Recently, the senior author (M. P. S.)1 presented a study which offered clinical evidence for a correlation between nasal polyps and an abnormal carbohydrate metabolism. Patients presenting the typical “allergic” nose with pale, edematous mucous membranes demonstrated few positive allergic reactions but frequently showed some carbohydrate dysfunction. Over half of these patients had a family history of diabetes mellitus. A common finding in the patients studied was a pale nasal mucosa, the paleness seemingly attributable to a polysaccharide abnormality rather than to an atopy.The present research was initiated in an effort to elucidate the etiology of the pale nasal mucosa. Biopsies of nine patients with pale mucous membranes were taken and analyzed by means of electron microscopy in order to relate clinical and ultrastructural findings. The most striking result was lamination in basement membrane structure. Specifically, membrane thickness and lamination were more prominent in those patients with a positive family history of diabetes; furthermore, multiple membrane duplication was particularly outstanding in those individuals demonstrating an abnormal glucose tolerance. Although clinical evidence has strongly indicated that paleness results from vascular changes as well as from an accumulation of polysaccharides in the nasal ground substance, no positive correlation could be made between the degree of paleness and the multiplicity of lamination. Several factors were suggested which may have limited the probability of showing a significant correlation: the small sample of patients studied, the relatively small amount of biopsy material obtained, and perhaps most important, the unpredictable variability in paleness.The authors suggest that a carbohydrate dysfunction could explain the physical changes observed in the basement membranes. A high glucose level would increase the availability of substrate to the cells involved in basement membrane synthesis, resulting in increased concentrations of free glucose and of glucose‐galactose disaccharides in the glycoproteins of the membrane material. The abnormally high percentage of glucose in the molecules could lead to structural defects in the basement membrane which would no doubt substantially interfere with its function as a filtration barrier. Vascular changes are not always related to the duration or the severity of the disease; thus, statistically, hypertrophy or lamination of the basement membrane would not necessarily correlate with the extent of carbohydrate dysfunction.