Main outcome measures-Annual incidence and prevalence rate for Scotland; time trend in incidence over the 10 years; diVerences in incidence between the three diVerent age groups; and completeness of the register. Results-The average annual incidence for Scotland was 23.9/100 000 children. The prevalence rate was 1.5/1000 in 1993. A total of 2326 cases was identified from the three sources. Capture-recapture analysis suggests a case ascertainment of 98.6%. The annual incidence rates increased at a rate of 2% each year (rate ratio = 1.02, 95% confidence interval (CI) 1.01 to 1.03). The incidence was higher in boys than girls (rate ratio = 1.08, 95% CI 1.00 to 1.18), and the incidence rates increased with age: 15.3/100 000/year for age 0-4 years, 24.4/ 100 000/year for age 5-9 years, and 31.9/ 100 000/year for age 10-14 years. Conclusions-The incidence of type 1 diabetes in Scotland is increasing and the prevalence is relatively high. These findings have important implications for health service resource allocation. The Scottish Study Group for the Care of Young Diabetics' register provides a base for monitoring and research.

The overall glycemic control of diabetic young people in Scotland is equivalent to a Diabetes Control and Complications Trial HbA1c concentration of 8.7%, placing the majority at a high risk of the complications of diabetes in adulthood. Although factors were significantly associated with poor HbA1c adjustment for these did not explain the differences between centers. We suggest that factors not analyzed in DIABAUD2 (e.g., deployment of resources, organization of the clinical structure, strategies of care, and clinic philosophy) are the determinants of HbA1c. We speculate that the style of utilization of optimum resources is the key to achieving good glycemic control.

Environmental influences are thought to have an aetiological role in onset of diabetes in children. Month of onset in over 2000 children in Scotland was established and there was an excess in colder/darker months than in warmer/lighter months. A meta-analysis of 21 previous studies with over 13,000 patients gave the same result at a much higher level of significance. A mechanism is postulated based on previous viral induced islet cell damage with ongoing progressive auto-immune destruction. There may be physiological seasonal changes with winter stress on carbohydrate and lipid metabolism. The raised winter levels of pituitary, adrenal and thyroid hormones fail to be antagonised by falling level of insulin. A role for seasonal variation in exercise and nutrition is considered.

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