2026 Volume 2 Issue 1 Pages 169-181
Background: Depression accounts for a substantial share of the global disease burden, yet current treatme nts avert less than half of it, prompting interest in modifiable risk factors. Within nutritional psychiatry, the consumption of ultra-processed food (UPF), as defined by the NOVA classification, has attracted growing attention in relation to depressive symptoms.
Objective: This review synthesises the pathophysiological background, putative molecular mechanisms, cl inical epidemiological evidence, and practical implications for psychiatric care regarding the association be tween UPF consumption and depression, while rigorously distinguishing observational correlation from int erventional causation.
Main Text: A meta-analysis of observational studies reported that higher UPF consumption was cross-sect ionally associated with increased odds of depressive symptoms (odds ratio 1.44), anxiety symptoms (1.48) and common mental disorders (1.53), and a pooled analysis of prospective studies indicated an increased ri sk of subsequent depression (hazard ratio 1.22). An umbrella review graded the association with common mental disorders as convincing and that with incident depression as highly suggestive. A 60-country surve y suggested a dose-dependent relationship with mental wellbeing. Proposed mechanisms include gut micro biome alterations and intestinal barrier disruption arising from low fibre and high additive content, systemi c low-grade inflammation, hypothalamic-pituitary-adrenal axis dysregulation, and the effects of emulsifier s and artificial sweeteners; however, much of this evidence derives from animal models and cross-sectional studies, and causality in humans has not been established. Cross-sectional neuroimaging has also linked hi gher UPF intake to lower mesocorticolimbic grey-matter volume, with peripheral inflammation proposed a s a mediator. Prospective data in Japanese populations remain scarce.
Conclusion: The association between UPF consumption and depression is robust as observational evidenc e, but reverse causation and residual confounding cannot be excluded, and causality remains unproven. Die tary modification should not replace standard psychiatric treatment but may serve as a complementary opti on, supported by dietary assessment, multidisciplinary collaboration, and public-health improvements to th e food environment.
