Journal of affective disorders · 2025
High ultra-processed food intake is associated with altered brain perfusion, depressive symptomatology, and increased inflammatory profile.
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Alvarez-Monell Adam, Fernández-Barrès Sílvia, Biarnés Carles, Motger-Albertí Anna, Blasco Gerard, Puig Josep, Fernández-Real José Manuel, Contreras-Rodríguez Oren
Аннотация
INTRODUCTION: Cumulative evidence links ultra-processed foods (UPF) consumption and depression. This association may be explained by a pro-inflammatory profile following high UPF consumption along with changes in brain perfusion. We investigate these previous assumptions considering interactions with the comorbid presence of obesity.
METHODS: 149 participants answered food frequency questionnaires and NOVA classification determined UPF consumption. They were grouped by obesity status (BMI ≥ 30 = OB and BMI < 30 = nonOB) and UPF consumption (lowest T1 and highest T3 tertiles). Self-reports to the PHQ-9 characterized depressive symptoms. Brain perfusion was measured through the IVIM magnetic resonance imaging sequence, and white blood cells were quantified via laboratory tests. Analyses were run controlling and in interaction with the obesity status. First, t-tests and ANOVA analyses assessed group differences in the association between UPF consumption and brain perfusion. Then, regressions analyses explored associations between UPF consumption and leukocyte subtype, and the relationship between the UPF-associated blood leukocytes subtypes and the perfusion fraction in the brain regions showing a significant between-group effect in the imaging models. Finally, we also tested mediation effects between UPF consumption, depressive symptoms, brain perfusion, and inflammation.
RESULTS: The T3-OB group showed increased perfusion in the dorsal anterior cingulate cortex (dACC), amygdala, and cerebellum compared to the T3-NonOB group. UPF consumption was positively associated with the blood lymphocytes and monocytes count. In addition, blood lymphocyte showed a positive association with the perfusion in the dACC in the T3-OB group and in the whole sample, and a negative association with the perfusion in the amygdala. In the whole sample, the perfusion in the cerebellum mediated the association between UPF consumption and depressive symptoms, whereas the blood lymphocyte count mediated the association between UPF consumption and the perfusion in the dACC.
CONCLUSION: We found a complex association between UPF consumption and the fractional perfusion in brain regions implicated in executive, reward and salience processing. The increased brain perfusion may serve as a compensatory mechanism for an initial loss of brain endothelial cell functions and UPF-related innate inflammatory response may play a role.
METHODS: 149 participants answered food frequency questionnaires and NOVA classification determined UPF consumption. They were grouped by obesity status (BMI ≥ 30 = OB and BMI < 30 = nonOB) and UPF consumption (lowest T1 and highest T3 tertiles). Self-reports to the PHQ-9 characterized depressive symptoms. Brain perfusion was measured through the IVIM magnetic resonance imaging sequence, and white blood cells were quantified via laboratory tests. Analyses were run controlling and in interaction with the obesity status. First, t-tests and ANOVA analyses assessed group differences in the association between UPF consumption and brain perfusion. Then, regressions analyses explored associations between UPF consumption and leukocyte subtype, and the relationship between the UPF-associated blood leukocytes subtypes and the perfusion fraction in the brain regions showing a significant between-group effect in the imaging models. Finally, we also tested mediation effects between UPF consumption, depressive symptoms, brain perfusion, and inflammation.
RESULTS: The T3-OB group showed increased perfusion in the dorsal anterior cingulate cortex (dACC), amygdala, and cerebellum compared to the T3-NonOB group. UPF consumption was positively associated with the blood lymphocytes and monocytes count. In addition, blood lymphocyte showed a positive association with the perfusion in the dACC in the T3-OB group and in the whole sample, and a negative association with the perfusion in the amygdala. In the whole sample, the perfusion in the cerebellum mediated the association between UPF consumption and depressive symptoms, whereas the blood lymphocyte count mediated the association between UPF consumption and the perfusion in the dACC.
CONCLUSION: We found a complex association between UPF consumption and the fractional perfusion in brain regions implicated in executive, reward and salience processing. The increased brain perfusion may serve as a compensatory mechanism for an initial loss of brain endothelial cell functions and UPF-related innate inflammatory response may play a role.