Chronic low-grade inflammation driven by dietary advanced glycation end products (AGEs), lipid peroxidation products, oxysterols, trans fats, and microbiome-derived metabolites activates pattern recognition receptors and NF-κB cascades central to cardiovascular disease, neurodegeneration, and metabolic syndrome. Counteracting these, polyphenols including quercetin, EGCG, resveratrol, and curcumin suppress pro-inflammatory signaling while activating sirtuin and Nrf2 pathways; omega-3 fatty acids shift eicosanoid balance toward pro-resolving mediators; and microelements selenium, zinc, and magnesium modulate oxidative and immune responses.
While this review synthesizes substantial mechanistic depth, it is ultimately a narrative synthesis rather than original data — and must be read as such. The core framework it assembles is nonetheless valuable: it operationalizes the Dietary Inflammatory Index as a translational bridge between bench findings and clinical practice, which remains underutilized in precision nutrition. The critical admission that human evidence is confined largely to biomarker endpoints — not lifespan extension — is exactly the honesty the field needs more of. The polyphenol-sirtuin-Nrf2 axis is well-trodden territory; the more compelling signal here is the framing of dietary AGEs and oxysterols as upstream pattern-recognition activators, which shifts responsibility from generic 'anti-inflammatory eating' toward specific food processing choices. For adults prioritizing longevity, the practical takeaway is clear and evidence-anchored: minimize processed and heat-damaged fats, maximize phytochemical diversity. Incremental as a contribution, but consolidating as a clinical reference.
