Elisa Domi, Malvina Hoxha, Bruno Zappacosta, Ruden Cakoni, Mariagrazia Abbasciano, Domenico Tricarico
Mycotoxins are fungal contaminants frequently detected in staple foods worldwide. While their toxic effects on growth and organ function are well recognized, their contribution to cardiometabolic disease programming during early life has received less attention. This review highlights the role of developmental exposure to major mycotoxins, including aflatoxins, ochratoxins, fumonisins, zearalenone, and deoxynivalenol, as a hidden driver of long-term cardiometabolic risk. Evidence indicates that exposure occurs during fetal life through placental transfer and after birth through breast milk, infant formula, and contaminated complementary foods. Because detoxification pathways and physiological systems are still developing, fetuses, infants, and young children are particularly vulnerable to mycotoxin-induced damage. Experimental and epidemiological studies show that early exposure can impair endocrine signaling, promote oxidative stress and chronic inflammation, alter lipid and glucose metabolism, induce gut microbiome dysbiosis, promote vascular injury, and trigger epigenetic changes. These interconnected mechanisms contribute to metabolic dysregulation and increase susceptibility to obesity, insulin resistance, hypertension, and cardiovascular disease later in life. Overall, current evidence supports the concept that mycotoxins represent an underrecognized environmental factor in the onset of cardiometabolic disease. Greater attention to exposure monitoring, risk assessment, and preventive interventions, especially during critical developmental periods may help reduce the long-term burden of metabolic disorders.