Short-term animal product dietary restriction alters metabolic profiles and modulates immune function.
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Abstract
BACKGROUND: Dietary interventions are powerful tools for disease prevention and health promotion, yet the molecular mechanisms by which diet influences health remain incompletely understood. Investigating the effects of diet in healthy individuals enables characterization of molecular and physiological responses in the absence of disease-related confounders and facilitates the identification of diet-responsive pathways underlying physiological regulation. METHODS: We investigated the metabolic and immune effects of short-term dietary restriction of animal products in a unique group of apparently healthy individuals (N = 200) who alternate between omnivory and animal product restriction for religious reasons. We profiled clinical biomarkers and immune parameters during both dietary states, alongside a control group of continuously omnivorous individuals (N = 211). RESULTS: Short-term restriction is associated with reductions in total and non-high-density lipoprotein cholesterol, urea, creatinine, alanine aminotransferase, and gamma-glutamyltransferase, and a concurrent 73% reduction of normal-range C-reactive protein levels. Immune profiling reveals reductions in frequencies of non-classical monocytes, CD56⁺ natural killer cells, and CD8⁺ memory T cells, accompanied by an increased response of cytokine IL-10, suggesting enhanced immune regulation against inflammation. Although most changes are in a direction suggesting beneficial health effects, levels of alkaline phosphatase increase upon restriction, implying possible negative effects on bone turnover or liver function. CONCLUSIONS: Short-term animal product restriction mostly improves systemic metabolic and immune health markers and may lower chronic inflammatory disease risk. Our findings highlight the value of studying diet in the absence of disease to reveal adaptive molecular changes and emphasize the translational potential of short-term dietary interventions in altering health-related risks.
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Acknowledgements: The authors would like to thank the FastBio study participants and the Interbalkan Hospital staff. We would also like to thank Dr Dimitrios Rouskas, Dr Loukas Kipouros and Dr Allen Seylani for their invaluable help. Finally, we would like to thank Professor Stylianos Antonarakis for his helpful comments on this work. The FastBio study was supported through a European Research Council Grant to Antigone Dimas (FastBio– 716998). Research at the University of California, Riverside was supported by the National Institutes of Health (R01AI19470), the UCR School of Medicine (Research Core, Dean’s Research Innovation fund to A. Seylani), and the UCR Opportunities to Advance Sustainability Innovation and Social Inclusion (OASIS) Internal Award. Mihalis Verykokakis is supported by a grant from the Hellenic Foundation for Research and Innovation (HFRI-14762).
Publication status: Published
Funder: Hellenic Foundation for Research and Innovation (HFRI - 14762)
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2730-664X

