PubMed1975
Historical evidence suggests that the Maori people of New Zealand were virtually untroubled by gout or obesity at a time when these disorders, along with other elements of the gouty diathesis, were rife in the best fed and hardest drinking sections of the Northern European population. By the mid 20th century, however, the apparent decline of the gout in Europe and North America and the breakup of the gouty diathesis in those lands had been more than compensated by their large-scale reappearance in the Maori and in other indigenous inhabitants of the Pacific Basin who, at first sight, appeared to have become one large gouty family. Half the Polynesian population of New Zealand, Rarotonga, Puka Puka, and the Tokelau Islands proved to be hyperuricemic by accepted European and North American standards, the associated gout rate reaching 10.2% in Maori males aged 20 and over. The trends towards hyperuricemia and gout, on the one hand, and towards obesity, diabetes mellitus, hypertension, and associated degenerative vascular disorders, on the other hand, which manifest themselves separately in some Polynesian Pacific Islanders, run together in the Maori and Samoan people, presenting a combined problem of considerable importance to the public health. The appearance of these traits under conditions of plenty in the descendants of hardy and wide-ranging Polynesian voyagers, suggests the emergence of a formerly favorable ancestral polygenic variation through selection for survival under harder conditions. This may now have lost its primitive survival value with a paradoxic shift towards increased prevalence of obesity and the gouty diathesis in more affluent environmental conditions. This may now constitute a genetic load, with recent environmentally determined increase in morbidity and mortality rates from degenerative vascular disorders. There is no satisfactory evidence that overproduction of uric acid differs in mechanism from its European counterparts, although more work remains to be done to determine whether there is any difficulty in renal handling of an increased uric acid load. A high Maori morbidity rate from gout and morbidity and mortality rates from associated components of the gouty diathesis in the face of readily available skilled medical advice and care, indicate the need for greater future attention to help education and health care delivery, at least while conditions of plenty continue. Continuation of previous epidemiologic surveillance may then be required in order to provide a continuing index of the effectiveness of these measures, as well as an opportunity for further research into the interrelationships of these associated disorders.