Earlier more enthusiastic reviews of the results of partial gastrectomy for the treatment of peptic ulcer such as those of Lake (1948) and Ross and Walsh (1949) make an interesting contrast to the more recent reports detailing various complications following this operation such as anaemia (Pitney, 1955; Maclntyre and Stent, 1956; MacLean and Sundberg, 1956; Welbourn, Nelson, and Zacharias, 1956; Lous and Schwarz, 1959; Baird, Blackburn, and Wilson, 1959; Hobbs, 1961; Deller, 1962; Deller, Richards, and Witts, 1962) and bone disease (Deller and Begley, 1963). Nutritional complications are amongst the most serious seen and a large number of papers have appeared in recent years on the incidence and causes of the excessive weight loss seen in a proportion of postgastrectomy patients. The reported incidence of weight loss varies but is in most cases substantial (Muir, 1949; Ivy, Grossman, and Bachrach, 1950; Rauch, 1952; Baron, 1954; Wallensten, 1954; Zollinger and Ellison, 1954; Ellison, 1955; Kiefer, 1959; Brookes, Waterhouse, and Thorn, 1960; Postlethwait, Shingleton, Dillon, and Willis, 1961; Culver, 1962). In a series of 100 postgastrectomy patients operated upon a year or more previously reviewed by the writer at the Repatriation General Hospital, Heidelberg, 25 were found to be 6 kg or more below their usual preoperative weight. Most explanations as to the cause of the weight loss have included dietary deficiency (Johnston, Welbourn, and Acheson, 1958; Lawrence, Vanamee, Peterson, McNeer, Levin, and Randall, 1960; Culver, 1962) and defective absorption (Wollaeger, Comfort, Weir, and Osterberg, 1946; Muir, 1949; Baron, 1954; Ellison, 1955; Lawrence et al, 1960; Barker, Malm, and Reemtsma, 1960). The alleged causes of defective absorption included intestinal hurry (Glazebrook and Welbourn, 1952), the type of operation performed (Butler, Capper, and Naish, 1954; Stammers, 1955), loss of reservoir function of the stomach (Brain and Stammers, 1951; Hedenstedt, 1959; Annersten, 1959), intestinal stasis with bacterial proliferation (Duncan, Goudie, MacKie, and Howie, 1954; Kinsella, Hennessy, and George, 1961), jejunal atrophy (Paulley, Fairweather, and Leeming, 1957; Lees, and Grandjean, 1958; Joske and Blackwell, 1959; Rubin, Branborg, Phelps, and Taylor, 1960; Deller et al, 1962; Jones, Williams, Cox, Meynell, Cooke, and Stammers, 1962; Scott, Williams, and Clark, 1964), and inadequate mixing with or secretion of bile and pancreatic juice (Annis and Hallenbeck, 1952; Polak and Pontes, 1956; Shingleton, Isley, Floyd, Sanders, Baylin, Postlethwait, and Ruffin, 1957; Herner and Ysander, 1960; White, Lundh, and Magee, 1960; Butler, 1961; Gastroenterology, 1962).
