Invited Commentary

The case for prospective longitudinal studies in child maltreatment research: commentary on Dube, Williamson, Thompson, Felitti, and Anda (2004)

Longitudinal studies consistently report adverse long-term outcomes of childhood maltreatment. Little is known about the impact of childhood maltreatment on mental health among a marginalized population (New Zealand Māori); therefore, we cannot assume the effects of maltreatment are the same across the population.

Associations were examined between childhood sexual abuse (CSA), childhood physical punishment (CPP) and childhood neglect (CN) (<16 years) and mental health outcomes 18–40 years, by ethnicity (Māori/non-Māori).

Data from the Christchurch Health and Development Study, a study of a birth cohort of 1265 children born in Christchurch in 1977. By age 40, 17.8 % (n = 191) reported New Zealand Māori ethnic identity; 82.2 % (n = 883) were non-Māori.

CSA, CPP (<16 years) were measured at 18, 21 years; CN was measured at 40 years. Major depression, anxiety disorder, suicidal ideation, alcohol abuse/dependence and cannabis abuse/dependence were measured at ages 21, 25, 30, 35 and 40 years. Childhood confounding variables controlled. Analyses were extended to include Māori ethnicity.

After statistical adjustment, experience of severe childhood maltreatment increased odds of mental health problems 1.8–2.6×, compared to no maltreatment; the effects of maltreatment were similar for males and females. For Māori, some higher rates of mental health problems were seen among those maltreated, no statistically significant associations were detected after Bonferroni correction (among severe maltreatment vs. no maltreatment). Limitations should be considered when interpreting results.

Exposure to childhood maltreatment has long-term effects into middle-age. Further research employing culturally-sensitive approaches may help clarify Māori childhood maltreatment outcomes.

This meta-analysis aimed to examine the association of child abuse with adult coronary heart disease risk and separately by abuse subtypes, including emotional abuse, sexual abuse, and physical abuse.

Data were extracted from studies published up through December 2021 and on the basis of research from PubMed, Embase, CINAHL, and PsycINFO. Studies were selected if they included adults with or without any type of child abuse and measured the risk of any type of coronary heart disease. Statistical analyses were conducted in 2022. The random effects model was used to pool the effect estimates presented by RRs with 95% CIs. Heterogeneity was assessed using Q and I² statistics.

The pooled estimates were synthesized using 24 effect sizes from 10 studies with a sample size of 343,371 adults. Adults with child abuse were associated with a higher risk of coronary heart disease than those without (RR=1.52; 95% CI=1.29, 1.79), and the association was similar for myocardial infarction (RR=1.50; 95 % CI=1.08, 2.10) and unspecified coronary heart disease (RR=1.58; 95% CI=1.23, 2.02). Moreover, emotional (RR=1.48; 95% CI=1.29, 1.71), sexual (RR=1.47; 95% CI=1.15, 1.88), and physical (RR=1.48; 95% CI=1.22, 1.79) abuse were associated with increased risk of coronary heart disease.

Child abuse was associated with an increased risk of adult coronary heart disease. Results were generally consistent across abuse subtypes and sex. This study advocates further research on biological mechanisms linking child abuse to coronary heart disease as well as improvement in coronary heart disease risk prediction and targeted prevention approaches.

A sizeable literature documents the associations between adverse childhood experiences (ACEs) and poor health in later life. By and large, ACEs are measured using retrospective self-reports. Little is known about the longitudinal consistency of these self-reports in panel data with multiple measurements. This is especially true in adolescence, as most studies using ACEs self-reports have been conducted among adults. Furthermore, very few studies have explored the consistency of ACEs self-reports in low- and middle-income countries, where the reported prevalence of ACEs tends to be higher than in high-income countries. Addressing these gaps, the current study examines the consistency of ACEs self-reports among a cohort of adolescents (N = 1,878, age 10 to 16 at survey baseline) in rural Malawi. We use data from two waves of the ACE project of the Malawi Longitudinal Study of Families and Health carried out in 2017-18 and 2021. In addition to the high prevalence of self-reported ACEs among adolescents in our sample, we document very low consistency of self-reports over time (average Kappa coefficient of 0.11). This low consistency is attributable not only to adolescents reporting more ACEs over time, which could be due to new exposures, but also to adolescents reporting fewer ACEs over time. Analyses of survey vignettes indicate that individual and sociocultural perceptions of abuse do not explain this low consistency. We find that external events (such as changes in socioeconomic status and negative economic shocks) and internal psychological states (such as depression and post-traumatic stress disorder) both predict inconsistencies in ACEs self-reports. Compared with results from prior studies, our findings indicate that the longitudinal consistency of ACEs self-reports may be lower in adolescence than in adulthood. Taken together, these findings suggest that ACEs self-reports provided by adults may be biased by key processes unfolding in adolescence.

Exposure to early-life adversity (ELA) is associated with elevated risk for depression and anxiety disorders in adolescence. Identifying mechanisms through which ELA contributes to the emergence of depression and anxiety is necessary to design preventive interventions. One potential mechanism linking exposure to ELA with psychopathology is accelerated pubertal development. Exposure to trauma—specifically interpersonal violence—is associated with earlier pubertal timing, which in turn predicts adolescent-onset depression and anxiety disorders. We review the recent literature on adversity and accelerated pubertal development, exploring specific associations between trauma and accelerated pubertal development as a mechanism linking adversity with depression and anxiety disorders in adolescence. Finally, we suggest future directions for research exploring mechanisms linking ELA with accelerated pubertal development as well as pubertal timing and psychopathology in adolescence.