<unk>  is caused by the destruction of β-cells – the only cells in the body that produce insulin – and the consequent progressive insulin deficiency. Without insulin, the body is unable to respond effectively to increases in blood sugar and diabetics have persistent hyperglycemia. In 70–90% of cases, β-cells are destroyed by someone's own immune system, for reasons that are not entirely clear. The best-studied components of this autoimmune response are β-cell-targeted antibodies that begin to develop in the months or years before symptoms arise. Typically someone will first develop antibodies against insulin or the protein GAD65, followed eventually by antibodies against the proteins IA-2, IA-2β, and/or ZNT8. People with more of these antibodies, and who develop them earlier in life, are at higher risk for developing symptomatic<unk> . The trigger for the development of these antibodies remains unclear. A number of explanatory theories have been put forward, and the cause may involve genetic susceptibility, a diabetogenic trigger, and/or exposure to an antigen. The remaining<unk> 0-30% of type<unk>  diabetics have β-cell destruction but no sign of autoimmunity; this is called idiopathic<unk>  and its cause remains unclear. Environmental Various environmental risks have been studied in an attempt to understand what triggers β-cell autoimmunity. Many aspects of environment and life history are associated with slight increases in<unk>  risk, however the connection between each risk and diabetes often remains unclear.<unk>  risk is slightly higher for children whose mothers are obese or older than 35, or for children born by caesarean section. Similarly, a child's weight gain in the first year of life, total weight, and BMI are associated with slightly increased<unk>  risk. Some dietary habits have also been associated with<unk>  risk, namely consumption of cow's milk and dietary sugar intake. Animal studies and some large human studies have found small associations between<unk>  risk and intake of gluten or dietary fiber; however, other large human studies have found no such association. Many potential environmental triggers have been investigated in large human studies and found to be unassociated with<unk>  risk including duration of breastfeeding, time of introduction of cow milk into the diet, vitamin D consumption, blood levels of active vitamin D, and maternal intake of omega-3 fatty acids. A longstanding hypothesis for an environmental trigger is that some viral infection early in life contributes to<unk>  development. Much of this work has focused on enteroviruses, with some studies finding slight associations with<unk> , and others finding none. Large human studies have searched for, but not yet found an association between<unk>  and various other viral infections, including infections of the mother during pregnancy. Conversely, some have postulated that reduced exposure to pathogens in the developed world increases the risk of autoimmune diseases, often called the hygiene hypothesis. Various studies of hygiene-related factors – including household crowding, daycare attendance, population density, childhood vaccinations, antihelminth medication, and antibiotic usage during early life or pregnancy – show no association with<unk> . Genetics<unk>  is partially caused by genetics, and family members of type<unk>  diabetics have a higher risk of developing the disease themselves. In the general population, the risk of developing<unk>  is around<unk>  in 250. For someone whose parent has<unk> , the risk rises to<unk> –9%. If a sibling has<unk> , the risk is 6–7%. If someone's identical twin has<unk> , they have a 30–70% risk of developing it themselves. About half of the disease's heritability is due to variations in three HLA class 2 genes involved in antigen presentation: HLA-DRB1, HLA-DQA1, and HLA-DQB1. The variation patterns associated with increased risk of<unk>  are called HLA-DR3 and HLA-DR4-HLA-DQ8, and are common in people of European descent. A pattern associated with reduced risk of<unk>  is called HLA-DR15-HLA-DQ6. Large genome-wide association studies have identified dozens of other genes associated with<unk>  risk, mostly genes involved in the immune system. Chemicals and drugs Some medicines can reduce insulin production or damage β cells, resulting in disease that resembles<unk> . The antiviral drug didanosine triggers pancreas inflammation in 5 to<unk> 0% of those who take it, sometimes causing lasting β-cell damage. Similarly, up to 5% of those who take the anti-protozoal drug pentamidine experience β-cell destruction and diabetes. Several other drugs cause diabetes by reversibly reducing insulin secretion, namely statins (which may also damage β cells), the post-transplant immunosuppressants cyclosporin A and tacrolimus, the leukemia drug L-asparaginase, and the antibiotic gatifloxicin. Pyrinuron (Vacor), a rodenticide introduced in the United States in<unk> 976, selectively destroys pancreatic beta cells, resulting in<unk>  after accidental poisoning. Pyrinuron was withdrawn from the U.S. market in<unk> 979.
Type 1 diabetes
Diabulimia
Type 3 diabetes
Type 3c diabetes
Maturity onset diabetes of the young
Cystic fibrosis–related diabetes
Lipoatrophic diabetes
Type 2 diabetes