Childhood Trauma Exposure Associated With a More Severe Course of Metabolic Disturbances in Bipolar Disorder: A 36‐Month Longitudinal Prospective Cohort Study
Juan F. Galvez‐Florez, Hernán F. Guillen‐Burgos, Sergio Moreno‐López, Mariana Ramírez‐Posada, Juan‐Manuel Anaya, Roger S. McIntyreABSTRACT
Background
Childhood trauma (CT) is a recognized risk factor for adverse psychiatric and physical health outcomes in individuals with bipolar disorder (BD). However, few prospective studies have examined how CT relates to the longitudinal course of metabolic dysregulation in BD. This study aimed to describe the association between CT exposure and the progression of metabolic disturbances over 36 months in adults with BD.
Methods
In this prospective cohort study, 305 adults diagnosed with BD (Types I and II) were followed across 13 visits over 36 months. Participants were stratified according to CT exposure using the Childhood Trauma Questionnaire—Short Form (CTQ—SF). Metabolic outcomes (HbA1c, BMI, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, and hs‐CRP) were analyzed with inverse probability of treatment weighting (IPTW) and linear mixed‐effects models incorporating a group‐by‐time interaction.
Results
Of the 305 participants enrolled, 53 (17.4%) were lost to follow‐up. Longitudinal analyses showed significant CT‐by‐time interactions for all metabolic markers ( p < 0.001). At 36 months, participants exposed to CT showed greater increases than non‐exposed participants in HbA1c (adjusted least‐squares mean difference 1.11%, 95% CI 0.89–1.33), BMI (4.46 kg/m 2 , 95% CI 3.90–5.03), and hs‐CRP (2.68 mg/L, 95% CI 2.52–2.84), together with unfavorable changes in the lipid profile. Effect sizes were large (Cohen's d > 0.8). These associations persisted after IPTW weighting for measured baseline covariates.
Conclusions
In this observational cohort, CT exposure was associated with an accelerated trajectory of metabolic deterioration in individuals with BD after weighting for measured baseline characteristics. Because the design is observational and several behavioral, socioeconomic, and illness‐course determinants of metabolic risk were not measured, these findings should be interpreted as associations rather than as causal effects. They nonetheless support the value of early trauma‐informed assessment and of integrated care strategies addressing both psychiatric and physical health in BD. Future research should incorporate detailed lifestyle and treatment‐exposure data, additional inflammatory biomarkers, and preventive interventions to mitigate long‐term cardiometabolic risk in this vulnerable population.