Diabetes is classified by the
World Health Organization into six categories: •
Type 1 diabetes •
Type 2 diabetes • Hybrid forms of diabetes(including
slowly evolving, immune-mediated diabetes of adults and
ketosis-prone type 2 diabetes) •
Hyperglycemia first detected during pregnancy • Other specific types • Unclassified diabetes Diabetes is a more variable disease than once thought, and individuals may have a combination of forms.
Type 1 Type 1 accounts for 5 to 10% of diabetes cases and is the most common type of diabetes diagnosed in patients under 20 years; however, the older term "juvenile-onset diabetes" is no longer used as onset in adulthood is possible. Patients often have irregular and unpredictable blood sugar levels due to very low insulin and an impaired counter-response to hypoglycemia. Type 1 diabetes is partly
inherited, with multiple genes, including certain
HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes 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. The genes that are responsible for diabetes are still being researched, but scientists have narrowed them down by investigating the gene mutations related to the capability of the body’s β-cells to produce insulin. Genes related to environmental responses (metabolism, pregnancy symptoms, autoimmune disorder development, etc.) also contribute to a person’s amount of genetic risk for diabetes. The occurrence of diabetes in monozygotic and dizygotic twins has been tested, and these rates can give insight into the genetic component of diabetes. In type 1 diabetes, the chance of monozygotic twins both developing the disease was greater than the risk for dizygotic twins. However, the rate of any siblings contracting the disease was much greater with type 2 diabetes. This indicates that there must be a large environmental factor involved in type 2, and some genetic factor with type 1. Type 1 diabetes has only about a 50% concordance rate (the percentage of two identical twins both having the condition). So, it is not fully genetic, but the results from the twin studies point to some inherited risk. Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood.
Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes 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 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause. LADA leaves adults with higher levels of insulin production than type 1 diabetes, but not enough insulin production for healthy blood sugar levels.
Type 2 Type 2 diabetes 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. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or
medications that improve insulin sensitivity or reduce the
liver's glucose production. Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 diabetes, including
obesity (defined by a
body mass index of greater than 30), lack of
physical activity, poor
diet such as
Western Pattern Diet, and
stress. 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. 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.
Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with
neglect having the strongest effect.
Antipsychotic medication,
SSRI, and
SNRI side effects (specifically metabolic abnormalities,
dyslipidemia and weight gain) are also potential risk factors.
Gestational diabetes Gestational diabetes resembles type 2 diabetes 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. Though it may be transient, untreated gestational diabetes 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. As the risk of developing type 2 diabetes is about 10 times higher in women with a history of gestational diabetes, postpartum screening may involve dietary, lifestyle, and drug interventions to prevent or delay its progression.
Maturity-onset diabetes of the young Maturity-onset diabetes of the young (MODY) is a rare
autosomal dominant inherited form of diabetes, 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 14 subtypes of MODY. People with MODY often can control it without using insulin.
Type 5 (malnutrition-related) Malnutrition-related diabetes, also termed
Type 5 diabetes, involves decreased insulin production, similar to Type 1 diabetes, but is primarily related to malnutrition rather than autoimmune damage of pancreas beta cells. Unlike in Type 1 diabetes, patients with Type 5 diabetes do not develop ketonuria or ketosis. The
ICD-10 (1992) diagnostic entity,
malnutrition-related diabetes mellitus (ICD-10 code E12), was previously deprecated by the
World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Other types Some cases of diabetes 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 diabetes); 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 diabetes (for example,
chronic pancreatitis and
cystic fibrosis). Diseases associated with excessive secretion of
insulin-antagonistic hormones can cause diabetes (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 diabetes"). It was first discovered in 1990 or 1991. The following is a list of disorders that may increase the risk of diabetes: • Genetic defects of β-cell function •
Maturity onset diabetes of the young • Mitochondrial DNA mutations • Genetic defects in insulin processing or insulin action • Defects in
proinsulin conversion • Insulin gene mutations • Insulin receptor mutations • Exocrine pancreatic defects (see
Type 3c diabetes, i.e. pancreatogenic diabetes) •
Chronic pancreatitis •
Pancreatectomy •
Pancreatic neoplasia •
Cystic fibrosis •
Hemochromatosis •
Fibrocalculous pancreatopathy •
Endocrinopathies • Growth hormone excess (
acromegaly) •
Cushing syndrome •
Hyperthyroidism •
Hypothyroidism •
Pheochromocytoma •
Glucagonoma • Infections •
Cytomegalovirus infection •
Coxsackievirus B • Drugs •
Glucocorticoids •
Thyroid hormone •
β-adrenergic agonists •
Statins Unofficial Insulin resistance in the brain caused by
Alzheimer's disease has been termed by some researchers as
Type 3 diabetes, though this label is also rejected by some to avoid confusion with other types classified as Type 3. "Type 4 diabetes" has been used to describe age-related insulin resistance in lean mice. Neither of these terms are commonly used in human health care. ==Pathophysiology==