The global distribution of childhood type 1 diabetes clearly indicates large area to area variations. This variability may partly be due to different distributions of risk genes for the disease as well as different distributions of environmental exposures, but part of the apparent variability both between countries and regions in the estimates in the Diabetes Atlas may also be due to methodological problems. Further details about methodology are available in the Diabetes Atlas, second edition.
In addition to the geographical variation in the incidence of childhood type 1 diabetes, there are also well-documented secular trends over time, which may also differ from country to country and from region to region within a country. Such time trends have not explicitly been incorporated in the estimates in the Atlas since reliable data are available for only a very small number of countries, but these trends are of considerable importance for healthcare planning.
The causes of such changes over time are unknown and although migration might slowly change the genetic background within a population, the rapid changes in incidence rate reported to occur within comparatively short time spans are more likely to be due to changes in environmental risk factors. These environmental risk factors may initiate autoimmunity or accelerate and precipitate an already ongoing beta cell destruction1Dahlquist G. Diabetes in children: The etiology in an epidemiological perspective. In The Diabetes Annual WHO vol 8, eds Home PD, Marshall SM. Amsterdam:Elsevier, 1994..
Potential risk factors which may initiate the autoimmune process include early fetal events eg blood group incompatibility2Dahlquist G, Kallen B. Maternal-child blood group incompatibility and other perinatal events increase the risk for early-onset type 1 (insulin-dependent) diabetes mellitus. Diabetologia 1992; 35(7):671-675., maternal viral infections during pregnancy3Dahlquist GG, Ivarsson S, Lindberg B, Forsgren M. Maternal enteroviral infection during pregnancy as a risk factor for childhood IDDM. A population-based case-control study. Diabetes 1995; 44(4):408-413. 4Hyoty H, Hiltunen M, Knip M, et al. A prospective study of the role of coxsackie B and other enterovirus infections in the pathogenesis of IDDM. Childhood Diabetes in Finland (DiMe) Study Group. Diabetes 1995; 44(6):652-657., early exposure to cow's milk components and other nutritional factors such as nitrosamines5Akerblom HK, Vaarala O, Hyoty H, Ilonen J, Knip M. Environmental factors in the etiology of type 1 diabetes. Am J Med Genet 2002; 115(1):18-29.. Population-based case-control studies have identified some protective factors, including a long duration of breast feeding5Akerblom HK, Vaarala O, Hyoty H, Ilonen J, Knip M. Environmental factors in the etiology of type 1 diabetes. Am J Med Genet 2002; 115(1):18-29., early vitamin D supplementation6EURODIAB Substudy 2 Study Group. Vitamin D supplement in early childhood and risk for Type I (insulin-dependent) diabetes mellitus. Diabetologia 1999; 42(1):51-54., pre-school day care (as a proxy measure of infections)7EURODIAB Substudy 2 Study Group. Infections and vaccinations as risk factors for childhood type I (insulin-dependent) diabetes mellitus: a multicentre case-control investigation. Diabetologia 2000; 43(1):47-53. and atopic diseases8EURODIAB Substudy 2 Study Group. Decreased prevalence of atopic diseases in children with diabetes. J Pediatr 2000; 137(4):470-474..
Since type 1 diabetes in childhood is associated with estimates of general wealth such as gross domestic product (GDP)9Patterson CC, Dahlquist G, Soltesz G, Green A. Is childhood-onset type I diabetes a wealth-related disease? An ecological analysis of European incidence rates. Diabetologia 2001; 44 Suppl 3:B9-16. it has been suggested that lifestyle habits related to welfare might be responsible for the changes in trend. Wealth is a well-known determinant of birth weight and childhood growth.
Different estimates of child growth such as high birth weight, an increased height, weight, weight for height and body mass index (BMI) have repeatedly been shown to be risk factors for childhood onset diabetes10Blom L, Persson LA, Dahlquist G. A high linear growth is associated with an increased risk of childhood diabetes mellitus. Diabetologia 1992; 35(6):528-533. 11Dahlquist G, Bennich SS, Kallen B. Intrauterine growth pattern and risk of childhood onset insulin dependent (type I) diabetes: population based case-control study. BMJ 1996; 313(7066):1174-1177. 12Stene LC, Magnus P, Lie RT, Sovik O, Joner G. Birth weight and childhood onset type 1 diabetes: population based cohort study. BMJ 2001; 322(7291):889-892. 13Hypponen E, Virtanen SM, Kenward MG, Knip M, Akerblom HK. Obesity, increased linear growth, and risk of type 1 diabetes in children. Diabetes Care 2000;23(12):1755-1760. 14EURODIAB Substudy 2 Study Group. Rapid early growth is associated with increased risk of childhood type 1 diabetes in various European populations. Diabetes Care 2002; 25(10):1755-1760.. Rapid growth is associated with high growth hormone levels and an increased number of fat cells both leading to insulin resistance and thereby an overloading of the beta cell. Although autoimmune mechanisms are responsible for the beta cell destruction leading to type 1 diabetes, overload factors may accelerate this process15Bjork E, Kampe O, Karlsson FA, et al. Glucose regulation of the autoantigen GAD65 in human pancreatic islets. J Clin Endocrinol Metab 1992; 75(6):1574-1576. 16Mandrup-Poulsen T. The role of interleukin-1 in the pathogenesis of IDDM. Diabetologia 1996; 39(9):1005-1029. 17Pipeleers D, Hoorens A, Marichal-Pipeleers M, et al. Role of pancreatic beta-cells in the process of beta-cell death. Diabetes 2001; 50 Suppl 1:S52-S57.. Overload through accelerated child growth and body fat accumulation in association with a lifestyle with a low physical activity are potentially preventable risk factors.