Principal findings

Our study provides a thorough analysis of how childhood psychosocial adjustment (CPA) affects the likelihood of developing cardiometabolic diseases (CMDs) during mid-life. Utilising data from two sizeable birth cohorts, our findings indicate a significant association between poor CPA and an elevated likelihood of hypertension, diabetes and obesity in mid-life. Specifically, emotional problems, hyperactivity and miscellaneous CPA subtypes were linked to all three CMDs, while conduct problems correlated with hypertension and diabetes. Additionally, mediation analysis suggested that both lower educational attainment and early-life depression partially contributed to the connection between CPA and CMDs

Comparison with other studies

In support of our results, prior research has identified various CPA factors (e.g. conduct problems, mental health problems, attention-deficit hyperactivity disorder (ADHD)) as predictors of adverse adult outcomes.^{Reference Galéra, Bouvard, Lagarde, Michel, Touchette and Fombonne12,Reference Clayborne, Varin and Colman16,Reference Canino, Shrout, Wall, Alegria, Duarte and Bird17} Colman and colleagues noted that adolescents with severe externalising behaviours face a range of social and health challenges, including mental health issues, strained family life, and poor employment and educational outcomes in adulthood,^{Reference Colman, Murray, Abbott, Maughan, Kuh and Croudace18} which also extend to physical health.^{Reference Melaku, Appleton, Reynolds, Sweetman, Stevens and Lack19} Similarly, Hoffmann and colleagues found enduring links between adolescent mental health problems (reported by parents or teachers) and negative educational, economic, social, health and psychological outcomes later in life.^{Reference Hoffmann, Evans-Lacko, Collishaw, Knapp, Pickles and Shearer20} Recent meta-analyses have also connected ADHD with adverse academic, mental health, substance use and employment outcomes.^{Reference Erskine, Norman, Ferrari, Chan, Copeland and Whiteford21} Nevertheless, the evidence directly associating CPA with mid-life CMDs remains scarce. Drawing on the National Child Development Study (NCDS), Ploubidis and colleagues explored early-life mental health's relationship with cardiometabolic biomarkers at age 42, identifying associations with elevated fibrinogen levels and blood pressure.^{Reference Ploubidis, Batty, Patalay, Bann and Goodman9} Thapar and colleagues also reported correlations between ADHD symptoms and higher body mass index (BMI), blood pressure and triglyceride levels, using the same analytical approach as Ploubidis et al.^{Reference Thapar, Riglin, Blakey, Collishaw and Davey Smith22} Our study extends and refines this body of evidence, delivering a detailed evaluation of childhood psychosocial conditions, integrating data from all life-course stages, rather than a single time point, to capture comprehensive information on hypertension, diabetes and obesity. Moreover, besides using NCDS data, we explored this relationship with the 1970 British Cohort Study (BCS70) and conducted a meta-analysis of these cohorts to further strengthen the reliability and validity of our findings.

Potential mechanism

The mechanisms through which poor CPA might be associated with increased odds of CMDs are likely multifaceted. Our analysis indicates that lower educational attainment partly mediates this relationship. Education, a precursor to socioeconomic factors such as occupation and income, is crucial for maintaining healthy lifestyles and accessing healthcare.^{Reference Stringhini, Carmeli, Jokela, Avendaño, Muennig and Guida23} Individuals with lower educational attainment may be more likely to occupy jobs that are physically demanding, low-paid and offer little control, which are stressors that have been linked to poor health outcomes.^{Reference Stormacq, Van den Broucke and Wosinski24} Limited income also restricts access to healthcare, nutritious food and safe living environments, further heightening the risk of CMDs.^{Reference Raghupathi and Raghupathi25} Furthermore, individuals with lower educational levels are more likely to smoke, have poor diets and lead sedentary lifestyles, and they are also less likely to follow medical advice,^{Reference Zhang, Lu, Wu, Cui, Wu and Hu26} which diminishes the effectiveness of CMD prevention measures in primary and secondary care, leaving them more susceptible to these diseases. Early adulthood depression also emerged as a notable mediator in the CPA–CMD relationship. Depression can encourage development of CMDs through behavioural pathways (e.g. physical inactivity, unhealthy eating)^{Reference Opie, Abbott, Crawford and Ball27,Reference Roshanaei-Moghaddam, Katon and Russo28} and has significant biological impacts on the development of CMDs. For instance, depression is associated with increased systemic inflammation, insulin resistance and endothelial dysfunction, all of which contribute to CMDs.^{Reference Goldstein, Carnethon, Matthews, McIntyre, Miller and Raghuveer29} Our findings did not identify early-life smoking as a significant mediator in the CPA–CMD relationship, which contrasts with previous studies that have highlighted smoking as a critical risk factor for CMDs. This discrepancy might arise from two factors. First, our study defined smoking habits as either ‘ever smoking’ or ‘never smoking’, which may not account for those who quit smoking later, thus reducing their duration of exposure. Second, our participants were relatively young (aged ≤55 years in the NCDS and ≤46 in BCS70), meaning the cumulative harm from smoking was likely lower and its dose-response effect on additional cardiometabolic risks had not fully manifested.^{Reference Inoue-Choi, Christensen, Rostron, Cosgrove, Reyes-Guzman and Apelberg30} It is important to acknowledge that other factors, including sleep patterns, diet and physical inactivity, may also serve as mediators. Further research is essential to explore and quantify these additional indirect pathways connecting CPA to CMDs.

Apart from the indirect effect between global CPA and mid-life CMDs, our study also suggested direct effects linking subtypes of CPA to mid-life CMDs. Specifically, childhood hyperactivity significantly increased the odds of hypertension, diabetes and obesity in mid-life. Although hyperactivity might intuitively seem protective against obesity owing to increased physical activity, observational studies have shown that those with ADHD often experience dysregulation of eating behaviour.^{Reference Khalife, Kantomaa, Glover, Tammelin, Laitinen and Ebeling31} Additionally, recent studies indicate genetic overlaps between ADHD and BMI,^{Reference Peters, Nullig, Antel, Naaresh, Laabs and Tegeler32} and a causal relationship between childhood ADHD and obesity was revealed by a Mendelian randomisation study.^{Reference Leppert, Riglin, Wootton, Dardani, Thapar and Staley3} Childhood hyperactivity also increased the odds of hypertension. Besides the similar pathways shared with obesity, medications used to treat hyperactivity may partly account for this relationship.^{Reference Thumfart, Jawaid, Bright, Flachsmann and Mansuy33} However, some studies have found conflicting results, suggesting that hyperactivity could be protective against obesity and showing no significant relationship with blood pressure.^{Reference Lundgren, Henriksson, Delisle Nyström, Silfvernagel and Löf34,Reference Saad, Randhawa and Pang35} These discrepancies indicate that the relationship between hyperactivity and CMDs may be influenced by the severity of exposure and the treatment received. Psychological factors are well-documented risk factors for CMDs. Our findings indicate that children with emotional problems are more likely to develop hypertension, diabetes and obesity in mid-life. Psychological disorders serve as a source of chronic stress, which can alter neuroendocrinological mechanisms such as the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system.^{Reference Kivimaki, Bartolomucci and Kawachi36} Persistent chronic stress can lead to continuous activation of these systems, negatively affecting cardiometabolic functions such as immune response, blood pressure and lipid metabolism.^{Reference Burford, Webster and Cruz-Topete37} Long-term epigenetic alterations induced by chronic stress, affecting the HPA system and resulting in elevated cortisol levels, have also been observed.^{Reference Thumfart, Jawaid, Bright, Flachsmann and Mansuy33,Reference Kuzawa and Sweet38} However, a multi-ethnic cross-sectional study found no relationship between depression and diabetes,^{Reference Golden, Lazo, Carnethon, Bertoni, Schreiner and Diez Roux39} suggesting that the effect of emotional problems on CMDs could be dose-responsive, with those experiencing childhood emotional problems being at higher risk of CMDs because of prolonged exposure to chronic stress. Childhood conduct problems also increased the odds of hypertension and diabetes. This may be attributed to the antisocial behaviour patterns developed in childhood that tend to persist across the lifespan, which are associated with poorer health and inadequate healthcare provision.^{Reference von Stumm, Deary, Kivimäki, Jokela, Clark and Batty40} Our findings of links with all four subtypes suggest that poor CPA could serve as a broad indicator of underlying socioeconomic disadvantages (e.g. poverty, poor living environment) and exposure to chronic stress (e.g. childhood maltreatment, recurrent illness). This broader context aligns with the concept of biological embedding, where early psychosocial stressors influence long-term health outcomes through complex physiological and behavioural pathways.

Policy implications

The prevention of CMDs presents a multifaceted challenge that necessitates collaboration across various disciplines, such as psychology, paediatrics, sociology, cardiology and endocrinology. Detailed documentation of children's psychosocial health in medical records should be prioritised. These records should be readily accessible to primary healthcare providers, regardless of the patient's age or geographical location. This integration would enable early identification and continuous monitoring of at-risk individuals throughout their lifespan. Children exhibiting psychosocial maladjustment should be identified as a high-risk group for future CMDs, similar to the recognition afforded to smokers and individuals with obesity. This categorisation can inform targeted prevention strategies, including regular screening for CMDs and tailored health interventions. Implementing early intervention programmes that focus on improving CPA is crucial. These programmes should address educational inequalities and mental health issues among young people. Interventions could include school-based mental health services, behavioural therapy and family support programmes. Policymakers should prioritise funding for research and interventions aimed at improving CPA. Investments in mental health services for children and adolescents, particularly in underserved communities, can have long-term benefits in reducing the prevalence of CMDs.

Strengthens and limitations

A principal strength of our study is the employment of two large, well-characterised cohorts, which bolsters the reliability of our findings. The longitudinal design facilitates a robust temporal analysis of the relationship between CPA and CMDs. Additionally, the extensive data collection process allows for the assessment of a wide range of confounders and mediators. A further notable strength is the intricate classification of CPA subtypes, as reported by parents and teachers, affording a nuanced understanding of how various psychosocial adjustment issues may influence risk of CMDs.

Despite these strengths, several limitations warrant attention. First, the presence of missing data for mediators and outcomes, which amounts to approximately 20%, poses a risk of bias if the missingness correlates with both exposure and outcome. We addressed this issue by employing multiple imputation to create complete data-sets, and our findings remained consistent after pooling the results. Second, there is a persistent possibility of residual confounding despite adjusting for a range of early-life factors in our models. For instance, disparities in social class may have widened during the long-term follow-up. Sensitivity analyses across different social classes confirmed the robustness of the association between CPA and mid-life CMDs, reinforcing our results. Third, although our analysis accounted for select mediators, it did not encompass all conceivable factors, such as diet, physical activity and genetics. We chose three representative mediators for this study: smoking habits (a behavioural factor), educational level (a socioeconomic factor) and depression (a psychological factor). We conducted subgroup analyses to test interaction effects between mediators (Supplementary Table 19) and no interaction effect was found. It is important to acknowledge that the interplay among mediators is complex, and incorporating an excessive number of mediators could lead to redundancy and overestimation of indirect effects. Fourth, the reliance on self-reported measures for certain variables could be perceived as a limitation. To mitigate recall bias, we ascertained early-life factors from the initial survey conducted at birth and assessed CMDs at short intervals. Fifth, caution should be exercised when extrapolating these results to populations outside the UK, since our study focused on two cohorts from the UK. Differences in healthcare systems, socioeconomic factors and lifestyle between countries could significantly affect the generalisability of the findings. Sixth, the use of different tools (the BSAG and RCBS) and different timing to assess childhood psychosocial adjustment across cohorts could lead to measurement inconsistencies. Additionally, the assessment at different ages (10 years old for the NCDS and 11 years old for the BCS70) might introduce a developmental bias. These factors could potentially influence the comparability of the results between cohorts. Last, although our study's prospective design is a strong point, it is essential to recognise that it does not establish causality owing to its observational nature and the potential for residual confounders.