Since our study was conducted on subjects with gastro-enteric disorders, it remains to be determined whether such deficit of association between food intake and glycemia is limited to this patient population or is a more general mechanism involved in other metabolic disorders, as suggested by findings on IgE and antibody to H. pylori plasma levels [13,14], and by preliminary studies on overweight and insulin-resistant adults [21,22]. This evidence concerns the gene IGHE and Other metabolic disease.