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

TL;DR

Anxiety in young adults is linked to higher levels of pro-inflammatory cytokines and minor changes in certain plasma lipids.

Contribution

The study identifies a reproducible pro-inflammatory profile in anxiety and suggests potential lipid alterations requiring further validation.

Findings

Anxiety group had elevated IL-6, MCP-1, and TNF-α compared to controls.

Selected glycerolipids and lysophospholipids showed modest reductions in the anxiety group.

MCP-1 and TNF-α levels correlated with anxiety severity in the clinical group.

Abstract

Systemic inflammation and altered lipid metabolism have been implicated in anxiety disorders, but the relationship between circulating cytokines, plasma lipid species and symptom severity remains unclear.

We studied 34 young adults (17 healthy controls, 17 with clinician-confirmed anxiety; age 21–27 years). Anxiety severity was assessed with standardized clinical instruments. Plasma cytokines were quantified by multiplex immunoassay and targeted lipid profiling was performed by mass spectrometry. Group comparisons used nonparametric tests (Mann-Whitney U), and associations were examined with Spearman correlations and robust regression models appropriate for nonparametric data.

Compared with controls, individuals with anxiety showed elevated plasma IL-6, MCP-1 and TNF-α and reduced IL-17A. Targeted lipidomics detected no group differences in total ceramides, dihydroceramides, hexosylceramides or lactosylceramides; nominal reductions were observed for DG 18:2/22:4, DG 18:2/22:6, LPC 24:1 and TG 60:11 (FA 22:5). None of the lipid species correlated with anxiety severity, and combined lipid-cytokine regression models failed to identify independent lipid predictors. MCP-1 and TNF-α showed associations with anxiety severity that were restricted to the clinical group. (All results are presented as unadjusted values; lipid findings did not remain significant after correction for multiple testing.)

The data indicate a reproducible pro-inflammatory signal in clinical anxiety and point to modest, exploratory alterations in selected glycerolipids and lysophospholipids that require validation. These results should be considered hypothesis-generating; larger, longitudinal studies are needed to determine causality and the clinical relevance of immunometabolic signatures in anxiety.

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