Anxiety is associated with systemic pro-inflammatory profile and plasma lipid changes in Mexican young adults

Sofía Bernal-Vega¹Natalia Vázquez-Manjarrez²Mariana Villegas-Romero²ROCIO ORTIZ-LOPEZ³José Alfonso Ontiveros-Sánchez de la Barquera⁴Antonio Ali Perez-Maya⁴Alberto Camacho-Morales^4*

• ¹Universidad Autonoma de Nuevo Leon, San Nicolás de los Garza, Mexico
• ²Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Mexico City, Mexico
• ³Tecnologico de Monterrey, Monterrey, Mexico
• ⁴Autonomous University of Nuevo León, San Nicolás de los Garza, Mexico

Anxiety disorders are highly prevalent psychiatric conditions characterized by persistent fear, hypervigilance, and physiological dysregulation. Emerging evidence suggests that systemic inflammation and disrupted lipid metabolism contribute to their pathophysiology; however, the biological basis of this relationship remains unclear. Here, we assessed the association between plasma lipid alterations, inflammatory cytokine levels, and anxiety symptom severity in individuals with clinically diagnosed anxiety. Thirty-four participants aged 21–27 years were included, comprising 17 healthy controls and 17 individuals with diagnostic criteria for anxiety. Anxiety symptoms were assessed using standardized clinical scales, and plasma cytokines and lipid species were quantified by multiplex immunoassay and targeted mass spectrometry. Group comparisons used nonparametric tests, and associations were evaluated using Spearman correlations and robust multiple regression models. We found that individuals with anxiety exhibited higher plasma levels of IL-6, MCP-1, and TNF-α, and lower levels of IL-17A. Targeted lipidomics revealed no differences in total ceramides, dihydroceramides, hexosylceramides, or lactosylceramides. Also, anxious individuals showed reduced levels of DG 18:2/22:4, DG 18:2/22:6, LPC 24:1, and TG 60:11 (FA 22:5), nonetheless, these data showed no association with anxiety severity. MCP-1 and TNF-α showed group-specific associations restricted to individuals with clinical anxiety, whereas no lipid species correlated with symptom severity, and combined lipid–cytokine models did not identify independent predictors. These data suggest a pro-inflammatory signature in clinical anxiety. The current data are proposed as an exploratory analysis and hypothesis-generating data. Larger longitudinal studies are needed to determine the causality and clinical relevance of immunometabolic mechanisms underlying psychiatric disorders.