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The prevalence and 14 year incidence of clinical gout and its precursors were investigated in the Polynesian population of Tokelauans living in the Pacific basin, non-migrant Tokelauans living in their isolated atoll homeland being compared with migrant Tokelauans living in urban New Zealand. The age standardised prevalence of gout in Tokelauan men in New Zealand was higher than that in non-migrant Tokelauan men, being 21.0 and 19.5/1000 subjects at the beginning of the study and 51.0 and 14.6/1000 at the end of study, respectively. Migrant men in New Zealand aged under 55 had higher mean serum uric acid concentrations than non-migrant men of the same age. The prevalence of gout was low in women in both environments. The age standardised relative risk of developing gout between 1968 and 1982 was 9.0 times higher in the migrant men than in the non-migrant men. Age, serum uric acid concentration, serum cholesterol concentration, and self reported alcohol consumption at entry to the study were the best set of predictors of gout in men. Preventive strategies to change body mass, diet, and patterns of alcohol use need to be developed in this population.

When human serum must be stored for extended periods before analysis, conditions must be such that samples give results comparable with those for "fresh" (unstored) samples. In a balanced experiment with statistically pre-determined sample size, we assessed, at three-weekly intervals for 18 weeks, the stability of total cholesterol, high-density-lipoprotein cholesterol, and triglycerides in human serum stored at -15 degrees C. No significant changes were observed.

The migration of Tokelauans from a traditional atoll in the Pacific to urban New Zealand is associated with an increased prevalence and incidence of Type 2 (non-insulin-dependent) diabetes mellitus over the period 1968-1982. During the same period, a lesser but definite increase is seen among non-migrants in Tokelau. The age standardised prevalence rates rose from 7.5 and 11.7 to 10.8 and 19.9 per 100 respectively in the male and female migrants compared with an increase from 3.0 and 8.7 to 7.0 and 14.3 per 100 in the non-migrant males and females respectively. The incidence of diabetes is shown to be consistently higher in the migrants compared to the non-migrants giving relative risks of 1.5 in males and 1.9 in females. The factors most likely contributing to this difference, are changes to a higher calorie, high protein diet, higher alcohol consumption, a greater weight gain and altered levels of physical activity in the migrants. A number of populations in the Pacific have been shown to have a low rate of diabetes in their traditional setting, but may have a genetic predisposition for diabetes which responds to factors in the urban industrialised environment and life-style. The social and economic changes taking place in Tokelau are also clearly increasing the risk of diabetes. To reverse these trends and prevent the development of complications of Type 2 diabetes, it will be important to institute preventive programmes and to follow up the population in both environments for long-term outcomes, including mortality.