Genetics of hyperuricaemia in Blackfeet and Pima Indians.

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