Association of early life adversity and peer victimisation with psychopathology and inflammatory-metabolic risk in adolescents from the eBRAIN study: the role of sex and diet.

Abstract

Background: Adolescence is a sensitive developmental period during which psychosocial stress can become biologically embedded, increasing risk for psychopathology and inflammatory-metabolic dysregulation. Early life adversity (ELA, such as maltreatment and household dysfunction) and peer victimisation frequently co‑occur, yet their cumulative association with adolescent psychopathology and inflammatory-metabolic risk remains poorly understood. Diet may be a modifiable pathway linking stress to both psychopathology and inflammatory and metabolic processes, yet evidence integrating multiple adversities with both subjective and objective dietary measures is limited. This study aimed to investigate whether co-occurring ELA and peer victimisation were associated with adolescent psychopathology and inflammatory-metabolic markers, and to test whether diet mediated these associations.

Methods: In an ethically and socio-economic diverse community sample of adolescents (N = 230, age: 12.9 ± 0.9 years), we assessed: 1) exposure to ELA and peer victimisation via structured interviews; 2) Internalising and externalising symptoms, using the Strengths and Difficulties Questionnaire (SDQ); 3) Age‑adjusted body mass index (BMI) and plasma levels of C‑reactive protein (CRP), as indicators of metabolic and inflammatory risk; and 4) Diet, using self‑reported dietary intake from a Food Frequency Questionnaire (FFQ) and urinary metabolic signatures of diet from spot urine samples measured via ultra-high-performance liquid chromatography and triple-quadrupole mass spectrometry (UHPLC-Q-q-Q MS). Linear regression models examined the associations between multiple exposures to ELA and peer victimisation with psychopathology, CRP and age-adjusted BMI, and mediation models tested the role of diet.

Results: Participants exposed to both ELA and peer victimisation showed more internalising (B = 3.3, 95%CI: 2.0 to 4.6) and externalising symptoms (B = 3.9, 95%CI: 2.5 to 5.3), higher log₁₀CRP (B = 0.4, 95%CI: 0.1 to 0.7) and age-adjusted BMI (B = 1.0, 95%CI: 0.3 to 1.6), and a higher likelihood of unhealthy dietary patterns (76% vs. 51%, pairwise p = 0.020), compared to those with no exposure. However, urinary metabolic signatures were not associated with adversity exposure. An unhealthy diet was associated with higher CRP (1.2 ± 3.8 vs. 0.4 ± 0.6 mg/L; p = 0.013), but not with psychopathology, and did not mediate associations between adversity and outcomes. Exploratory sex‑stratified analyses suggested that associations between multiple adversities and higher CRP and BMI were stronger in boys (log₁₀CRP: B = 0.6, 95% CI: 0.2 to 1.1; age-adjusted BMI: B = 1.2, 95% CI: 0.2 to 2.2) than in girls (log₁₀CRP: B = 0.2, 95% CI: -0.2 to 0.6; age-adjusted BMI: B = 0.6, 95% CI: -0.2 to 1.6), though the moderation effect for BMI did not reach statistical significance, but, again, diet did not mediate these differential associations.

Conclusions: Risk for both behavioural difficulties and elevated CRP and BMI was higher among adolescents exposed to multiple forms of adversity, especially boys. Although diet alone may not explain these associations, it remains a relevant target for reducing inflammation and metabolic risk. Future longitudinal research should explore how diet and other modifiable lifestyle behaviours can mitigate the long-term impacts of adolescent adversity.