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  • 1. Diabetes mellitus From Wikipedia, the free encyclopedia (Redirected from Diabetes) • Ten things you may not know about images on Wikipedia • Jump to: navigation, search Diabetes mellitus Classification and external resources United Nations blue circle symbol for diabetes.[1] ICD-10 E10.–E14. ICD-9 250 MedlinePlus 001214 eMedicine med/546 emerg/134 MeSH C18.452.394.750 For the disease characterized by excretion of large amounts of very dilute urine, see diabetes insipidus. For diabetes mellitus in pets, see diabetes in cats and dogs. Diabetes mellitus (IPA: /ˌdaɪəˈbiːtiːz/ or /ˌdaɪəˈbiːtəs/, /məˈlaɪtəs/ or /ˈmɛlətəs/), often referred to simply as diabetes (Greek: διαβήτης), is a syndrome characterized by disordered metabolism and abnormally high blood sugar (hyperglycaemia) resulting from low levels of the hormone insulin with or without abnormal resistance to insulin's effects.[2] The characteristic symptoms are excessive urine production (polyuria), excessive thirst and increased fluid intake (polydipsia), blurred vision, unexplained weight loss and lethargy. These symptoms are likely to be absent if the blood sugar is only mildly elevated. The World Health Organization recognizes three main forms of diabetes mellitus: type 1, type 2, and gestational diabetes (occurring during pregnancy),[3] which have different causes and population distributions. While, ultimately, all forms are due to the beta cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia, the causes are different.[4] Type 1 diabetes is usually due to autoimmune destruction of the pancreatic beta cells. Type 2 diabetes is characterized by insulin resistance in target tissues. This causes a need for abnormally high amounts of insulin and diabetes develops when the beta cells cannot meet this demand. Gestational diabetes is similar to type 2 diabetes in that it involves insulin resistance; the hormones of pregnancy can cause insulin resistance in women genetically predisposed to developing this condition. A 2008 study completed in the U.S. found that more American women are entering pregnancy with diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. [5] This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future. Gestational diabetes typically resolves with delivery of the child, however types 1 and 2 diabetes are chronic conditions.[2] All types have been treatable since insulin became medically available in 192 Type 1 diabetes, in which insulin is not secreted by the 1. pancreas, is directly treatable only with injected insulin, although dietary and other lifestyle adjustments are part of management. Type 2 may be managed with a combination of dietary treatment, tablets and injections and, frequently, insulin supplementation. While insulin was originally produced from natural sources such as porcine pancreas, most insulin
  • 2. used today is produced through genetic engineering, either as a direct copy of human insulin, or human insulin with modified molecules that provide different onset and duration of action. Insulin can also be delivered continuously by a specialized pump which subcutaneously provides insulin through a changeable catheter. Diabetes can cause many complications. Acute complications (hypoglycemia, ketoacidosis or nonketotic hyperosmolar coma) may occur if the disease is not adequately controlled. Serious long-term complications include cardiovascular disease (doubled risk), chronic renal failure, retinal damage (which can lead to blindness), nerve damage (of several kinds), and microvascular damage, which may cause impotence and poor healing. Poor healing of wounds, particularly of the feet, can lead to gangrene, which may require amputation. Adequate treatment of diabetes, as well as increased emphasis on blood pressure control and lifestyle factors (such as not smoking and keeping a healthy body weight), may improve the risk profile of most aforementioned complications. In the developed world, diabetes is the most significant cause of adult blindness in the non-elderly and the leading cause of non-traumatic amputatio in adults, and diabetic nephropathy is n the main illness requiring renal dialysis in the United States.[6] Diabetes mellitus Types of Diabetes Diabetes mellitus type 1 Diabetes mellitus type 2 Gestational diabetes Pre-diabetes: Impaired fasting glycaemia Impaired glucose tolerance Disease Management Diabetes management: •Diabetic diet •Anti-diabetic drugs •Conventional insulinotherapy •Intensive insulinotherapy Other Concerns Cardiovascular disease Diabetic comas: •Diabetic hypoglycemia •Diabetic ketoacidosis •Nonketotic hyperosmolar Diabetic myonecrosis Diabetic nephropathy Diabetic neuropathy Diabetic retinopathy Diabetes and pregnancy Blood tests Blood sugar
  • 3. Fructosamine Glucose tolerance test Glycosylated hemoglobin Contents [hide] * 1 Classification o 1.1 Type 1 diabetes mellitus o 1.2 Type 2 diabetes mellitus o 1.3 Gestational diabetes o 1.4 Other types * 2 Signs and symptoms * 3 Genetics * 4 Pathophysiology * 5 Diagnosis * 6 Screening * 7 Prevention * 8 Treatment and management * 9 Cure o 9.1 Cures for type 1 diabetes o 9.2 Cures for type 2 diabetes * 10 Prognosis o 10.1 Acute complications o 10.2 Chronic complications * 11 Epidemiology * 12 History * 13 Social issues * 14 See also * 15 References * 16 External links [edit] Classification The term diabetes, without qualification, usually refers to diabetes mellitus, which is associated with excessive sweet urine (known asquot;glycosuriaquot;) but there are several rarer conditions also named diabetes. The most common of these is diabetes insipidus in which the urine is not sweet (insipidus meaning quot;without tastequot; in Latin); it can be caused by either kidney (nephrogenic DI) or pituitary gland (central DI) damage. The principal two idiopathic forms of diabetes mellitus are known as types 1 and 2. The term quot;type 1 diabetesquot; has uni ersally replaced several former terms, including childhood- v onset diabetes, juvenile diabetes, and insulin-dependent diabetes (IDDM). Likewise, the term quot;type 2 diabetesquot; has replacedseveral former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. Various sources have defined quot;type 3 diabetesquot; as, among others, gestational diabetes,[7] insulin-resistant type 1 diabetes (or quot;double diabetesquot;), type 2 diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of adults (or LADA or quot;type 1.5quot; diabetes.[8]) There is also
  • 4. maturity onset diabetes of the young (MODY) which is a group of several single gene disorders with strong family histories that present as type 2 diabetes before30 years of age. [edit] Type 1 diabetes mellitus Main article: Diabetes mellitus type 1 Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas, leading to a deficiency of insulin. The main cause of this beta cell loss is a T-cell mediated autoimmune attack.[4] There is no known preventative measure that can be taken against type 1 diabetes, which comprises up to 10% of diabetes mellitus cases in North America and Europe (though this varies by geographical location). 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. Type 1 diabetes can affect children or adults but was traditionally termed quot;juvenile diabetesquot; because it represents amajority of cases of diabetes affecting children. The principal treatment of type 1 diabetes, even from the earliest stages, is replacement of insulin combined with careful monitoring of blood glucose levels using blood testing monitors. Without insulin, diabetic ketoacidosis can develop and may result in coma or death. Emphasis is also placed on lifestyle adjustments (diet and exercise) though these can do absolutely nothing to reverse the loss. Apart from the common subcutaneous injections, it is also possible to deliver insulin by a pump, which allows continuous infusion of insulin 24 hours a day at preset levels, and the ability to program doses (a bolus) of insulin as needed at meal times. An inhaled form of insulin, Exubera, was approved by the FDA in January 2006, although Pfizer discontinued Exubera in October 2007. [9] Type 1 treatment must be continued indefinitely. Treatment does not significantly impair normal activities, if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken. However, treatment is burdensome for patients, and insulin is replaced in a non-physiological manner, and is therefore far from ideal. The average glucose level for the type 1 patient should be as close to normal (80–120 mg/dl, 4– 6 mmol/l) as is safely possible. Some physicians suggest up to 140–150 mg/dl (7-7.5 mmol/l) for those having trouble with lower values, such as frequent hypoglycemic events. Values above 200 mg/dl (10 mmol/l) is sometimes accompanied by discomfort and frequent urination leading to dehydration. Values above 300 mg/dl (15 mmol/l) usually require treatment and may lead to ketoacidosis, although is not immediately life- threatening. However, low levels of blood glucose, called hypoglycemia, may lead to seizures or episodes of unconsciousness and absolutely must be treated immediately. [edit] Type 2 diabetes mellitus Main article: Diabetes mellitus type 2 Type 2 diabetes mellitus is characterized differently due to insulin resistance or reduced insulin sensitivity, combined with reduced insulin secretion. The defective responsiveness of body tissues to insulin almost certainly involves the insulin receptor in cell membranes. In the early stage the predominant abnormality s reduced insulin sensitivity, characterized i
  • 5. by elevated levels of insulin in the blood. At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary. There are numerous theories as to the exact cause and mechanism in type 2 diabetes. Central obesity (fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat) is known to predispose individuals for insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes.[10] Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have hadit). In the last decade, type 2 diabetes has increasingly begun to affect children and adolescents, likely in connection with the increased prevalence of childhood obesity seen in recent decades in some places.[11] Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no ketoacidotic episodes. However, severe long-term complications can result from unnoticed type 2 diabetes, including renal failure due to diabetic nephropathy, vascular disease (including coronary artery disease), vision damage due to diabetic retinopathy, loss of sensation or pain due to diabetic neuropathy, and liver damage from non-alcoholic steatohepatitis. Type 2 diabetes is usually first treated by increasing phy sical activity, decreasing carbohydrate intake, and losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. It is sometimes possible to achieve long-term, satisfactory glucose control with these measures alone. However, the underlying tendency to insulin resistance is not lost, and so attention to diet, exercise, and weight loss must continue. The usual next step, if necessary, is treatment with oral antidiabetic drugs. Insulin production is initially only moderately impaired in type 2 diabetes, so oral medication (often used in variou s combinations) can be used to improve insulin production (e.g., sulfonylureas), to regulate inappropriate release of glucose by the liver and attenuate insulin resistance to some extent (e.g., metformin), and to substantially attenuate insulin resistance (e.g., thiazolidinediones). According to one study, overweight patients treated with metformin compared with diet alone, had relative risk reductions of 32% for any diabetes endpoint, 42% for diabetes related death and 36% for all cause mortality and stroke.[12] Oral medication may eventually fail due to further impairment of beta cell insulin secretion. At this point, insulin therapy is necessary to maintain normal or near normal glucose levels. [edit] Gestational diabetes Main article: Gestational diabetes Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires carefulmedical supervision throughout
  • 6. the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life. Even 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 cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental profusion due to vascular impairment. Induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia. [edit] Other types There are several rare causes of diabetes mellitus that do not fit into type 1, type 2, or gestational diabetes; attempts to classify them remain controversial. 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. The ICD-10 (1992) diagnostic entity, malnutrition- related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.[3] [edit] Signs and symptoms The classical triad of diabetes symptoms is po lyuria, polydipsia and polyphagia, which are, respectively, frequent urination; increased thirst and consequent increased fluid intake; and increased appetite. Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes the symptoms develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled. When the glucose concentration in the blood is raised beyond the renal threshold, reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits the reabsorption of water by the kidney, resulting in increased urine product on i (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells, causing dehydration and increased thirst. Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes. Blurred vision is a common
  • 7. complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change whereas type 2 is generally more gradual, but should still be suspected. Patients (usually with type 1 diabetes) may also present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires hospital admission. A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydrati due to loss of body on water. Often, the patient has been drinking extreme amounts of sugar-contain drinks, ing leading to a vicious circle in regard to the water loss. [edit] Genetics Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by some (mainly viral) infections, or in a less common group, by stress or environmental exposure (such as exposure to certain chemicals or drugs). There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic quot;selfquot; identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger. A small proportion of people with type 1 diabetes carry a mutated gene that causes maturity onset d iabetes of the young (MODY). There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Candidate genes include KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), which encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7–like 2), which regulates proglucagon gene expression and thus the production of glucagon-like peptide-1.[4] Moreover, obesity (which is an independen risk factor for type 2 diabetes) is t strongly inherited.[13] Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.[14] [edit] Pathophysiology Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is triggered by increased blood glucose levels. Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or
  • 8. less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is triggered by increased blood glucose levels. Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus. Much of the carbohydrate in food is converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism. Higher insulin levels increase some anabolic (quot;building upquot;) processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolismfrom a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase). If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis. [edit] Diagnosis The diagnosis of type 1 diabetes, and many cases of type 2, is usually prompted by recent- onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia), often accompanied by weight loss. These symptoms typically worsen over days to weeks; about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes,such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.
  • 9. Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:[3] * fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/l). * plasma glucose at or above 200 mg/dL (11.1 mmol/l) two hours after a 75 g oral glucose load as in a glucose tolerance test. * random plasma glucose at or above 200 mg/dL (11.1 mmol/l). A positive result, in the absence of clinical symptoms of diabetes, should be confirmed by another of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/l) is considered diagnostic for diabetes mellitus. Patients with fasting glucose levels between 110 and 125 mg/dL (6.1 and 7.0 mmol/l) are considered to have impaired fasting glycemia. Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/l two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease. While not used for diagnosis, an elevated level of gluco irreversibly bound to se hemoglobin (termed glycosylated hemoglobin or HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is <7.0%, which is considered good glycemic control, although some guidelines are stricter (<6.5%). People with diabetes who have HbA1c levels within this range have a significantly lower incidence of complications from diabetes, including retinopathy and diabetic nephropathy.[15][16] [edit] Screening Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. The screening test varies according to circumstances and local policy, and may be a random blood glucose test, a fasting blood glucose test, a blood glucose test two hours after 75 g of glucose, or an even more formal glucose tolerance test. Many healthcare providers recommend universal screening for adults at age 40 or 50, and often periodically thereafter. Earlier screening is typically recommended for those with risk factors such as obesity, family history of diabetes, high-risk ethnicity (Hispanic, Native American, Afro-Caribbean, Pacific Island, and South Asian ancestry).[17][18] Many medical conditions are associated with diabetes and warrant screening. A partial list includes: high blood pressure, elevated cholesterol levels, coronary artery disease, past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, fatty liver, hemochromatosis, cystic fibrosis, several mitochondrial neuropathies and myopathies,
  • 10. myotonic dystrophy, Friedreich's ataxia, some of the inherited forms of neonatal hyperinsulinism. The risk of diabetes is higher with chronic use of several medications, including high-dose glucocorticoids, some chemotherapy agents (especially L- asparaginase), as well as some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics). People with a confirmed diagnosis of diabetes are screened routinely for complications. This includes yearly urine testing for microalbuminuria and examination ofthe retina (retinal photography) for retinopathy. In the UK, screening for diabetic retinopathy has helped reduce the incidence of legal blindness since its implementation.[citation needed] [edit] Prevention Type 1 diabetes risk is known to depend upon a genetic predisposition based on HLA types (particularly types DR3 and DR4), an unknown environmental trigger (suspected to be an infection, although none has proven definitive in all cases), and an uncontrolled autoimmune response that attacks the insulin producing beta cells.[19] Some research has suggested that breastfeeding decreased the risk; [20][21] various other nutritional risk factors are being studied, but no firm evidence has been found. [22] Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes. [23] Children with antibodies but no overt diabetes treated with vitamin B-3 (niacin) had less than half the onset of diabetes incidence in a 7-year time span as the general population and even lower incidence relative to those with antibodies as above, but no vitamin B-3 [24] Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity.[25][26] The American Diabetes Association (ADA) recommends maintaining a healthy weight, getting at least 2½ hours of exercise per week (a brisk sustained walk appears sufficient), having a modest fat intake, and eating a good amount of fiber and whole grains. The ADA does not recommend alcohol consumption as a preventative, but it is interesting to note that moderate alcohol intake may reduce the risk (though heavy consumption clearly increases damage to body systems significantly). There is inadequate evidence that eating foods of low glycemic index is clinically helpful.[27] Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin,[26] rosiglitazone,[28] or valsartan.[29] In patients on hydroxychloroquine for rheumatoid arthritis, incidence of diabetes was reduced by 77%.[30] Breastfeeding might also be associated wih the prevention of type 2 of the t disease in mothers.[31] [edit] Treatment and management Main article: Diabetes management Diabetes mellitus is currently a chronic disease, without a cure, and medical emphasis must necessarily be on managing/avoiding possible short-term as well as long-term diabetes- related problems. There is an exceptionally important role for patient education, dietetic
  • 11. support, sensible exercise, self glucose monitoring, with the goal of keeping both short- term blood glucose levels, and long term levels as well, within acceptable bounds. Careful control is needed to reduce the risk of long term complications. This is theoretically achievable with combinations of diet, exercise and weight loss (type 2), various oral diabetic drugs (type 2 only), and insulin use (type 1 and increasingly for type 2 not responding to oral medications). In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications should be undertaken to control blood pressure[32] and cholesterol by exercising more, smoking cessation, consuming an appropriate diet, wearing diabetic socks, and if necessary, taking any of several drugs to reduce pressure. Many Type 1 treatments include the combination use of regular or NPH insulin, and/or synthetic insulin analogs such as Humalog, Novolog or Apidra; the combination of Lantus/Levemir and Humalog, Novolog or Apidra. Another Type 1 treatment option is the use of the insulin pump with some of the most popular pump brands being: Cozmo, Animas, Medtronic Minimed, and Omnipod. In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care of a patient in a team approach. Optometrists, podiatrists/chiropodists, dietitians, physiotherapists, clinical nurse specialists (eg, Certified Diabetes Educators and DSNs (Diabetic Specialist Nurse)), or nurse practitioners may jointly provide multidisciplinary expertise. In countries where patients must provide their own healt care (i.e., the United States in the developed world),the h impact of out-of-pocket costs of diabetic care can be high. In addition to the medications and supplies needed, patients are often advised to receive regular consultation from a physician (e.g., at least every three to six months). [edit] Cure [edit] Cures for type 1 diabetes Main article: Cure for diabetes mellitus type 1 There is no practical cure now for type 1 diabetes. The fact that type 1 diabetes is due to the failure of one of the cell types of a single organ with a relatively simple function (i.e. the failure of the islets of Langerhans) has led to the study of several possible schemes to cure this form diabetes mostly by replacing the pancreasor just the beta cells.[33] Only those type 1 diabetics who have received either a pancreas or a kidney-pancreas transplant (when they have developed diabetic nephropathy) and become insulin-independent may now be considered quot;curedquot; from their diabetes. A simultaneous pancreas-kidney transplant is a promising solution, showing similar or improved survival rates over a kidney transplant alone.[34] Still, they generally remain on long-term immunosuppressive drugs and there is a possibility that the immune system will mount a host versus graft response against the transplanted organ.[33] Transplants of exogenous beta cells have been performed experimentally in both mice and humans, but this measure is not yet practical in regular clin practice partly due to the ical limited number of beta cell donors. Thus far,like any such transplant, it has provoked an
  • 12. immune reaction and long-term immunosuppressive drugs will be needed to protect the transplanted tissue.[35] An alternative technique has been proposed to place transplanted beta cells in a semi-permeable container, isolating and protecting them from the immune system. Stem cell research has also been suggested as a potential avenue for a cure since it may permit regrowth of Islet cells which are genetically part of the treated individual, thus perhaps eliminating the need for immuno-suppressants.[33] A 2007 trial of 15 newly diagnosed patients with type 1 diabetes treated wit stem cells raised from their own bone h marrow after immune suppression showed that the majority did not require any insulin treatment for prolonged periods of time.[36] Microscopic or nanotechnological approaches are under investigation as well, in one proposed case with implanted stores of insulin metered out by a rapid response valve sensitive to blood glucose levels. At least two approaches havebeen demonstrated in vitro. These are, in some sense, closed-loop insulin pumps. [edit] Cures for type 2 diabetes Type 2 diabetes can be cured by one type of gastric bypass surgery in 80-10 of severely 0% obese patients. The effect is not due to weight loss because it usually occurs within days of surgery, which is before significant weight loss occurs. The pattern of secretion of gastrointestinal hormones is changed by the bypass and removal of the duodenum and proximal jejunum, which together form the upper (proximal) part of the small intestine.[37] One hypothesis is that the proximal small intestine is dysfunctional in type 2 diabetes; its removal eliminates the source of an unknown hormone that contributes to insulin resistance.[38] This surgery has been widely performed on morbidly obese patients and has the benefit of reducing the death rate from all causes by up to 40%.[39] A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.[40][41] [edit] Prognosis Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-controlled blood sugar levels.[42][43] Wider health problems accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise. According to a study, women with high blood pressure have a threefold risk of developing diabetes. Anecdotal evidence suggests that some of those with type 2 diabetes who exercise regularly, lose weight, and eat healthy diets may be able to keep some of the disease or some of the effects of the disease in 'remission.' Certainly these tips can help prevent people predisposed to type 2 diabetes and those at pre-diabetic stages from actually developing the disorder as it helps restore insulin sensitivity. However patients should talk to their doctors about this for real expectations before undertaking it (esp. to avoid hypoglycemia or other complications); few people actually seem to go into total 'remission,' but some may find they need less of their insulin medications since the body tends to have lower insulin requirements during and shorty following exercise. Regardless l of whether it works that way or not for an individual, there are certainly other benefits to
  • 13. this healthy lifestyle for both diabetics and nondiabetics. The way diabetes is managed changes with age. Insulin production decreases because of age-related impairment of pancreatic beta cells. Additionally, insulin resistance increases because of the loss of lean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population.[44] Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people. [45] Treatment goals for older patients with diabetes vary with the individual, and take into account health status, as well as life expectancy, level of dependence, and willingness to adhere to a treatment regimen.[46] [edit] Acute complications Main articles: Diabetic ketoacidosis , Nonketotic hyperosmolar coma , Hypoglycemia , and Diabetic coma Diabetic ketoacidosis Diabetic ketoacidosis (DKA) is an acute and dangerous complication that is always a medical emergency. Lack of insulin causes the liver to turn fatinto ketone bodies, a fuel mainly used by the brain. Elevated levels of ketone bodies in the blood decrease the blood's pH, leading to most of the symptoms of DKA. On presentation at hospital, the patient in DKA is typically dehydrated and is breathin rapidly and deeply. Abdominal pain is g common and may be severe. The level of consciousness is typically normal until late in the process, when lethargy may progress to coma. Ketoacidosis can become severe enough to cause hypotension, shock, and death. Analysis of the urine reveals significant levels of ketone bodies present (which spill over from the blood when the kidneys filter blood). Prompt proper treatment usually results in full recovery, though death can result from inadequate or delayed treatment, or from complications. Ketoacidosis is much more common in type 1 diabetes than type 2. Nonketotic hyperosmolar coma The hyperosmolar nonketotic state (HNS) is an acute complication with many symptoms in common with DKA, but an entirely different cause and different treatment. In a person with very high blood glucose levels (usually considered to be above 300 mg/dl (16 mmol/l)), water is drawn out of cells into the blood by osmosis and the kidneys dump glucose into the urine. This results in loss of water and an increase in blood osmolarity. If fluid is not replaced (by mouth or intravenously), the osmotic effect of high glucose levels combined with the loss of water will eventually lead to dehydration. The body's cells become progressively dehydrated as water is taken from them and excreted. Electrolyte imbalances are also common and dangerous. As with DKA, urgent medical treatment is necessary, especially volume replacement. Lethargy may ultimately progress to a coma, which is more common in type 2 diabetes than type 1. Hypoglycemia
  • 14. Hypoglycemia, or abnormally low blood glucose, is a complication of several diabetes treatments. It may develop if the glucose intake does not cover the treatment. The patient may become agitated, sweaty, and have many symptoms of sympathetic activation of the autonomic nervous system resulting in feelings similar to dread and immobilized panic. Consciousness can be altered or even lost in extreme cases, leading to coma, seizures, or even brain damage and death. In patients with diabetes, this may be caused by several factors, such as too much or incorrectly timed insulin, too much or incorrectly timed exercise (exercise decreases insulin requirements) or not enough food (specifically glucose- producing carbohydrates), but this is an over-simplification. It is more accurate to note that iatrogenic hypoglycemia is typically the result of the interplay of absolute (or relative) insulin excess and compromised glucose counterregulation in type 1 and advanced type 2 diabetes. Decrements in insulin, increments in glucagon, and, absent the latter, increments in epinephrine stand high in the hierarchy of redundant glucose counterregulatory factors that normally prevent orrapidly correct hypoglycemia. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephr ine responses causes defective glucose coun terregulation. Furthermore, reduced sympathoadrenal responses cancause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. In many cases (but not all), short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in most affected patients, although this is easier in theory than it is in practice. In most cases, hypoglycemia is treated with sugary drinks or food. In severe cases, an injection of glucagon (a hormone with the opposite effects of insulin) or an intravenous infusion of dextrose is used for treatment, but usually only if the person is unconscious. In hospitals, intravenous dextrose is often used. [edit] Chronic complications Vascular disease Chronic elevation of blood glucose level leads to damage of blood vessels (angiopathy). The endothelial cells lining the blood vessels take in more glucose than normal, since they don't depend on insulin. They then form more surface glycoproteins than normal, and cause the basement membrane to grow thicker and weaker. In diabetes, the resulting problems are grouped under quot;microvasculardiseasequot; (due to damage to small blood vessels) and quot;macrovascular diseasequot; (due to damage to the arteries). Image of fundus showing scatter laser surgery for diabetic retinopathy Image of fundus showing scatter laser surgery for diabetic retinopathy
  • 15. The damage to small blood vessels leads to a microangiopathy, which can cause one or more of the following: * Diabetic retinopathy, growth of friable and poor-quality new blood vessels in the retina as well as macular edema (swelling of the macula), which can lead to severe vision loss or blindness. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US. * Diabetic neuropathy, abnormal and decreased sensation, usually in a 'glove and stocking' distribution starting with the feet but potentially in other nerves, later often fingers and hands. When combined with damaged blood vessels this can lead to diabetic foot (see below). Other forms of diabetic neuropathy may present as mononeuritis or autonomic neuropathy. Diabetic amyotrophy is muscle weakness due to neuropath y. * Diabetic nephropathy, damage to the kidney which can lead to chronic renal failure, eventually requiring dialysis. Diabetes mellitus is the most common cause of adult kidney failure worldwide in the developed world. Macrovascular disease leads to cardiovascu disease, to which accelerated atherosclerosis lar is a contributor: * Coronary artery disease, leading to angina or myocardial infarction (quot;heart attackquot;) * Stroke (mainly the ischemic type) * Peripheral vascular disease, which contributes to intermittent claudication (exertion- related leg and foot pain) as well as diabetic foot. * Diabetic myonecrosis ('musclewasting') Diabetic foot, often due to a combination of neuropathy and arterial disease, may cause skin ulcer and infection and, in serious cases, necrosis and gangrene. It is why diabetics are prone to leg and foot infections and why it takes longer for them to heal from leg and foot wounds. It is the most common cause of adult amputation, usually of toes and or feet, in the developed world. Carotid artery stenosis does not occur more often in diabetes, and there appears to be a lower prevalence of abdominal aortic aneurysm.However, diabetes does cause higher morbidity, mortality and operative risks with these conditions.[47] [edit] Epidemiology In 2000, according to the World Health Organization, at least 171 million people worldwide suffer from diabetes. Its incidence is increasing rapid and it is estimated that ly, by the year 2030, this number will double. Diabetes mellitus occurs throughout the world, but is more common (especially type 2) in the more developed countries. The greatest increase in prevalence is, however, expected to occur in Asia and Africa, where most patients will likely be found by 2030. The increase in incidence of diabetes in developing countries follows the trend of urbanization and lifestyle changes, perhaps most importantly a quot;Western-stylequot; diet. This has suggested an environmental (i.e., dietary) effect, but there is little understanding of the mechanism(s) at present, though there is much speculation, some of it most compellingly presented.
  • 16. Diabetes is in the top 10, and perhaps the top 5, of the most significant diseases in the developed world, and is gaining in significance there and elsewhere (see big killers). For at least 20 years, diabetes rates in North America have been increasing substantially. In 2005 there were about 20.8 million people with diabetes in the United States alone. According to the American Diabetes Association, there are about 6.2 million people undiagnosed and about 41 million people that would be considered prediabetic.[48] However, the criteria for diagnosing diabetes in the USA mean that it is more readily diagnosed than in some other countries. The Centers for Disease Control has termed the change an epidemic. The National Diabetes Information Clearinghouse estimates that diabetes costs $132 billion in the United States alone every year. About 5%–10% of diabetes cases in North Americaare type 1, with the rest being type 2. The fraction of type 1 in other parts of the world differs; this is likely due to both differences in the rate of type 1 and differences in the rate of other types, most prominently type 2. Most of this difference is not currently understood. The American Diabetes Association point out the 2003 assessment of the National Center for Chronic Disease Prevention and Health Promotion (Centers for Disease Control and Prevention) that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime.[49][48] According to the American Diabetes Association, approximately 18.3% (8.6 million) of Americans age 60 and older have diabetes. [50] Diabetes mellitus prevalence increases with age, and the numbers of older persons with diabetes are expected to grow as the elderly population increases in number. The National Health and Nutrition Examination Survey (NHANES III) demonstrated that, in the population over 65 years old, 18% to 20% have diabetes, with 40% having either diabetes or its precursor form of impaired glucose tolerance.[44] Indigenous populations in first world countries have a higher prevalence and increasing incidence of diabetes than their correspond non-indigenous populations. In Australia the ing age-standardised prevalence of self-reported diabetes in Indigenous Australians is almost 4 times that of non-indigenous Australians.[51] Preventative community health programs such as Sugar Man (diabetes educatio are showing some success in tackling this problem. n) [edit] History The term diabetes (Greek: διαβήτης, diabētēs) was coined by Aretaeus of Cappadocia. It was derived from the Greek verb διαβαίνειν, diabaínein, itself formed from the prefix dia-, quot;across, apart,quot; and the verb bainein, quot;to walk, stand.quot; The verb diabeinein meant quot;to stride, walk, or stand with legs asunderquot;; hence, its derivative diabētēs meant quot;one that straddles,quot; or specifically quot;a compass, siphon.quot; The sense quot;siphonquot; gave rise to the use of diabētēs as the name for a disease involving the discharge of excessive amounts of urine. Diabetes is first recorded in English, in the form diabete, in a medical text written around 1425. In 1675, Thomas Willis added the word mellitus, from the Latin meaning quot;honeyquot;, a reference to the sweet taste of the urine. This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, and Indians. In 1776, Matthew Dobson confirmed that the sweet taste was because of an excess of a kind of sugar in the urine and blood of people with diabetes.[52]
  • 17. The ancient Indians tested for diabetes by observing whether ants were attracted to a person's urine, and called the ailment quot;sweet urine diseasequot; (Madhumeha). The Korean, Chinese, and Japanese words for diabetes are based on the same ideographs (糖尿病) which mean quot;sugar urine diseasequot;. Although diabetes has been recognized since antiquity, and treatments of various efficacy have been known in various regions since the Middle Ages, and in legend for much longer, pathogenesis of diabetes has only been understo experimentally since about 190 od 0.[53] The discovery of a role for the pancreas in diabetes is generally ascribed to Josep von h Mering and Oskar Minkowski, who in 1889 found that dogs whose pancreas was removed developed all the signs and symptoms of diabetes and died shortly afterwards.[54] In 1910, Sir Edward Albert Sharpey-Schafer suggested that people with diabetes were deficient in a single chemical that was normally producedby the pancreas—he proposed call ng this i substance insulin, from the Latin insula, meaning island, in reference to the insulin- producing islets of Langerhans in the pancreas.[53] The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not further clarified until 1921, when Sir Frederick Grant Banting and Charles Herbert Best repeated the work of Von Mering and Minkowski, and went further to demonstrate they could reverse induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs.[55] Banting, Best, and colleagues (especially the chemist Collip) went on to purify the hormone insulin from bovine pancreases at the University of Toronto. This led to the availability of an effective treatment—insulin injections—and the first patient was treated in 1922. For this, Banting and laboratory director MacLeod received the Nobel Prize in Physiology or Medicine in 1923; both shared their Prize money with others in the team who were not recognized, in particular Best and Collip. Banting and Best made the patent available without charge and did not attempt to control commercial production. Insulin production and therapy rapidly spread around the world,largely as a result of this decision. The distinction between what is now known as type 1 diabetes and type 2 diabetes was first clearly made by Sir Harold Percival (Harry) Himsworth, and published in January 1936.[56] Despite the availability of treatment, diabetes has remained a major cause of death. For instance, statistics reveal that the cause-specific mortality rateduring 1927 amounted to about 47.7 per 100,000 population in Malta.[57] Other landmark discoveries include:[53] * identification of the first of the sulfonylureas in 1942 * reintroduction of the use of biguanides for Type 2 diabetes in the late 1950s. The initial phenformin was withdrawn worldwide (in the U.S. in 1977) due to its potential for sometimes fatal lactic acidosis and metformin was first marketed in France in 1979, but not until 1994 in the US. * the determination of the amino acid sequence of insulin (by Sir Frederick Sanger, for which he received a Nobel Prize) * the radioimmunoassay for insulin, as discovered by Rosalyn Yalow and Solomon
  • 18. Berson (gaining Yalow the 1977 Nobe Prize in Physiology or Medicine)[58] l * the three-dimensional structure of insulin (PDB 2INS) * Dr Gerald Reaven's identification of the constellation of symptoms now called metabolic syndrome in 1988 * demonstration that intensive glycemic control in type 1 diabetes reduces chronic side effects more as glucose levels approach 'normal' in a large longitudinal study,[59] and also in type 2 diabetics in other large studies * identification of the first thiazolidinedione as an effective insulin sensitizer during the 1990s -In 1980, U.S. biotech company Genentech developed human insulin. The insulin is isolated from genetically-altered bacteria (the bacteria contain the human gene for synthesizing human insulin), which produce large quantities of insulin. Scientists then purify the insulin and distribute it to pharmacies for use by diabetes patients. (2004. Thieman,W.J. and Palladino,M.A. Introduction To Biotechnology. page 6. Pearson, Benjamin Cummings) [edit] Social issues The 1989 Declaration of St Vincent was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important both in terms of quality of life and life expectancy but also economically - expenses to diabetes have been shown to be a major drain on health- and product vity-related resources for healthcare systems and i governments. Several countries established more and less successful national diabetes programmes to improve treatment of the disease.[60] A study shows that diabetic patients with neuropathic symptoms such as numbness or tingling in feet or hands are twice more likely to be unemployed than those without the symptoms.[61] [edit] See also * List of terms associated with diabetes [edit] References 1. ^ IDF Chooses Blue Circle to Represent UN Resolution Campaign. Unite for Diabetes (17 March 2006). 2. ^ a b L M Tierney, S J McPhee, M A Papadakis (2002). Current medical Diagnosis & Treatment. International edition. New York: Lange Medical Books/McGraw-Hill, 1203- 1215. ISBN 0-07-137688-7.Check 1cate! 3. ^ a b c World Health Organisation Department of Noncommunicable Disease Surveillance (1999). Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications (PDF). 4. ^ a b c Rother, KI (2007). quot;Diabetes Treatment — Bridging the Dividequot;. N Engl J Med 356 (15): 1499-1501.Check 1cate!
  • 19. 5. ^ [1] 6. ^ Mailloux, Lionel (2007-02-13). [[[:Template:Cite web /url=http://patients.uptodate.com/topic.asp?file=dial sis/15147 /title=UpToDate Dialysis in y diabetic nephropathy /accessdate=2007-12-07 /format= /work=]] UpToDate Dialysis in diabetic nephropathy]. UpToDate. Retrieved on 2007-12-07. 7. ^ Other quot;typesquot; of diabetes. American Diabetes Association (August 25, 2005). 8. ^ Diseases: Johns Hopkins Autoimmune Disease Research Center. Retrieved on 2007- 09-23. 9. ^ FDA Approves First Ever Inhaled Insulin Combination Product for Treatment of Diabetes. Retrieved on 2007-09-09. 10. ^ Eberhart, MS; Ogden C, Engelgau M, Cadwell B, Hedley AA, Saydah SH (November 19, 2004). quot;Prevalence of Overweight and Obesity Among Adults with Diagnosed Diabetes --- United States, 1988--1994 and 1999--2002quot;. Morbidity and Mortality Weekly Report 53 (45): 1066-1068. Centers for Disease Control and Prevention. Retrieved on 2007-03-11.Check 1cate! 11. ^ Arlan Rosenbloom, Janet H Silverstein (2003). Type 2 Diabetes in Children and Adolescents: A Clinician's Guide to Diagnosis, Epidemiology, Pathogenesis, Prevention, and Treatment. American Diabetes Association,U.S., 1. ISBN 978-1580401555.Check 1cate! 12. ^ quot;Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Groupquot; (1998). Lancet 352 (9131): 854-6 PMID 9742977.Check 1cate! 5. 13. ^ Walley AJ, Blakemore AI, Froguel P (2006). quot;Genetics of obesity and the prediction of risk for healthquot;. Hum. Mol. Genet. 15 Spec No 2: R124-30. doi:10.1093/hmg/ddl215. PMID 16987875.Check 1cate! 14. ^ Barrett TG (2001). quot;Mitochondrial diabetes, DIDMOAD and other inheri ed t diabetes syndromesquot;. Best Pract. Res. Clin. Endocrinol. Metab. 15 (3): 325-43. doi:10.1053/beem.2001.0149. PMID 11554774.Check 1cate! 15. ^ Sniderman, AD; Bhopal R, Prabhakaran D, Sarrafzadegan N, Tchernof A (2007). quot;Why might South Asians be so susceptible to central obesity and its atherogenic consequences? The adipose tissue overflow hypothesisquot;. International journal of epidemiology 36 (1): 220–225. doi:10.1093/ije/dyl245. PMID 17510078.Check 1cate! 16. ^ Genuth S (Jan-Feb 2006). quot;Insights from the diabetes control and complications trial/epidemiology of diabetes interventions and complications study on the use of intensive glycemic treatment to reduce the risk of complications of type 1 diabetes.quot;. Endocr Pract 12 (Suppl 1): 34-41. ISSN 1530-891X. PMID 16627378.Check 1cate! 17. ^ Lee CM, Huxley RR, Lam TH, et al (2007). quot;Prevalence of diabetes mellitus and population attributable fractions for coronary heart disease and stroke mortality in the WHO South-East Asia and Western Pacific regionsquot;. Asia Pacific journal of clinical nutrition 16 (1): 187–92. PMID 17215197.Check 1cate! 18. ^ Seidell JC (2000). quot;Obesity, insulin resistance and diabetes--a worldwide epidemicquot;. Br. J. Nutr. 83 Suppl 1: S5–8. PMID 10889785.Check 1cate! 19. ^ Daneman D (2006). quot;Type 1 diabetesquot;. Lancet 367 (9513): 847-58. doi:10.1016/S0140-6736(06)68341-4. PMID 16530579.Check 1cate! 20. ^ Borch-Johnsen K, Joner G, Mandrup-Poulsen T, Christy M, Zachau-Christiansen B, Kastrup K, Nerup J (1984). quot;Relation between breast-feeding and incidence rates of insulin-dependent diabetes mellitus. A hypothesisquot;. Lancet 2 (8411): 1083-6. PMID 6150150.Check 1cate!
  • 20. 21. ^ Naim Shehadeh, Raanan Shamir, Moshe Berant, Amos Etzioni (2001). quot;Insulin in human milk and the prevention of type 1 diabetesquot;. Pediatric Diabetes 2 (4): 175-177. doi:10.1034/j.1399-5448.2001.20406.x.Check 1cate! 22. ^ Virtanen S, Knip M (2003). quot;Nutritional risk predictors of beta cell autoimmunity and type 1 diabetes at a young agequot;. Am J Clin Nutr 78 (6): 1053-67. PMID 14668264.Check 1cate! 23. ^ Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM (2001). quot;Intake of vitamin D and risk of type 1 diabetes: a birth-cohort studyquot;. Lancet 358: 1500. doi:10.1016/S0140-6736(01)06580-1. PMID 11705562.Check 1cate! 24. ^ Elliott RB Pilcher CC Fergusson DM Stewart AW 1996 A population based strategy to prevent insulin-dependent diabetes using nicotinamide. J Pediatr Endocrinol Metab. 1996 Sep-Oct;9(5):501-9. 25. ^ Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson J, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle T, Uusitupa M, Tuomilehto J (2006). quot;Sustained reduction in the incidence of type 2 diabetes by lifes tyle intervention: follow-up of the Finnish Diabetes Prevention Study.quot;. Lancet 368 (9548): 1673-9. doi:10.1016/S0140- 6736(06)69701-8. PMID 17098085.Check 1cate! 26. ^ a b Knowler W, Barrett-Connor E, Fowler S, Hamman R, Lachin J, Walker E, Nathan D (2002). quot;Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.quot;. N Engl J Med 346 (6): 393-403. doi:10.1056/NEJMoa012512. PMID 11832527.Check 1cate! 27. ^ Bantle JP, Wylie-Rosett J, Albright AL, et al (2006). quot;Nutrition recommendations and interventions for diabetes--2006: a position statement of the American Diabetes Associationquot;. Diabetes Care 29 (9): 2140–57. doi:10.2337/dc06-9914. PMID 16936169.Check 1cate! 28. ^ Gerstein H, Yusuf S, Bosch J, Pogue J, Sheridan P, Dinccag N, Hanefeld M, Hoogwerf B, Laakso M, Mohan V, Shaw J, Zinman B, Holman R (2006). quot;Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trialquot;. Lancet 368 (9541): 1096-105. PMID 16997664.Check 1cate! 29. ^ Kjeldsen SE, Julius S, Mancia G, McInnes GT, Hua T, Weber MA, Coca A, Ekman S, Girerd X, Jamerson K, Larochelle P, Macdonald TM, Schmieder RE, Schork MA, Stolt P, Viskoper R, Widimsky J, Zanchetti A; for the VALUE Trial Investigators (2006). quot;Effects of valsartan compared to amlodipine on preventing type 2 diabetes in high-risk hypertensive patients: the VALUE trial.quot;. J Hypertens 24 (7): 1405-1412. doi:10.1097/01.hjh.0000234122.55895.5b. PMID 16794491.Check 1cate! 30. ^ Wasko MC, Hubert HB, Lingala VB, et al (2007). quot;Hydroxychloroquine and risk of diabetes in patients with rheumatoid arthritisquot;. JAMA 298 (2): 187-93. doi:10.1001/jama.298.2.187. PMID 17622600.Check 1cate! 31. ^ Stuebe AM, Rich-Edwards JW, Willett WC, Manson JE, Michels KB (2005). quot;Duration of lactation and incidence of type 2 diabetesquot;. JAMA 294 (20): 2601–10. doi:10.1001/jama.294.20.2601. PMID 16304074.Check 1cate! 32. ^ Adler, A.I.; Stratton, I. M.; Neil, H.A.; et al (2000). quot;Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observational studyquot;. BMJ 321 (7258): 412–419. doi:10.1136/bmj.321.7258.412. ISSN 0959-8146. PMID 10938049.Check 1cate! 33. ^ a b c Vinik AI, Fishwick DT, Pittenger G (2004). quot;Advances in diabetes for the
  • 21. millennium: toward a cure for diabetesquot;. MedGenMed : Medscape generalmedicine 6 (3 Suppl): 12. PMID 15647717.Check 1cate! 34. ^ Stratta RJ, Alloway RR. (1998). quot;Pancreas transplantation for diabetes mellitus: a guide to recipient selection and optimum immunosuppression.quot;. BioDrugs. 10 (5): 347- 357. PMID 18020607.Check 1cate! 35. ^ Shapiro AM, Ricordi C, Hering BJ, et al (2006). quot;International trial of the Edmonton protocol for islet transplantationquot;. N. Engl. J. Med. 355 (13): 1318-30. doi:10.1056/NEJMoa061267. PMID 17005949.Check 1cate! 36. ^ Voltarelli, JC; Couri CE, Stracieri AB, Oliveira MC, Moraes DA, Pieroni F, Coutinho M, Malmegrim KC, Foss-Freitas MC, Simoes BP, Foss MC, Squiers E, Burt RK. (2007). quot;Autologous nonmyeloablative hematopoietic stem cell transplantation in newly diagnosed type 1 diabetes mellitus.quot;. JAMA 297 (14): 1568-76. PMID 17426276.Check 1cate! 37. ^ Rubino, F; Gagner M (2002). quot;Potential of surgery for curing type 2 diabetes mellitusquot;. Ann. Surg. 236 (5): 554-9. ISSN 0003-4932. PMID 12409659.Check 1cate! 38. ^ Rubino, F; Forgione A, Cummings DE, et al (2006). quot;The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetesquot;. Ann. Surg. 244 (5): 741–9. PMID 17060767.Check 1cate! 39. ^ Adams, TD; Gress RE, Smith SC, et al (2007). quot;Long-term mortality after gastric bypass surgeryquot;. N. Engl. J. Med. 357 (8): 753–61. doi:10.1056/NEJMoa066603. ISSN 0028-4793. PMID 17715409.Check 1cate! 40. ^ Cohen, RV; Schiavon CA, Pinheiro JS, Correa JL, Rubino F (2007). quot;Duodenal- jejunal bypass for the treatment of type 2 diabetes in patients with body mass index of 22- 34 kg/m2: a report of 2 casesquot;. Surg Obes Relat Dis. 3 (2): 195–7. doi:10.1016/j.soard.2007.01.009. PMID 17386401.Check 1cate! 41. ^ Vasonconcelos, Alberto (2007-09-01). quot;Could type 2 diabetes be reversed using surgery?quot;. New Scientist (2619): 11-13. Retrieved on 2007-09-26.Check 1cate! 42. ^ Nathan, D.M.; Cleary P.A., Backlund J.Y., et al (2005). quot;Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetesquot;. N. Engl. J. Med. 353 (25): 2643-53. doi:10.1056/NEJMoa052187. PMID 16371630.Check 1cate! 43. ^ The Diabetes Control and Complication Trial Research Group (1995). quot;The effect s of intensive diabetes therapy on the development and progression of neuropathyquot;. Annals of Internal Medicine 122 (8): 561-568. ISSN0003-4819. PMID 7887548.Check 1cate! 44. ^ a b Harris MI, Flegal KM, Cowie CC, et al (1998). quot;Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994quot;. Diabetes Care 21 (4): 518-24. doi:10.2337/diacare.21.4.518. PMID 9571335.Check 1cate! 45. ^ Annette M. Chang and Jeffrey B. Halter (2003). Aging and insulin secretion. AJP - Endocrinology and Metabolism. Retrieved on 2007-05-14. 46. ^ Diabetes and Aging. Diabetes Dateline. National Institute of Diabetes and Digestive and Kidney Diseases (2002). Retrieved on 2007-05-14. 47. ^ Weiss J, Sumpio B (2006). quot;Review of prevalence and outcome of vascular disease in patients with diabetes mel litus.quot;. Eur J Vasc Endovasc Surg 31 (2): 143-50. doi:10.1016/j.ejvs.2005.08.015. PMID 16203161.Check 1cate! 48. ^ a b American Diabetes Association (2005). Total Prevalence of Diabetes & Pre- diabetes. Retrieved on 2006-03-17.
  • 22. 49. ^ Narayan K, Boyle J, Thompson T, Sorensen S, Williamson D (2003). quot;Lifetime risk for diabetes mellitus in the United Statesquot;. JAMA 290 (14): 1884-90. doi:10.1001/jama.290.14.1884. PMID 14532317.Check 1cate! 50. ^ Seniors and Diabetes. Elderly And Diabetes - Diabetes and Seniors. LifeMed Media (2006). Retrieved on 2007-05-14. 51. ^ http://www.aihw.gov.au/indigenous/health/diabetes.cfm 52. ^ Dobson, M. (1776). quot;Nature of the urine in diabetesquot;. Medical Observations and Inquiries 5: 298–310.Check 1cate! 53. ^ a b c Patlak M (2002). quot;New weapons to combat an ancient disease: treating diabetesquot;. FASEB J 16 (14): 1853. PMID 12468446.Check 1cate! 54. ^ Von Mehring J, Minkowski O. (1890). quot;Diabetes mellitus nach pankreasexstirpation.quot;. Arch Exp Pathol Pharmakol 26: 371-387.Check 1cate! 55. ^ Banting FG, Best CH, Collip JB, Campbell WR, Fletcher AA (1922). quot;Pancreatic extracts in the treatment of diabetes mellitusquot;. Canad Med Assoc J 12: 141– 146.Check 1cate! 56. ^ Himsworth (1936). quot;Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive typesquot;. Lancet i: 127–130.Check 1cate! 57. ^ Department of Health (Malta), 1897–1972:Annual Reports. 58. ^ Yalow RS, Berson SA (1960). quot;Immunoassay of endogenous plasma insulin in manquot;. J. Clin. Invest. 39: 1157-75. doi:10.1172/JCI104130. PMID 13846364.Check 1cate! 59. ^ quot;The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group.quot; (1993). N Engl J Med 329 (14): 977-86. PMID 8366922.Check 1cate! 60. ^ Dubois, HFW and Bankauskaite, V (2005). quot;Type 2 diabetes programmesin Europequot; (PDF). Euro Observer 7 (2): 5–6.Check 1cate! 61. ^ Stewart WF, Ricci JA, Chee E, Hirsch AG, Brandenburg NA (2007). quot;Lost productive time and costs due to diabetes and diabetic neuropathic pain in the US workforcequot;. J. Occup. Environ. Med. 49 (6): 672–9. doi:10.1097/JOM.0b013e318065b83a. PMID 17563611.Check 1cate! [edit] External links * American Diabetes Association * MedlinePlus Diabetes from the U.S. National Library of Medicine * National Diabetes Education Program [hide] v•d•e Endocrine pathology: endocrine diseases (E00-35, 240-259) Thyroid Hypothyroidism (Iodine deficiency, Cretinism, Congenital hypothyroidism, Goitre, Myxedema) - Hyperthyroidism (Graves disease, Toxic multinodular goitre, Teratoma with thyroid tissue or Struma ovarii) - Thyroiditis (De Quervain's thyroiditis, Hashimoto's thyroiditis, Riedel's thyroiditis) - Euthyroid sick syndrome Pancreas Diabetes mellitus (type 1, type 2, coma, angiopathy, ketoacidosis, nephropathy,
  • 23. neuropathy, retinopathy) - Hypoglycemia - Hyperinsulinism - Zollinger-Ellison syndrome - insulin receptor (Rabson-Mendenhall syndrome) Parathyroid Hypoparathyroidism (Pseudohypoparathyroidism) - Hyperparathyroidism (Primary, Secondary, Tertiary) Pituitary Hyperpituitarism (Acromegaly, Hyperprolactinaemia, SIADH) - Hypopituitarism (Simmonds' disease/Sheehan's syndrome,Kallmann syndrome, Growth hormone deficiency, Diabetes insipidus) - Adiposogenital dystrophy - Empty sella syndrome Adrenal Cushing's syndrome (Nelson's syndrome, Pseudo-Cushing's syndrome) - CAH (Lipoid, 3β, 11β, 17α, 21α) - Hyperaldosteronism (Conn syndrome, Bartter syndrome) - Adrenal insufficiency (Addison's disease) - Hypoaldosteronism Gonads ovarian dysfunction (Polycystic ovary syndrome, Premature ovarian failure) - testicular dysfunction (5-alpha-reductase deficiency)- testosterone biosynthesis (17-beta- hydroxysteroid dehydrogenase deficiency) - general (Hypogonadism, Delayed puberty, Precocious puberty) Other Androgen insensitivity syndrome - Autoimmune polyendocrine syndrome - Carcinoid syndrome - Gigantism - Short stature (Laron syndrome, Psychogenic dwarfism) - Multiple endocrine neoplasia (1, 2) - Progeria - Woodhouse-Sakati syndrome Retrieved from quot;http://en.wikipedia.org/wiki/Diabetes_mellitusquot; Categories: Diabetes | Med conditions related to obesity | Nutrition ical Hidden categories: All articles with unsourced statements | Artic with unsourced les statements since March 2008 Views * Article * Discussion * Edit this page * History Personal tools * Log in / create account Navigation * Main Page * Contents * Featured content * Current events * Random article Interaction
  • 24. * About Wikipedia * Community portal * Recent changes * Contact Wikipedia * Donate to Wikipedia * Help Search Toolbox * What links here * Related changes * Upload file * Special pages * Printable version * Permanent link * Cite this page Languages * Afrikaans * ‫العربية‬ * Asturianu * Български * Bosanski * Català * Česky * Cymraeg * Dansk * Deutsch * Ελληνικά * Esperanto * Español * Eesti * Euskara * ‫فارسی‬ * Suomi * Français * Galego * ‫עברית‬ * ििहन दी * Hrvatski * Magyar * Interlingua * Bahasa Indonesia * Íslenska * Italiano
  • 25. * 日本語 * ქართული * 한국어 * Lëtzebuergesch * Lietuvių * മലയാളം * Bahasa Melayu * नेपाली * नेपाल भाषा * Nederlands * Norsk (nynorsk) * Norsk (bokmål) * Oromoo * Kapampangan * Polski * Português * Runa Simi * Română * Русский * Srpskohrvatski / Српскохрватски * Simple English * Slovenčina * Slovenščina * Shqip * Српски / Srpski * Svenska * தமிழ் * తెలుగు * ไทย * Türkçe * Українська * Tiếng Việt * ‫יידיש‬ ִ * 中文 * Bân-lâm-gú Powered by MediaWiki Wikimedia Foundation * This page was last modified on 7 May 2008, at 01:58. * All text is available under the terms of the GNU Free Documentation License. (See Copyrights for details.) Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a U.S. registered 501(c)(3) tax-deductible nonprofit charity. * Privac
  • 26. Framingham Heart Study From Wikipedia, the free encyclopedia • Ten things you may not know about Wikipedia • Jump to: navigation, search The Framingham Heart Study is a cardiovascular study based in Framingham, Massachusetts. The study began in 1948 with 5,209 adult subjects from Framingham, and is now on its third generation of participan Much of the now-common knowledge ts. concerning heart disease, such as the effects of diet, exercise, and common medications such as aspirin, is based on this longitudinal study. It is a project of the National Heart, Lung, and Blood Institute, in collaboration with (since 1971) Boston University. Various health professionals from the hospitals and universities of Greater Boston staff the project. Thomas Royle Dawber (1949-66) was appointed as chief epidemiologist shortly after the start of the project, when it was not progressing well.[1] The study had been intended to last 20 years, but at that time Dawber moved to Boston and became a preventive medicine chair, raising funds to continue the project and taking it with him. One of the crucial questions in evidence-based medicine is how closely the people in a study resemble the patient you are dealing with.[2] Recently the Framingham studies have become regarded as overestimating risk, particularly in the lower risk groups, for UK populations.[3] There has been widespread discussion of the study, and it is generally accepted that the work is outstanding in its scope and duration, and is overall considered very useful. Researchers recently used contact information gi en by subjects over the last v 30 years to map the social network of friends and family in the study.[4] The initial population was 5,209 healthy men and women aged 30 to 60, not the whole of the town population, as is sometimes assumed. A similar longitudinal study has been carried out in a high proportion of the residents of Busselton, a town in Western Australia, over a period of many years;[5] however, Framingham is more widely cited. [edit] Footnotes 1. ^ Richmond (2006). quot;Obituary: Thomas Royle Dawberquot; (fee required). BMJ 332: 122.Check 1cate! 2. ^ David Hadden (7 September 2002). quot;Holidays in Framingham?quot;. BMJ 325: 544.Check 1cate! 3. ^ Brindle P, Emberson J, Lampe F, et al (2003). quot;Predictive accuracy of the Framingham coronary risk score in British men: prospective cohort studyquot;. BMJ 327 (7426): 1267. doi:10.1136/bmj.327.7426.1267. PMID 14644971.Check 1cate!
  • 27. 4. ^ Nicholas A. Christakis and James H. Fowler. (2007). quot;The Spread of Obesity in a Large Social Network Over 32 Years,quot; New England Journal of Medicine 357 (4): 370-379 5. ^ A list of publications from the Busselton study [edit] References  Daniel Levy and Susan Brink. (2005). A Change of Heart: How the People of Framingham, Massachusetts, Helped Unravel the Mysteries of Cardiovascular Disease. Knopf. ISBN 0-375-41275-1. [edit] External links  Framingham Heart Study - official web site  Framingham Heart Study - National Heart, Lung, and Blood Institute  Heart Center of MetroWest - Cardiology group including William P. Castelli, MD - Former Director of Framingham Heart Study
  • 28. [hide] v•d•e Framingham, Massach [hide] v•d•e Framingham, Massach [hide] v•d•e Framingham, Massach Articles Main · Government · Education · Religion · History Framingham High School · Framingham State College · Marian High School Minuteman statue at the intersection of Main St. and Union Ave. Related Articles
  • 29. Retrieved from quot;http://en.wikipedia.org/wiki/Framingham_Heart_Studyquot; Categories: 1948 establishments | Framingham, Massachusetts | Clinical trials Views  Article  Discussion  Edit this page  History Personal tools  Log in / create account Navigation  Main Page  Contents  Featured content  Current events  Random article Interaction  About Wikipedia  Community portal  Recent changes  Contact Wikipedia  Donate to Wikipedia  Help Search Toolbox  What links here  Related changes  Upload file  Special pages  Printable version  Permanent link  Cite this page
  • 30. Languages  Deutsch  Hrvatski  Norsk (bokmål)  This page was last modified on 29 April 200 at 02:29. 8,  All text is available under the terms of the GNU Free Documentation License. (See Copyrights for details.) Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a U.S. registered 501(c)(3) tax-deductible nonprofit charity.  Privacy policy  About Wikipedia Early registration for Wikimania 2008 is now open. DESMOND (diabetes) From Wikipedia, the free encyclopedia • Learn more about citing Wikipedia • Jump to: navigation, search DESMOND (Diabetes Education and Self Management for Ongoing and Newly Diagnosed) is an UK NHS training course for people with type 2 diabetes that helps people to identify their own health risks and to set their own goals.
  • 31. Diabetes mellitus Types of Diabetes Diabetes mellitus type 1 Diabetes mellitus type 2 Gestational diabetes Pre-diabetes: Impaired fasting glycaemia Impaired glucose tolerance Disease Management Diabetes management: •Diabetic diet •Anti-diabetic drugs •Conventional insulinotherapy •Intensive insulinotherapy Other Concerns Cardiovascular disease Diabetic comas: •Diabetic hypoglycemia •Diabetic ketoacidosis •Nonketotic hyperosmolar Diabetic myonecrosis Diabetic nephropathy Diabetic neuropathy Diabetic retinopathy Diabetes and pregnancy Blood tests Blood sugar Fructosamine Glucose tolerance test Glycosylated hemoglobin
  • 32. Contents [hide]  1 Background  2 Course details o 2.1 Format o 2.2 Content  3 References  4 See also  5 External links [edit] Background DESMOND is the first nat onal education programme created for people with Type 2 i diabetes. DESMOND meets the criteria NICE identified as being the characteristics of a quality, evidence-based structured education programme. A NHS training course is available for type 1 diabetics called DAFNE (Dose Adjustment for Normal Eating). [edit] Course details [edit] Format Each programme is run in a group setting, consisting of not more than 10 people newly diagnosed with Type 2 diabetes (normally wit in the last 12 months), accompanied, if they h so choose, by a partner, family member, or friend. The programme may be run as a one day, or two part (2 x half-day) course. The DESMOND programme is facilitated by two health care professionals who have been formally trained. [edit] Content Topics covered in the DESMOND curriculum: 1. The patient story 2. What diabetes is 3. Main ways to manage diabetes 4. Consequences of diabetes and personal risk from having diabetes 5. Monitoring your diabetes 6. Ways to take action to improve the control of your diabetes
  • 33. 7. Food choices for diabetics 8. Physical activity and diabetes 9. Stress and emotions and diabetes 10. The purpose and content of annual diabetic review and screening in diabetics [edit] References  Department of Health Structured patient education in diabetes: Leaflet  NHS Get Educated page for diabetes  NHS NICE criteria for diabetes training courses [edit] See also  Diabetes mellitus type 2 [edit] External links  DESMOND NHS project website  Diabetes UK charity website Retrieved from quot;http://en.wikipedia.org/wiki/DESMOND_%28diabetes%29quot; Categories: Diabetes Views  Article  Discussion  Edit this page  History Personal tools  Log in / create account Navigation  Main Page  Contents  Featured content  Current events  Random article Interaction
  • 34.  About Wikipedia  Community portal  Recent changes  Contact Wikipedia  Donate to Wikipedia  Help Search Toolbox  What links here  Related changes  Upload file  Special pages  Printable version  Permanent link  Cite this page  This page was last modified on 3 February 2008, at 12:15.  All text is available under the terms of the GNU Free Documentation License. (See Copyrights for details.) Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a U.S. registered 501(c)(3) tax-deductible nonprofit charity.  Privacy policy  About Wikipedia  Disclaimers Help us improve Wikipedia by supporting it financially.  Disclaimers