This may indicate that (i) small intestinal damage does not occur so soon after intrapartum infection; (ii) structural and immunological damage to the intestine is not reflected in circulating I-FABP levels [40]; (iii) other exposures are more critical determinants of I-FABP at a time of dynamic intestinal adaptation; or (iv) there is such extensive intestinal damage that enterocytes at the villus tip have been lost and are unable to release I-FABP, as in severe celiac disease [41]. This evidence concerns the gene FABP2 and infection.