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Venous plasma glucose levels two hours after a 75 gm. carbohydrate load were determined on over 2,900 Pima Indians, a population known to have an extremely high prevalence of diabetes mellitus. In each sex and in each decade above twenty-five years of age, the frequency distributions of the logarithms of the glucose levels were clearly bimodal, but below this age a single symmetrical unimodal distribution was found. A maximum likelihood procedure was used to derive the best fitting theoretical gaussian distributions for each group of data, together with the parameters of each distribution. The observed bimodal distributions were found to be in satisfactory agreement with a model of two overlapping gaussian distributions, indicating that a logical separation between those with normal and high levels of glucose is possible, although the presence of overlap indicates that some misclassification will occur if any finite level is used to subdivide the population. The data indicate that among the Pima: 1. The frequency distributions of two-hour glucose tolerance levels can be used to identify objectively and describe a hyperglycemic population without recourse to other criteria for diabetes. 2. There are small changes in the parameters of “normal” glucose tolerance between the ages of twenty-five and sixtyfour years. 3. The increase in mean glucose level found with rising age in this population is mainly the result of an increasing proportion of subjects who are in the group characterized by marked glucose intolerance. The bimodal distributions of plasma glucose levels The bimodal distributions of plasma glucose levels among the Pima Indians contrast with those described so far in other groups. It seems likely that differences are attributable to the lower prevalence of diabetes elsewhere which would obscure the identification of bimodality.

We report the results of typings, for immunoglobulin G allotypes, of 5392 Native Americans from ten samples, the typings having been performed over the last 20 years. Four cultural groups are represented: the Pimans-Pima and Papago; the Puebloans-Zuni and Hopi; the Pai-Walapai; and the Athabascans-Apache and Navajo. The haplotype Gm1;21 has the highest frequency in each population while Gm1,2;21 is polymorphic in all except the Hopi. The Mongoloid marker Gm1;11,13 is found primarily in the Athabascans. The Caucasian haplotype Gm3;5,11,13 is found at polymorphic frequencies in several of the populations but its frequency is very low or absent among nonadmixed individuals. Although Nei's standard genetic distance analysis demonstrates genetic similarity at the Gm and Km loci, the heterogeneity that does exist is consistent both with what is known about the prehistory of Native Americans and traditional cultural categories. When the current Gm distributions are analyzed with respect to the three-migration hypothesis, there are three distinct Gm distributions for the postulated migrants: Gm1;21 and Gm1,2;21 for the Paleo-Indians 16,000 to 40,000 years ago; Gm1;21, Gm1,2;21, and Gm1;11,13 for the second wave of Na-Dene hunters 12,000 to 14,000 years ago; and Gm1;21 and Gm1;11,13 for the Eskimo-Aleut migration 9,000 years ago. The Pimans, Puebloans, and the Pai are descendents of the Paleo-Indians while the Apache and Navajo are the contemporary populations related to the Na-Dene. Finally, the Gm distribution in Amerindians is found to be consistent with a hypothesis of one migration of Paleo-Indians to South American, while the most likely homeland for the three ancestral populations is found to be in northeastern Asia.

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Medical records of 1,207 Pima Indian children were examined for reported congenital anomalies. Anomalies occurred in eight (38.1 per cent) of twenty-one offspring born after the onset of diabetes to mothers whose disease was diagnosed before age twenty-five, but in only 3.7 per cent of the offspring of all other women. Children born after the onset of diabetes to mothers whose disease started at or after age twenty-five, and those born to prediabetic mothers had anomalies no more frequently than the children of nondiabetic mothers. Congenital anomalies were not related to paternal diabetes. Anomalies were more frequent in children from “diabetic” pregnancies during which the mother required hypoglycemic medication than from those during which medication was not required. Although a genetic mechanism cannot be completely excluded, the data better support the hypothesis that diabetes produced fetal anomalies among the Pima Indians by its influence upon the intrauterine environment during early pregnancy.

It is generally agreed that hyperuricaemia is inherited, although the exact mechanism of inheritance is not well understood. In the late 1940s two papers appeared in which hyperuricaemia was studied as a simple monofactorial trait. In neither case did the data fit simple genetic models well. Smyth, Cotterman, and Freyberg (1948) concluded it to be inherited as a simple monofactorial dominant in which only a portion of the heterozygotes manifested the trait, while Stecher, Hersh, and Solomon (1949) concluded it to be dominant with varying penetrance in some families and recessive with varying penetrance in others. The metric character of the trait and the necessity of invoking penetrance casts doubt on the hypothesis of simple inheritance. Hauge and Harvald (1955) studied the uric acid levels in siblings of probands with gout. The uric acid of brothers was 1 .0 mg. per cent. greater than controls, and of sisters 1 *4 mg. per cent. greater than controls; the distribution of urate levels was normal, and the authors suggested the trait was polygenic.The present study was undertaken to determine whether hyperuricaemia is, indeed, inherited, and, if so, what the mechanism of inheritance might be.Two populations were studied: the Blackfeet Indians of Montana, and the Pima Indians of Arizona; 86 per cent. of all individuals of the designated tribe aged 30 and over living on the reservation were studied. All matings in the population and their offspring were identified; paternities in the Pima Indians were checked by multiple blood groups. Uric acid determinations were made in duplicate by the uricase spectrophotometric method of Liddle, Seegmiller, and Laster (1959). Height and weight were recorded and a history obtained. Each individual was carefully examined for joint disease, and