Vol. 15Diet and anaemia '03 1000 develops megaloblastic anaemia. Often the cause does not seem to be due to direct dietary deficiency of folic acid. A survey of some 855 cases of macrocytic anaemia seen in our clinic in Edinburgh during the period 1940-54 indicates four points of special interest. Firstly, it does not follow that because a patient has a macrocytic anaemia, as judged by a high colour index and a high mean cell volume, he necessarily has a megaloblastic anaemia. Secondly, it is apparent that in Edinburgh if a patient has a macrocytic anaemia it is six chances to one that he has a megaloblastic anaemia. Thirdly, if he has a megaloblastic anaemia it is nearly six chances to one that he is suffering from Addisonian pernicious anaemia. Fourthly, excluding Addisonian pernicious anaemia, the only two forms of megaloblastic anaemia of numerical importance are those due to malabsorption and to pregnancy and the puerperium, unlike the megaloblastic anaemias in Africa and in the Far East, which are frequently due to direct nutritional deficiency. There are few physicians in Great Britain, in active practice in hospitals at the present time, who can say, like myself, that they were in charge of patients suffering from Addisonian pernicious anaemia for a period of 6 years before liver therapy was discovered. It is only those who personally watched the invariably tragic and fatal course of this disease who can appreciate the amazing results produced to-day by the injection of a few micrograms of cyanocobalamin. It is no exaggeration to say that the research work undertaken during the last 25 years, which has led to the unravelling of so many mysteries of the megaloblastic anaemias and which has produced such potent remedies as cyanocobalamin and folic acid, constitutes one of the greatest triumphs of science over disease.It is my pleasure to declare the one-hundredth meeting of The Nutrition Society open.