251 mellitus may well have existed in those monozygotic twins of Tattersall and Pyke who were discordant for diabetes mellitus at the time of study. The findings of Gottlieb and Root demonstrate that discordant monozygotic twins must be followed up for two to three decades before it is assumed that diabetes mellitus in younger patients does not have a genetic basis. In Tattersall and Pyke’s series approximately half the 28 discordant pairs of younger twins were followed up for less than 10 years. Since the data of Gottlieb and Root indicate that the rate of development of concordance is unchanged in younger diabetic twins for at least 24 years, had Tattersall and Pyke followed their twin pairs for an adequate time, concordance in the early and older onset diabetics may well have been comparable. We conclude that the evidence of Tattersall and Pyke and of Gottlieb and Root is consistent with the conclusion that diabetes mellitus in man, regardless of age at onset, is primarily genetic in origin, with environmental factors apparently influencing only the time of appearance of this disease. This study was performed under Veterans Administration projects MRIS 7927-01 and MRIS 3194-01 and was supported by program project grant HL-06285, projects A-9 and A-10, from the National Heart and Lung Institute. We thank Peter Martin and Vera Vaughn for their assistance. Metabolism Section, Medical Service, Veterans Administration Hospital, San Francisco, California 94121, U.S.A. and Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco

MONROE B. ROSENTHAL IRA D. GOLDFINE MARVIN D. SIPERSTEIN

glucose. 2 parents were found to have maturity-onset diabetes. No additional J .D.M. patients were found. Except for B7, there was no segregation distortion of the HLA antigens, irrespective of whether the sibs were diabetic or not. Of the 35 families 10 had one B7-positive parent. 8 of these were heterozygous; the other 2 were B7 homozygous. Data from several other informative families have been published (see table). Depending on whether 1 or both parents are B7 heterozygous, one expects, respectively, 50% or 75% of the children also to be B7 positive. This distribution is confirmed in the healthy sibs, but only 1 of the 16 diabetics is B7 positive (P