Bacterial Metabolites for Aflatoxin Control in Food Systems: Distinguishing Growth Suppression, Toxin Fate, and Biosynthetic Evidence

A large and growing body of literature reports that bacterial metabolites reduce aflatoxin levels, and these findings increasingly support proposed applications in food biopreservation and biocontrol. However, a lower measured aflatoxin concentration does not necessarily demonstrate inhibition of aflatoxin biosynthesis, because the same endpoint can result from suppression of fungal growth, adsorption of preformed toxin, degradation of preformed toxin, or genuine regulation of the biosynthetic pathway. These routes have different biological interpretations but are frequently conflated. This critical review examines the principal classes of bacterial metabolites associated with reduced aflatoxin levels, including organic and aromatic acids from lactic acid bacteria, Bacillus -derived lipopeptides, Streptomyces -derived inhibitors and diketopiperazines, and volatile compounds, while evaluating the strength of the underlying evidence. The distinction between growth, toxin-fate, and pathway effects is well recognized; the contribution of this review is to operationalize these concepts into a framework that applies three independent evidence axes- growth separation (G), toxin-fate validation (F), and mechanistic evidence (M) to each compound-level evidence package. Applied to selected high-information compound-level evidence packages, the framework indicates that growth-independent aflatoxin suppression has been demonstrated across chemical classes, with one package additionally reaching biochemical-target evidence. Among the selected evidence packages, no purified-compound package met the F1 criterion for toxin-fate validation, and none met the joint G2 + F1 + ≥M1 threshold. This evidence-based framework may improve the interpretation and translational assessment of bacterial-metabolite strategies for safer food and feed systems. We propose that these three axes be reported separately and that claims of pathway-level biosynthesis inhibition be reserved for evidence packages meeting all three thresholds (G2, F1, and at least M1).