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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

SO337

Diet, immunometabolic dysregulation, and brain structure: evidence from UK Biobank

DIET, IMMUNOMETABOLIC DYSREGULATION, AND BRAIN STRUCTURE: EVIDENCE FROM THE UK BIOBANK

A pro-inflammatory diet is associated with volume loss in subcortical reward structures through circulating triglyceride-rich lipoproteins and saturated fatty acids, and this structural impairment shares genetic signals with susceptibility to depression.

The study aimed to elucidate the biological pathways linking a pro-inflammatory diet to neurostructural impairment and depression along the diet–metabolite–brain structure axis. In UK Biobank data, dietary exposure was characterized using the Energy-adjusted Dietary Inflammatory Index (E-DII), derived from Oxford WebQ 24-hour dietary recalls administered five times between 2006 and 2010. Elastic net regression reduced 251 NMR metabolites to 32 core metabolic signatures, and structural MRI (gray matter volume, N=12,510) and diffusion MRI (white matter, FA, N=12,295) outcomes were obtained from imaging performed after 2014. Bayesian mediation analysis (BFDR<0.01), two-sample Mendelian randomization, colocalization, and FUMA were used for causal inference. Bayesian mediation analysis identified circulating lipoproteins and saturated fatty acids as key mediators that selectively remodel subcortical reward centers and limbic white matter. Colocalization identified shared genetic signals between saturated fatty acid percentage and the left ventral striatum (rs7412/150966173, 19q13.32/APOE cluster; PP.H4=0.996), small VLDL triglyceride percentage and the right caudate (rs6547692, 2p23.3/GCKR; PP.H4=0.796), and pyruvate and the left posterior limb of the internal capsule (rs12928099, 16p13.11/PDXDC1; PP.H4=0.989). The structural findings also shared genetic signals with depression: the bilateral ventral striatum with depression (rs13388394, 2p22.3/RASGRP3; PP.H4=0.949), and left thalamic volume with depression (rs55705857, 8q24.21/CCDC26; PP.H4=0.994). A shared signal was also identified between free cholesterol percentage in very small VLDL and Ruminococcus gauvreauii abundance (rs2412974, 22q12.2/HORMAD2; PP.H4=0.922), suggesting a feedback loop between the host and the microbiota. Overall, the study delineates a continuous immunometabolic pathway extending from diet to selective subcortical vulnerability, and its findings provide a mechanistic framework for precision nutrition interventions aimed at reducing depression risk.

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