Olakunle Ayokunmi Oginni

BackgroundNinety percent of the world’s children live in Low-/Middle-Income Countries (LMICs),but relatively little is known about children’s mental health risk in these settings. Using agenetically informative twin-family design, we estimated parent-child associations for mentalhealth symptoms (MHSs), indirect effects through specific risk/protective factors, and howparental MHSs impact genetic/environmental influences on child MHSs in Nigeria.MethodsWe recruited 320 twin pairs (aged 3-5 years) and both parents in two Nigerian towns.Participants were assessed for MHSs (emotional/behavioural symptoms in children; anxiety,depressive and Attention-Deficit Hyperactivity Disorder symptoms in parents), and selectedrisk/protective factors (adverse home environments, adverse childhood experiences, poorphysical health; and religiosity, parental warmth and prosociality). We used structural equationmodelling to test parent-child MHS associations, and mediation by risk/protective factors. Weestimated latent genetic (A), shared environmental (C) and individual-specific environmental(E) influences on child MHSs, and how parent MHSs impact these influences using univariatetwin models.ResultsChild MHSs were significantly associated with MHSs in both parents. The strongestindirect effects for parent-child MHS associations were through adverse childhood experiencesand diminished parental warmth. Others indirect pathways involved poor physical health anddiminished prosociality. Latent A and C influences each explained 22-29% of the individualdifferences in children’s MHSs. Independent of A influences, C influences were impacted byparents’ MHSs.ConclusionOur findings indicate that potentially modifiable environmental pathways are importantfor understanding parent-child MHS associations for very young children in a LMIC, and thesemay inform intervention design. Larger and more rigorous genetically informative designs areneeded to replicate and extend our findings.

Background: ADHD has been associated with BMI, across the lifespan. A possible mechanism linking ADHD and BMI is binge eating symptoms. Previous research has found associations between ADHD, binge eating symptoms, and BMI. However, the role of genetic and environmental influences on these associations remains unclear. Method: We utilized data from the Twins Early Development Study, comprising 4,363 monozygotic and 8,575 dizygotic twin pairs. ADHD symptoms in childhood and adolescence were assessed using parent-reported questionnaires. Adult ADHD symptoms were measured using both self-report and parent-report questionnaires. Phenotypic mediation models examined whether binge eating symptoms mediated the association between ADHD and BMI, without controlling for genetic confounding. Subsequently, the etiological architecture underlying the associations among the three traits across childhood, adolescence, and adulthood were investigated by incorporating genetic and environmental influences into the models. Results: Binge eating symptoms significantly mediated the association between ADHD symptoms and BMI in both adolescence and adulthood. However, these mediation effects were no longer present once genetic and environmental influences were incorporated into the models. The best-fitting model in childhood, adolescence, and adulthood was Cholesky decomposition models, where covariance between traits was explained by shared etiology. Conclusions: This twin study reveals shared liability across ADHD, binge eating symptoms, and BMI. The mediating role of binge eating symptoms in the relationship between ADHD symptoms and BMI was largely confounded by shared genetic influences. Intervention strategies could focus more on common underlying behavioral and self-regulatory mechanisms across these traits, as well as placing more emphasis on symptom patterns within families.

High or persistent levels of aggression are associated with psychopathology and difficulties with health and education as the child develops. Parenting behaviours have been frequently associated with childhood aggression, however much of this literature does not control for the shared genetics between parent and child or investigate the direction of effects. Here, we triangulated across two family-based designs, the Norwegian Mother Father and Child Cohort Study (MoBa) and the Early Growth and Development Study (EGDS) from the United States, both of which have comparable measures and allow for direction-of-causation analysis and control for shared genetics. Analyses were pre-registered.We found converging evidence across both studies for both genetic and environmental transmission in the relationship between parenting behaviours and child aggressive behaviour, with the association between positive parenting and lower child aggression being driven primarily by shared genetics. In MoBa, 47% of the association between inconsistent parenting and child aggression was explained by shared genetics. We found significant child-to-parent effects in both the MoBa and the EGDS samples. This work shows the strength of triangulation, allowing us to describe a pattern of intergenerational association that is not dependent on a specific sample or study design.

This study examined the prevalence of domestic violence (DV) exposure in in-school adolescents, the forms and ways in which adolescents get exposed or are involved in domestic violence, and factors that are associated with exposure to domestic violence. The study aimed to determine the pattern and factors associated with child exposure to domestic violence (CEDV) in Nigeria. A multistage sampling technique was used to recruit 406 students from four secondary schools in Ile-Ife, South-western Nigeria; the design was descriptive cross-sectional. Standardized, facilitated, self-administered, semi-structured questionnaires were administered to participants after obtaining their assent and parental consent. Information collected included sociodemographic data and details of exposure to DV using the CEDV questionnaire. Data collected were analyzed using descriptive and inferential statistics with IBM SPSS Statistics for Windows, version 25 (IBM Corp., Armonk, NY, USA). The prevalence of exposure to any form of domestic violence was 84.7%. Verbal abuse was the most prevalent form of abuse observed by 78.8% of the participants. A third (32.1%) of participants reported exposure to DV for at least 4 years. About 45.3% of those exposed were involved in the DV to varying degrees. Most of those exposed to DV experienced it as first-hand witnesses, and 58.1% were direct victims: physically, emotionally, or sexually. Low socioeconomic class was significantly associated with exposure to DV (χ² = 6.158 and p = .046). Participants had high exposure to DV, and a large proportion of them were involved, with those from lower socioeconomic classes being at higher risk. Efforts must be put in place in the home (family) to protect children and to facilitate optimal psychosocial development.

Globally, most children and adolescents live in low- and middle-income (LAMI) countries. Despite the high and under-recognized mental health burden in these settings, there is little systematic research to inform cost-effective mental health interventions. Identifying causal risk and protective mechanisms is important to inform such interventions. Longitudinal genetically informative designs can help identify potentially causal environmental mechanisms in the etiology of childhood psychopathology but few have been carried out in LAMI settings. We tested the feasibility of a twin-family study in a semi-urban setting in South-Western Nigeria. We recruited 320 family units, each comprising at least one parent and both twins aged 2.5–5.9 (x̄ = 4.0 ± 0.92) years from two towns using five strategies: direct and indirect contacts, radio adverts, cluster sampling (based on local administrative units) and snowball sampling. Participants were asked about their willingness to participate in future research including providing biological samples. These were supplemented with participant engagement activities before and after data collection. Snowball sampling was the most effective strategy while cluster sampling was the least effective (recruiting 46.3% and 8.3% of participants, respectively). Direct contacts and cluster sampling appeared prone to excluding under-represented participants. A large proportion of the participants (98–99%) were willing to participate in future studies. Challenges included grant administration (finance and ethical priorities) and desirability bias. Twin research is feasible in LAMI sub-Saharan Africa, with snowball sampling being an efficient means of recruiting a diverse sample. Participant involvement and engagement is useful to inform the execution of genetically-informative research in a LAMI context.

In the current study, we explored barriers to accessing gender-affirming care among transgender and gender-diverse (TGD) people in Nigeria. Between February and September 2021, we conducted focus group discussions with 25 adult TGD individuals residing in Nigeria. We found (1) a lack of trans-competent health care providers, (2) high medical costs, (3) limited access to accurate health information, (4) experiences of transphobia, and (5) a lack of trans-specific programming. Health care services that cater to the unique needs of TGD people in Nigeria are needed. ( Am J Public Health. 2025;115(8):1231–1235. https://doi.org/10.2105/AJPH.2025.308057 )

We assessed genetic and environmental influences on social isolation across childhood and the overlap between social isolation and mental health symptoms including depression symptoms, conduct problems, and psychotic-like experiences from adolescence to young adulthood. Participants included 2,232 children from the Environmental Risk Longitudinal Twin Study. Social isolation was measured at ages 5, 7, 10, 12, and 18. A Cholesky decomposition was specified to estimate the genetic and environmental influences on social isolation across ages 5, 7, 10, and 12. An independent pathway model was used to assess additive genetic (A), shared environmental (C), and non-shared environmental (E) influences on the overlap between social isolation and mental health problems from age 12 to 18. Genetic and non-shared environmental influences accounted for half of the variance in childhood social isolation. Genetic influences contributed to the continuity of social isolation across childhood, while non-shared environmental influences were age-specific. The longitudinal overlap between social isolation and mental health symptoms was largely explained by genetic influences for depression symptoms (r = 0.15–0.24: 82–84% A, 11–12% C, and 5–6% E) and psychotic-like experiences (r = 0.13–0.15: 81–91% A, 0–8% C, and 9–11% E) but not conduct problems (r = 0.13–0.16; 0–42% A, 42–81% C, 16–24% E). Our findings emphasise that rather than a risk factor or an outcome, social isolation is aetiologically intertwined with the experience of poor mental health. An integrative assessment of social isolation could be a helpful indicator of underlying mental health symptoms in young people.