To the Editor.
—In the February Archives (139:225-230, 1979), Colwell and colleagues rightly consider impaired transport of oxygen a causative factor for microvascular disease in diabetics. However, the role they attribute to glycosylated hemoglobin (Hb A1c) calls for comment. While normal (nondiabetic) children and adults of both sexes have 2% to 6% Hb A1c, glycosylated hemoglobin formed 4% to 16% of total hemoglobin in newly diagnosed (untreated) diabetics,1 with similar values in uncontrolled diabetes and cases of ketoacidosis. Thus, although Hb A1c per se does have a somewhat higher oxygen affinity than adult hemoglobin,2 the overall effect in unloading oxygen in vivo to the tissues is slight. Compared to the normal blood oxygen Po, at 50% oxygen saturation (P50) of 26 to 27 mm Hg, maturity-onset diabetics without ketoacidosis have a P50 of 24 to 26 mm Hg. Similarly, Ditzel3 found that 42 diabetic children had a mean