Type 1 diabetes is increasing rapidly in many parts of the Western wor
ld, most evidently in Scandinavia. A low concordance rate of insulin-d
ependent diabetes mellitus among monozygotic twins clearly indicates t
hat genetic risk factors may be necessary, but are not sufficient for
the disease to occur. The strongest genetic risk markers are located i
n the HLA region of chromosome 6, but these DNA specificities differ i
n different populations. Risk genes are indicated in other chromosomes
of the human genome, suggesting a complex interaction between genes a
nd environment as the cause of the disease. The pathogenesis of the di
sease is proposed to be autoimmune in nature and environmental risk fa
ctors may either initiate autoimmunity or accelerate an already ongoin
g P-cell destruction. Risk factors disclosed by epidemiological studie
s that may accelerate the pathogenetic process are: a cold environment
, a high growth rate, infections and stressful life events. Risk facto
rs that may initiate the autoimmune process include early exposure to
cow's milk proteins, nitrosamines or early foetal events such as blood
group incompatibility or foetal viral infections. In conclusion, popu
lation-based epidemiological studies have helped to confirm proposed a
etiological models that have arisen from experimental research. These
epidemiological studies have also introduced important new findings th
at may reveal the complex aetiology of the disease and advance underst
anding closer to the ultimate goal of primary prevention.