Emerging evidence highlights the role of chronic low-grade inflammation and dysregulated cytokines in both obesity and schizophrenia, suggesting overlapping immune system pathways that contribute to cognition and nervous system inflammation. Excess adipose tissue functions as an active endocrine organ, releasing pro-inflammatory mediators that may serve as potential biomarkers, while the use of antipsychotic agents in schizophrenia further modifies cytokine profiles and immune responses. A key knowledge gap lies in understanding how adipose-related inflammation modifies the severity of psychotic symptoms, cognitive deficits, and the efficacy of antipsychotic medications. This review aims to present excess adipose tissue as a potential contributor to the development of SCZ or a modifier of treatment efficacy, emphasizing the role of immune imbalance, inflammatory pathways, and metabolic dysfunction. By synthesizing current findings, we aim to present obesity not only as a frequent comorbidity in schizophrenia but also as a potential driver of neuroinflammation and disease progression. Here, we demonstrate that excess adiposity may perpetuate a vicious cycle linking metabolic dysfunction, immune activation, and psychiatric symptomatology. Situating these findings within a broader context, the review underscores the clinical need for inflammation-informed, individualized management strategies that integrate psychiatric care with metabolic monitoring. Ultimately, clarifying the shared inflammatory pathways of obesity and schizophrenia may open new avenues for biomarker development and targeted interventions.
Oracz et al. (Sat,) studied this question.