Early exposure to food contaminants reshapes maturation of the human brain-gut-microbiota axis

Figure 1 Hypothesis on the impact of food contaminants on prenatal and postnatal gut homeostasis mis-programming and its consequences on the etiology of non-communicable chronic diseases. During pregnancy and infancy, repeated exposure of fetus and then infant to food contaminants is presumed to be at the origin of altered gut homeostasis due to mis settlement of neuro-immuno-endocrine cross talks and microbiota diversification and densification. Furthermore, also due to these contaminants, the brain/gut axis exchanges might not settle properly. All these modifications during the perinatal period may, later in life, predispose to the appearance of non-communicable chronic diseases among which celiac disease, allergies, inflammatory bowel disease, metabolic syndrome, depression, etc. At the bottom of the figure, are presented the main consequences on gut homeostasis observed at each stage of life. MRPs: Maillard reaction products; POPs: Persistent organic pollutants.

Figure 2 Impact of food contaminants on gut homeostasis settlement and stability. A: At birth the intestinal epithelial environment is still immature with fairly no secretion, very few microorganisms and immature neuro-immuno-endocrine interactions; B: These interactions settle progressively during infancy and childhood to be fully functional at adulthood; C: However, when the conditions are not met and more especially if the child has been submitted during the fetal stage and infant stage to food contaminants, this might be at the origin of gut homeostasis misshaping observed at adulthood. This could then be responsible for gut permeability increase responsible for a mild “leaky gut”, predisposing to intestinal neuro-immuno-endocrine communications alterations. This will in turn be at the origin of systemic neuro-immuno-endocrine communication misshaping contributing to an alteration of crosstalk between the brain and the gut.