Incidence varies from eight to 17 per 100,000 in Northern Europe and the U.S., with a high of about 35 per 100,000 in Scandinavia, to a low of one per 100,000 in Japan and China.^[4]

Eventually, type 1 diabetes is fatal unless treated with insulin. Injection is the most common method of administering insulin; other methods are insulin pumps and inhaled insulin. Pancreatic transplants have been used. Pancreatic islet cell transplantation is experimental, though growing.^[5]

Most people who develop type 1 are otherwise healthy.^[6] Although the cause of type 1 diabetes is still not fully understood, it is believed to be of immunological origin.

Type 1 can be distinguished from type 2 diabetes via a C-peptide assay, which measures endogenous insulin production.

Type 1 treatment must be continued indefinitely in all cases. Treatment should not significantly impair normal activities, and can be done adequately if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken. However, treatment remains quite burdensome for many people. Complications may be associated with both low blood sugar and high blood sugar, both largely due to the nonphysiological manner in which insulin is replaced. Low blood sugar may lead to seizures or episodes of unconsciousness, and requires emergency treatment. High blood sugar may lead to increased fatigue and can also result in long-term damage to organs.

Diabetes mellitus type 1 (Type 1 diabetes, T1DM, formerly insulin dependent or juvenile diabetes) is a form of diabetes mellitus that results from autoimmune destruction of insulin-producing beta cells of the pancreas.^[2] The subsequent lack of insulin leads to increased blood and urine glucose. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.^[3]

Incidence varies from eight to 17 per 100,000 in Northern Europe and the U.S., with a high of about 35 per 100,000 in Scandinavia, to a low of one per 100,000 in Japan and China.^[4]

Eventually, type 1 diabetes is fatal unless treated with insulin. Injection is the most common method of administering insulin; other methods are insulin pumps and inhaled insulin. Pancreatic transplants have been used. Pancreatic islet cell transplantation is experimental, though growing.^[5]

Most people who develop type 1 are otherwise healthy.^[6] Although the cause of type 1 diabetes is still not fully understood, it is believed to be of immunological origin.

Type 1 can be distinguished from type 2 diabetes via a C-peptide assay, which measures endogenous insulin production.

Type 1 treatment must be continued indefinitely in all cases. Treatment should not significantly impair normal activities, and can be done adequately if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken. However, treatment remains quite burdensome for many people. Complications may be associated with both low blood sugar and high blood sugar, both largely due to the nonphysiological manner in which insulin is replaced. Low blood sugar may lead to seizures or episodes of unconsciousness, and requires emergency treatment. High blood sugar may lead to increased fatigue and can also result in long-term damage to organs.

Environmental

Environmental factors can influence expression of type 1. For identical twins, when one twin had type 1 diabetes, the other twin only had it 30%–50% of the time. Despite having exactly the same genome, one twin had the disease, where the other did not; this suggests environmental factors, in addition to genetic factors, can influence disease prevalence.^[12] Other indications of environmental influence include the presence of a 10-fold difference in occurrence among Caucasians living in different areas of Europe, and a tendency to acquire the incidence of the disease of the destination country for people who migrate.^[9]

Virus

One theory, discussed by DeLisa Fairweather and Noel R. Rose, among others,^[13] proposes that type 1 diabetes is a virus-triggered autoimmune response in which the immune system attacks virus-infected cells along with the beta cells in the pancreas. The Coxsackie virus family or rubella is implicated, although the evidence is inconclusive. In type 1, pancreatic beta cells in the islets of Langerhans are destroyed, decreasing endogenous insulin production. This distinguishes type 1's origin from type 2. The type of diabetes a patient has is determined only by the cause—fundamentally by whether the patient is insulin resistant (type 2) or insulin deficient without insulin resistance (type 1).

This vulnerability is not shared by everyone, for not everyone infected by the suspected virus develops type 1 diabetes. This has suggested presence of a genetic vulnerability^[14] and there is indeed an observed inherited tendency to develop type 1. It has been traced to particular HLA genotypes, though the connection between them and the triggering of an autoimmune reaction is still poorly understood.

Diet

Some researchers believe the autoimmune response is influenced by antibodies against cow's milk proteins.^[15] No connection has been established between autoantibodies, antibodies to cow's milk proteins, and type 1 diabetes. A subtype of type 1 (identifiable by the presence of antibodies against beta cells) typically develops slowly, so is often confused with type 2. In addition, a small proportion of type 2 cases manifest a genetic form of the disease called maturity onset diabetes of the young.^{[citation needed]}

Vitamin D in doses of 2000 IU per day given during the first year of a child's life has been connected in one study in northern Finland (where intrinsic production of Vitamin D is low due to low natural light levels) with an 80% reduction in the risk of getting type 1 diabetes later in life. The causal connection, if any, is obscure.

Short breastfeeding period and short attendance at day care is associated with the risk of type 1 diabetes in Czech children.^[16]

Chemicals and drugs

Some chemicals and drugs preferentially destroy pancreatic cells. Pyrinuron (Vacor, N-3-pyridylmethyl-N'-p-nitrophenyl urea), a rodenticide introduced in the United States in 1976, selectively destroys pancreatic beta cells, resulting in type 1 diabetes after accidental or intentional ingestion. Vacor was withdrawn from the U.S. market in 1979, but is still used in some countries. Zanosar is the trade name for streptozotocin, an antibiotic and antineoplastic agent used in chemotherapy for pancreatic cancer; it also kills beta cells, resulting in loss of insulin production. Other pancreatic problems, including trauma, pancreatitis or tumors (either malignant or benign), can also lead to loss of insulin production.

Pathophysiology

The pathophysiology in diabetes type 1 is basically a destruction of beta cells in the pancreas, regardless of which risk factors or causative entities have been present.

Individual risk factors can have separate pathophysiological processes to, in turn, cause this beta cell destruction. Still, a process that appears to be common to most risk factors is an autoimmune response towards beta cells, involving an expansion of autoreactive CD4+ and CD8+ T helper cells, autoantibody-producing B cells and activation of the innate immune system.^[10]