+Comparison of type 1 and 2<unk>  Feature Type 1<unk>  Type 2<unk>  Onset Sudden Gradual Age at onset Mostly in children Mostly in adults Body size Thin or normal Often obese Ketoacidosis Common Rare Autoantibodies Usually present Absent Endogenous insulin Low or absent Normal, decreased or increased Heritability 0.69 to 0.88 0.47 to 0.77 Prevalence (age standardized) <2 per 1,000 ~6% (men), ~5% (women)<unk>  mellitus is classified into six categories: type 1<unk> , type 2<unk> , hybrid forms of<unk> , hyperglycemia first detected during pregnancy, "unclassified<unk> ", and "other specific types". The "hybrid forms of<unk> " contains slowly evolving, immune-mediated<unk>  of adults and ketosis-prone type 2<unk> . The "hyperglycemia first detected during pregnancy" contains gestational<unk>  mellitus and<unk>  mellitus in pregnancy (type 1 or type 2<unk>  first diagnosed during pregnancy). The "other specific types" are a collection of a few dozen individual causes.<unk>  is a more variable disease than once thought and people may have combinations of forms. The term<unk> ", without qualification, refers to<unk>  mellitus. Type 1 Type 1<unk>  is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1<unk>  is of an immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of<unk>  mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Although it has been called "juvenile<unk> " due to the frequent onset in children, the majority of individuals living with type 1<unk>  are now adults. "Brittle"<unk> , also known as unstable<unk>  or labile<unk> , is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent<unk> . This term, however, has no biologic basis and should not be used. Still, type 1<unk>  can be accompanied by irregular and unpredictable high blood sugar levels, and the potential for<unk> etic ketoacidosis or serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease). These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1<unk> . Autoimmune attack in type 1<unk> . Type 1<unk>  is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of<unk> . In genetically susceptible people, the onset of<unk>  can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans. Among dietary factors, data suggest that gliadin (a protein present in gluten) may play a role in the development of type 1<unk> , but the mechanism is not fully understood. Type 1<unk>  can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune<unk>  of adults (LADA) is the diagnostic term applied when type 1<unk>  develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5<unk> " for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2<unk> , based on age rather than a cause. Type 2 Reduced insulin secretion and absorption leads to high glucose content in the blood. Type 2<unk>  is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known.<unk>  mellitus cases due to a known defect are classified separately. Type 2<unk>  is the most common type of<unk>  mellitus. Many people with type 2<unk>  have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2<unk> . The progression of prediabetes to overt type 2<unk>  can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production. Type 2<unk>  is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2<unk> , including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese may have a high waist–hip ratio. Dietary factors such as sugar-sweetened drinks are associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating white rice excessively may increase the risk of<unk> , especially in Chinese and Japanese people. Lack of physical activity may increase the risk of<unk>  in some people. Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2<unk>  later in life by 32%, with neglect having the strongest effect. Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors. Gestational<unk>  Gestational<unk>  resembles type 2<unk>  in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. However, after pregnancy approximately 5–10% of women with gestational<unk>  are found to have another form of<unk> , most commonly type 2. Gestational<unk>  is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required. Though it may be transient, untreated gestational<unk>  can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia. Other types Maturity onset<unk>  of the young (MODY) is a rare autosomal dominant inherited form of<unk> , due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin. Some cases of<unk>  are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2<unk> ; this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to<unk>  (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause<unk>  (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid<unk> "). The ICD-10 (1992) diagnostic entity, malnutrition-related<unk>  mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999. Yet another form of<unk>  that people may develop is double<unk> . This is when a type 1<unk> etic becomes insulin resistant, the hallmark for type 2<unk>  or has a family history for type 2<unk> . It was first discovered in 1990 or 1991. The following is a list of disorders that may increase the risk of<unk> :
Diabetes
Benign prostatic hyperplasia
Obesity
Terry's nails
Hypertension
Diabetes insipidus  Diabetes insipidus  1
Prediabetes
Prehypertension