Postprandial Inflammatory Stress: A Hypothesis-Generating Framework Linking Metabolic, Immune and Vascular Responses

Chronic low-grade inflammation accompanies cardiometabolic disease, while routine risk assessment is based mainly on fasting measurements. This structured narrative review summarises human evidence for discrete postprandial changes in triglyceride-rich lipoproteins and remnants, glucose and insulin, endotoxin-related markers, innate immune cells and endothelial function. The evidence is comparatively consistent for postprandial lipaemia, glycaemic excursions and acute flow-mediated dilation responses, whereas endotoxin, cytokine and cellular findings are smaller, assay-sensitive and less consistently replicated. Based on this evidence, we introduce PRISM-CM (Postprandial Inflammatory Stress Modules in CardioMetabolic disease) as an author-developed, hypothesis-generating evidence map. It comprises five candidate biological domains—lipid–remnant burden, glucose–insulin stress, endotoxin handling, innate immune-cell activation and endothelial response—with recovery kinetics treated as a cross-domain analytic dimension. The framework was not derived by clustering, consensus methods or predictive modelling; its illustrative response patterns are not validated endotypes. A composite score is not proposed because the independence, reproducibility and incremental predictive value of the candidate measurements have not been established. Potential future diagnostic and prognostic applications require prospective validation. Reference ranges, age- and sex-specific norms, within-person reproducibility, reproducible response patterns and outcome-linked thresholds remain unknown. PRISM-CM is therefore not a clinical algorithm, risk score or treatment-selection tool.