPATH consortium: the CoLaus (Lausanne, Switzerland), E3N (France), EPIC-Turin (Turin, Italy), EPIPorto (Porto, Portugal), Melbourne Collaborative Cohort Study (Melbourne, VIC, Australia), and Whitehall II (London, UK) cohorts. All participants with data on mortality, educational attainment, and neighbourhood deprivation were included in the present study. The data sources were the databases of each cohort study. Poisson regression was used to estimate the mortality rates and associations (relative risk, 95% CIs) with neighbourhood deprivation (Q1 being least deprived to Q5 being the most deprived). Baseline educational attainment was used as an indicator of individual socioeconomic position. Estimates were combined using pooled analysis and the relative excess risk due to the interaction was computed to identify additive interactions. FINDINGS: The cohorts comprised a total population of 168 801 individuals. The recruitment dates were 2003-06 for CoLaus, 1989-91 for E3N, 1992-98 for EPIC-Turin, 1999-2003 for EPIPorto, 1990-94 for MCCS, and 1991-94 for Whitehall II. We use baseline data only and mortality data obtained using record linkage. Age-adjusted mortality rates were higher among participants residing in more deprived neighbourhoods than those in the least deprived neighbourhoods (Q1 least deprived neighbourhoods, 369·7 per 100 000 person-years [95% CI 356·4-383·2] vs Q5-most deprived neighbourhoods 445·7 per 100 000 person-years [430·2-461·7]), but the magnitude of the association varied according to educational attainment (relative excess risk due to interaction=0·18, 95% CI 0·08-0·28). The relative risk for Q5 versus Q1 was 1·31 (1·23-1·40) among individuals with primary education or less, but less pronounced among those with secondary education (1·12; 1·04-1·21) and tertiary education (1·16; 1·07-1·27). Associations remained after adjustment for individual-level factors, such as smoking, physical activity, and alcohol intake, among others. INTERPRETATION: Our study suggests that the detrimental health effect of living in disadvantaged neighbourhoods is more pronounced among individuals with low education attainment, amplifying social inequalities in health. This finding is relevant to policies aimed at reducing health inequalities, suggesting that these issues should be addressed at both the individual level and the community level. FUNDING: The European Commission, European Regional Development Fund, the Portugese Foundation for Science and Technology

Patterning of educational attainment across inflammatory markers : Findings from a multi-cohort study

Background: Evidence suggests that the inflammatory reaction, an adaptive response triggered by a variety of harmful stimuli and conditions involved in the risk and development of many chronic diseases, is a potential pathway through which the socioeconomic environment is biologically embedded. Difficulty in interpreting the role of the inflammatory system in the embodiment dynamic arises because of heterogeneity across studies that use a limited but varied number of inflammatory markers. There is no consensus in the literature as to which inflammatory markers beyond the C-reactive protein and to a lesser extent interleukin 6 are related to the social environment. Accordingly, we aimed to investigate the association between educational attainment, and several markers of inflammation - C-reactive protein, fibrinogen, interleukin 6, interleukin 1 beta and tumor necrosis factor alpha- in 6 European cohort studies. Methods: Up to 17,470 participants from six European cohort studies with data on educational attainment, health behaviors and lifestyle factors, and at least two different inflammatory markers. Four sub-datasets were drawn with varying numbers of participants to allow pairwise comparison of the social patterning of C-reactive protein and any other inflammatory markers. To evaluate within each sub-dataset the importance of the context and cohort specificities, linear regression-based analyses were performed separately for each cohort and combined in a random effect meta-analysis to determine the relationship between educational attainment and inflammation. Results: We found that the magnitude of the relationship between educational attainment and five inflammatory biomarkers (C-reactive protein, fibrinogen, interleukin 6 and 1 beta and tumor necrosis factor alpha) was variable. By far the most socially patterned biomarker was C-reactive protein, followed by fibrinogen and to lesser extent interleukin 6, where a low educational attainment was associated with higher inflammation even after adjusting for health behaviours and body mass index. No association was found with interleukin 1 beta and tumor necrosis factor alpha. Conclusions: Our study suggests different educational patterning of inflammatory biomarkers. Further large-scale research is needed to explore social differences in the inflammatory cascade in greater detail and the extent to which these differences contribute to social inequalities in health.Peer reviewe

Multi-cohort study identifies social determinants of systemic inflammation over the life course

Chronic inflammation has been proposed as having a prominent role in the construction of social inequalities in health. Disentangling the effects of early life and adulthood social disadvantage on inflammation is key in elucidating biological mechanisms underlying socioeconomic disparities. Here we explore the relationship between socioeconomic position (SEP) across the life course and inflammation (as measured by CRP levels) in up to 23,008 participants from six European cohort studies from three countries conducted between 1958 and 2013. We find a consistent inverse association between SEP and CRP across cohorts, where participants with a less advantaged SEP have higher levels of inflammation. Educational attainment is most strongly related to inflammation, after adjusting for health behaviours, body mass index and later-in-life SEP. These findings suggest socioeconomic disadvantage in young adulthood is independently associated with later life inflammation calling for further studies of the pathways operating through educational processes.Peer reviewe