A review published in Toxicon synthesizes how emetic foodborne toxins — including the mycotoxins deoxynivalenol (DON), zearalenone (ZEA), and T-2 toxin — activate the brainstem's area postrema through gut barrier disruption, dysbiosis, and vagal signaling. Acute exposure triggers anorexia and nausea via AP and NTS receptor pathways; chronic exposure impairs the area postrema–hypothalamus–locus coeruleus axis, producing neuropsychiatric symptoms, cachexia-like metabolic reprogramming, and multi-organ dysfunction.
The authors describe how microbial dysbiosis and LPS translocation amplify systemic inflammation, and identify older adults, immunocompromised patients, and people with comorbidities as particularly vulnerable due to weakened intestinal barriers, immunosenescence, and polypharmacy. The paper outlines a toxin-induced acute-to-chronic cascade across the gut-brain-neuro-metabolic network and calls for further work on chronic pathogenic mechanisms underlying complex mycotoxin-related comorbidities.