Sacred cow

Amylase is found in saliva and breaks starch into maltose and dextrin. This form of amylase is also called "ptyalin" /ˈtaɪəlɪn/[4] It will break large, insoluble starch molecules into soluble starches (amylodextrin, erythrodextrin, and achrodextrin) producing successively smaller starches and ultimately maltose. Ptyalin acts on linear α(1,4) glycosidic linkages, but compound hydrolysis requires an enzyme that acts on branched products. Salivary amylase is inactivated in the stomach by gastric acid. In gastric juice adjusted to pH 3.3, ptyalin was totally inactivated in 20 minutes at 37°C. In contrast, 50% of amylase activity remained after 150 minutes of exposure to gastric juice at pH 4.3.[5] Both starch, the substrate for ptyalin, and the product (short chains of glucose) are able to partially protect it against inactivation by gastric acid. Ptyalin added to buffer at pH 3.0 underwent complete inactivation in 120 minutes; however, addition of starch at a 0.1% level resulted in 10% of the activity remaining, and similar addition of starch to a 1.0% level resulted in about 40% of the activity remaining at 120 minutes.[6]increased absorption of intact lactose, which in turn has a toxic effect on the whole organism, especially the kidneys. At present it appears best to separate the puzzling syndrome described by Durand from that of “benign” lactose in- tolerance described by Holzel and to regard Durand’s syndrome as a seperate entity rather than a more severe form of Holzel’s entity.
Congenital sucrose intolerance due to sucrose malabsorption was first reported in 1960 by Weijers et al. in three children, in one of whom maltose tolerance was also poor [27,77]. Five patients with sucrose intolerance described by Prader et al. in 1961 [22] were later shown to have an additional intolerance to isomaltose and palatinose [23-251 which are split by the same enzyme [26]. A total of thirty-four cases of congenital sucrose intolerance have increased absorption of intact lactose, which in turn has a toxic effect on the whole organism, especially the kidneys. At present it appears best to separate the puzzling syndrome described by Durand from that of “benign” lactose in- tolerance described by Holzel and to regard Durand’s syndrome as a seperate entity rather than a more severe form of Holzel’s entity.
Congenital sucrose intolerance due to sucrose malabsorption was first reported in 1960 by Weijers et al. in three children, in one of whom maltose tolerance was also poor [27,77]. Five patients with sucrose intolerance described by Prader et al. in 1961 [22] were later shown to have an additional intolerance to isomaltose and palatinose [23-251 which are split by the same enzyme [26]. A total of thirty-four cases of congenital sucrose intolerance have increased absorption of intact lactose, which in turn has a toxic effect on the whole organism, especially the kidneys. At present it appears best to separate the puzzling syndrome described by Durand from that of “benign” lactose in- tolerance described by Holzel and to regard Durand’s syndrome as a seperate entity rather than a more severe form of Holzel’s entity.
Congenital sucrose intolerance due to sucrose malabsorption was first reported in 1960 by Weijers et al. in three children, in one of whom maltose tolerance was also poor [27,77]. Five patients with sucrose intolerance described by Prader et al. in 1961 [22] were later shown to have an additional intolerance to isomaltose and palatinose [23-251 which are split by the same enzyme [26]. A total of thirty-four cases of congenital sucrose intolerance have no