#REDIRECT Diabetes mellitus
Diabetes mellitus is a medical disorder characterized by varying or persistent hyperglycemia (elevated blood sugar levels), especially after eating. All types of diabetes mellitus share similar symptoms and complications at advanced stages. Hyperglycemia itself can lead to dehydration and ketoacidosis. Longer-term complications include cardiovascular disease (doubled risk), chronic renal failure (it is the main cause for renal dialysis), diabetic retinopathy with eventual blindness, diabetic neuropathy and eventual gangrene with risk of amputation of toes, feet, and even legs. The most important forms of diabetes are due to decreased production of insulin (diabetes mellitus type 1, the first recognized form), or insulin resistance of body tissues to insulin (diabetes mellitus type 2, the more common form). The former requires insulin injections, while the latter is generally managed with oral medication and only requires insulin if the tablets are ineffective. Patient understanding and participation is vital as blood glucose levels change continuously, while successfully keeping blood sugar within normal limits has been compellingly shown to reduce or prevent development of some of the complications of diabetes. Other risk factors that can require addressing to reduce complications are: cessation of tobacco smoking, optimizing cholesterol levels, maintaining a stable human weight, controlling arterial hypertension and engaging in regular exercise. ==Statistics== In 2004, according to the World Health Organization, more than 150 million people worldwide suffer from diabetes. Its incidence is increasing rapidly, and it is estimated that by the year 2025 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 rate is, however, expected to occur in Asia and Africa, where most of the diabetic patients will be seen by 2025. The increase in incidence of diabetes in the developing countries follows the trend of urbanisation and life style changes. 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 (see big killers). For at least 20 years, diabetes rates in North America have been increasing substantially. In 2002 there were about 18.2 million diabetics in the United States alone. 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. ==Causes and types== ===The role of insulin=== Since insulin is the principal hormone that regulates uptake of glucose into cells (primarily muscle and fat cells) from the blood, deficiency of insulin or its action plays a central role in all forms of diabetes. Most of the carbohydrates in food are rapidly digested to glucose, the principal sugar in blood. Insulin is produced by beta cells in the pancreas in response to rising levels of glucose in the blood, as occurs after a meal. Insulin makes it possible for most body tissues to remove 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 (the basic sugar unit) to glycogen for storage in liver and muscle cells. Lowered insulin levels result in the reverse conversion of glycogen to glucose when glucose levels fall -- though only in the liver not muscle tissue. Higher insulin level increase many anabolic ("building up") processes such as cell growth, cellular protein synthesis, and fat storage. Insulin is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction. If the amount of insulin produced is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or insulin resistance), or if the insulin itself is defective, glucose is not handled properly by body cells (about 2/3 require it) nor stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements. ===Type 1 diabetes mellitus=== Type 1 diabetes is most commonly diagnosed in children and adolescents, but can occur in adults as well. It is an autoimmune disorder, in which the body's own immune system attacks the beta cells in the Islets of Langerhans of the pancreas, destroying them or damaging them sufficiently to reduce insulin production. The autoimmune attack may be triggered by reaction to an infection, for example by one of the viruses of the Coxsackie virus family. A subtype of type 1 (identifiable by the presence of antibodies against beta cells) develops slowly and so is often confused with Type 2. In addition, a small proportion of type 1 cases has the hereditary condition maturity onset diabetes of the young (MODY). Some poisons (e.g. certain rat poisons) work by selectively destroying certain types of cells, including pancreatic beta cells, thus producing "artificial" type 1 diabetes. Other pancreatic problems including trauma, pancreatitis or tumors (either malignant or benign) can also lead to loss of insulin production. As of 2004, type 1 is treated with insulin injections, lifestyle adjustments, and careful monitoring of blood glucose levels using blood test kits. Insulin delivery is also available by an insulin pump, which allows the infusion of insulin 24 hours a day at preset levels, and the ability to program push doses (bolus) of insulin as needed at meal times. The treatment must be continued indefinitely. Experimental replacement of beta cells (by transplant) is being investigated in several research programs and may become clinically available in the future. About 5-10% of all North American cases of diabetes are Type 1 diabetics. The fraction of type 1 diabetics 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. Formerly, type 1 diabetes was called "childhood" or "juvenile" diabetes or "insulin dependent" diabetes. Each term is a misnomer, especially since the obesity epidemic in recent years has led to increased incidence of type 2 diabetes in children and adolescents in the USA, and insulin is used in some type 2 cases. ===Type 2 diabetes mellitus=== Type 2 diabetes is characterized by "insulin resistance" as body cells do not respond appropriately when insulin is present. This is a more complex problem than type 1, but is sometimes easier to treat, since insulin is still produced, especially in the initial years. Type 2 may go unnoticed for years in a patient before diagnosis, since the symptoms are typically milder (no ketoacidosis) and can be sporadic. However, severe complications can result from unnoticed type 2 diabetes, including renal failure, and coronary artery disease. Type 2 diabetes was formerly known by a variety of partially misleading names, including "adult-onset diabetes", "obesity-related diabetes", "insulin-resistant diabetes", or "non-insulin-dependent diabetes" (NIDDM). It may be caused by a number of diseases, such as hemochromatosis and polycystic ovary syndrome, and can also be caused by certain types of medications (e.g. long-term steroid use). About 90-95% of all North American cases of diabetes are type 2, and about 20% of the population over the age of 65 is a type 2 diabetic. The fraction of type 2 diabetics in other parts of the world varies substantially, almost certainly for environmental and lifestyle reasons. There is also a strong inheritable genetics connection in type 2 diabetes: having relatives (especially first degree) with type 2 is a considerable risk factor for developing type 2 diabetes. The majority of patients with type 2 diabetes mellitus are obesity - chronic obesity leads to increased insulin resistance that can develop into diabetes, most likely because adipose tissue is a (recently identified) source of chemical signals (hormones and cytokines). Other research shows that type 2 diabetes causes obesity.12 Type 2 is initially treated by changes in diet and through weight loss. This can restore insulin sensitivity, even when the weight lost is modest e.g. around 5 kg (10 to 15 lb). The next step, if necessary, is treatment with oral antidiabetic drugs: the sulphonylureas, metformin, or (if these are insufficient) thiazolidinediones. When these have failed, insulin therapy may be necessary to maintain normal glucose levels. ===Type 3 diabetes mellitus=== All other specific forms of diabetes, accounting for up to 5% of all diagnosed cases of diabetes, are termed Type 3: * Type 3A: genetic defect in beta cells. * Type 3B: genetically related insulin resistance. * Type 3C: diseases of the pancreas. * Type 3D: caused by hormonal defects. * Type 3E: caused by chemicals or drugs. ===Type 4 diabetes mellitus=== ''Main article: Gestational diabetes'' Type 4 or ''gestational diabetes mellitus'' appears in about 2-5% of all pregnancy. It is temporary and fully treatable, but if untreated it may cause problems with the pregnancy, including macrosomia (high birth weight) of the child. It requires careful medical supervision during the pregnancy. In addition, about 20-50% of these women go on to develop type 2 diabetes. ===Genetics=== Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by infection, stress, or environmental factors (e.g. exposure to a causative agent). There is a genetic element in the susceptibility of individuals to some of these triggers which has been traced to particular HLA genotypes (i.e. genetic "self" identifiers used 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 type 1 diabetics carry a mutation that causes maturity onset diabetes of the young (MODY). There is an even stronger inheritance pattern for Type 2 diabetes; those with type 2 ancestors or relatives have very much higher chances of developing Type 2. It is also often connected to obesity, which is found in approximately 85% of (North American) patients diagnosed with that form of the disease, so inheriting a tendency toward obesity seems also to contribute. Age is also thought to be a contributing factor, as most type 2 patients in the past were older. The exact reasons for these connections are unknown. ==Diagnosis== ===Signs and symptoms=== Type 2 diabetes almost always has a slow onset (often years), but in type 1, particularly in children, onset may be quite fast (weeks or months). Early symptoms of type 1 diabetes are often polyuria (frequent urination) and polydipsia (increased thirst, and consequent increased fluid intake). There may also be weight loss (despite normal or increased eating), increased appetite, and irreduceable fatigue. These symptoms may also manifest in Type 2 diabetes in patients who present with frank poorly controlled diabetes. Thirst develops because of osmosis effects — sufficiently high glucose (above the 'renal threshold') in the blood is excreted by the kidneys but this requires water to carry it and causes increased fluid loss, which must be replaced. The lost blood volume will be replaced from water held inside body cells, causing dehydration. Another common presenting symptom is altered vision. Prolonged high blood glucose causes changes in the shape of the lens in the eye, leading to blurred vision and, perhaps, a visit to an optometry. All unexplained quick changes in eyesight should force a fasting blood glucose test. These are now quick (less than 5 minutes total), inexpensive (materials less than US$1), and can be safely performed by almost anyone with trivial training. Especially dangerous symptoms in diabetics include the smell of acetone on the patient's breath (a sign of Diabetic ketoacidosis), Kussmaul breathing (a rapid, deep breathing), and any altered state of consciousness or arousal (hostility and mania are both possible, as is confusion and lethargy). The most dangerous form of altered consciousness is the so-called "diabetic coma" which produces unconsciousness. Early symptoms of impending diabetic coma include polyuria, nausea, vomiting and abdominal pain, with lethargy and somnolence a later development, progressing to unconsciousness and death if untreated. ===Diagnostic approach=== 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 25% of people with new type 1 diabetes have developed a degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is made in many other ways. The most common are (1) health screening, (2) detection of hyperglycemia when a doctor is investigating a complication of longstanding, unrecognized diabetes, and less commonly (3) new signs and symptoms attributable to the diabetes. # Diabetes screening is recommended for many types of people at various stages of life or with several different risk factors. The screening test varies according to circumstances and local policy and may be a random glucose, a fasting glucose and insulin, a glucose 2 hours after 75 g of glucose, or a formal glucose tolerance test. Many health care recommendations for adults recommend universal screening at age 40 or 50 years, and sometimes occasionally thereafter. Earlier screening is recommended for those with risk factors such as obesity, family history of diabetes, high risk ethnicity (Hispanic [Latin American], American Indian, African American, Pacific Island, and South Asian ancestry). # Many medical conditions are associated with a higher risk of various types of diabetes and warrant screening. A partial list includes: arterial hypertension, dyslipidemia, coronary artery disease, past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, hepatic steatosis (fatty liver), cystic fibrosis, several mitochondrial neuropathies and myopathies, myotonic dystrophy, Friedreich's ataxia, some of the inherited forms of neonatal hyperinsulinism and many others. Risk of diabetes is higher with chronic use of several medications, including high dose glucocorticoids, some chemotherapy agents (especially L-asparaginase), and some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics). # Diabetes is often detected when a person suffers a problem 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. ===Criteria for diagnosis=== Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of # two fasting plasma glucose levels above 7 mmol/l (125 mg/dl) on different days; # plasma glucose above 11.1 mmol/l (200 mg/dl) two hours after a 75 g glucose load; or # symptoms of diabetes and a random glucose above 11 mmol/l (200 mg/dl). While not used for diagnosis, an elevated glucose bound to hemoglobin, HbA1c, of 6.0% or higher (2003 revised US standard); is a screening and treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). ===Diabetic ketoacidosis and coma=== ''See also the more detailed articles diabetic ketoacidosis and diabetic coma'' Diabetic ketoacidosis (DKA) is an acute, dangerous complication and is always a ''medical emergency''. Without prompt proper treatment, diabetic ketoacidosis leads to death. DKA occurs more commonly in type 1 diabetes because the insulin deficiency is more severe, though it can occur rarely in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, the insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. When a person is known to have diabetes and is being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis (the "flu"), or an overwhelming new health problem (e.g., bacterial infection, myocardial infarction). Insulin deficiency switches many aspects of metabolic balance in a catabolic direction. The liver becomes a net producer of glucose by way of gluconeogenesis and glycogenolysis. Fat in adipose tissue is reduced to triglycerides and fatty acids by lipolysis. Muscle is degraded to release amino acids for gluconeogenesis. The rise of fatty acid levels is accompanied by a rise of ketones (acetone, acetoacetate and beta-hydroxybutyrate). As the ketosis worsens, it produces a metabolic acidosis, with anorexia, abdominal distress, and eventually vomiting. The rising level of glucose increases the volume of urine produced by the kidneys (an ''osmolar diuresis''). The high volume of urination (polyuria) also produces increased losses of electrolytes, especially sodium, potassium, chloride, phosphate, and magnesium. Reduced fluid intake from vomiting combined with amplified urination produce dehydration. As the metabolic acidosis worsens, it induces obvious hyperventilation (termed Kussmaul respiration). On presentation to hospital, the patient in DKA is typically dehydrated and breathing both fast and deeply. Abdominal pain is common and may be severe. The level of consciousness is normal until late in the process, when obtundation may progress to coma. The dehydration can become severe enough to cause shock. Laboratory tests typically show hyperglycemia, metabolic acidosis, normal or hyperkalemia, and severe ketosis. Many other tests can be affected. At this point the patient is urgently in need of intravenous fluids. The basic principles of DKA treatment are #Rapid restoration of adequate circulation and perfusion with isotonic intravenous fluids #Gradual rehydration and restoration of depleted electrolytes (especially sodium and potassium) #Insulin to reverse the ketosis and lower the glucose #Careful monitoring to detect and treat complications Treatment usually results in full recovery, though death can result from inadequate treatment or a variety of complications. ===Hyperosmotic diabetic coma=== Hyperosmotic diabetic coma is another acute problem associated with improper management of diabetes mellitus. It has some symptoms in common with DKA, but a different cause, and requires different treatment. In anyone with very high blood glucose levels (usually considered to be above 300 mg/dl) water will be osmotically driven out of cells into the blood. The kidneys will also be "dumping" glucose into the urine, resulting in concomitant loss of water, causing an increase in blood osmolality. The osmotic effect of high glucose levels combined with the loss of water will eventually result in such a high serum osmolality that the body's cells may become directly affected as water is drawn out from them. Electrolyte imbalances are also common. This combination of changes, especially if prolonged, will result in symptoms similar to ketoacidosis, including loss of consciousness. As with DKA, urgent medical treatment is necessary. This is the diabetic coma to which type 2 diabetics are prone; it is less common in type 1 diabetics. ===Hypoglycemia=== Hypoglycemia in diabetic patients almost always arises as a result of poor management of the disease either from too much or poorly timed insulin or oral hypoglycemics or too much exercise, not enough food, or poor timing of either. If blood glucose levels are low enough, the patient may become agitated, sweaty, and have many symptoms of Autonomic nervous system activation of the autonomic nervous system - they may experience feelings similar to dread and immobilized panic. Consciousness can be altered, or even lost, in extreme cases, leading to coma and/or seizures or even death and brain damage. Experienced diabetics can often recognise the symptoms early on - all diabetics should always carry something sugary to eat or drink as these symptoms can be rapidly reduced if treated early enough. In the case of children, this can be a type of candy disliked by the patient, to prevent concerns about unnecessary use. Other ways of treating hypoglycemia include an injection of glucagon which causes the liver to convert its internal stores of glycogen to be released as glucose into the blood. Oral or intravenous dextrose can also be given. In most cases, recovery is rapid and troublefree. Longstanding hypoglycemia may require hospital admission to allow supervised recovery and adjustment of diabetic medications. ==Long-term complications== Among the major risks of the disorder are chronic problems affecting multiple organ systems which will eventually arise in patients with poor glycemic control. Many of these arise from damage to the blood vessels. These illnesses can be divided into those arising from large blood vessel diseases, macroangiopathy, and those arising from small blood vessel disease, microangiopathy. Interestingly, small vessel disease is minimized by tight blood glucose control, but large vessel disease is unaffected by tight blood glucose control. *Small vessel disease complications: **proliferative diabetic retinopathy which can lead to blindness; **peripheral diabetic neuropathy which, particularly when combined with damaged blood vessesls, can lead to foot ulcers, and possibly progressing to necrosis, infection and gangrene, sometimes requiring limb amputation, see below **diabetic nephropathy (due to microangiopathy) which can lead to renal failure *Large vessel disease complications: **ischemic heart disease caused by both large and small vessel disease **stroke **peripheral vascular disease which contributes to foot ulcers and the risk of amputation Diabetes mellitus is the most common cause of adult renal failure worldwide. It also the most common cause of amputation in the US, usually toes and feet, often as a result of gangrene, and almost always as a result of peripheral vascular disease. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US. ==Management of the disease== Diabetes is a chronic disease with no cure (except experimentally in type 1 diabetics) as of 2004. Management of this disease may include lifestyle modifications such as achieving and maintaining proper weight, diet, exercise and foot care. The most important is the hypoglycemic treatment with either oral hypoglycemics and/or insulin therapy. Nowadays, the goal for diabetics is to avoid or minimize chronic diabetic complications, as well as to avoid acute problems of hyperglycemia or hypoglycemia. Adequate control of diabetes leads to a lower risk of the complications of uncontrolled diabetes which include kidney failure (requiring dialysis or transplant), blindness, heart disease and limb amputation. Recent studies show that use of statins might be needed in primary and secondary prevention of cardiovascular complications and mortality. Ideal control of hypertension plays a pivotal role in preventing both diabetic nephropathy and cardiovascular disease. There is emerging solid evidence that full-blown diabetes mellitus type 2 can be evaded in those with only mildly impaired glucose tolerance6. Patients with type 1 diabetes mellitus require direct injection of insulin as their bodies cannot produce enough (or even any) insulin. As of 2004, there is no other clinically available form of insulin administration other than injection for patients with type 1: injection can be done by insulin pump, by jet injector, or any of several forms of hypodermic needle. There are several insulin application mechanisms under experimental development as of 2004. There have also been proposed vaccines for type I using glutamic acid decarboxylase (GAD), but these are currently not being tested by the pharmaceutical companies that have sublicensed the patents to them. For type 2 diabetics, diabetic management consists of a combination of diet (nutrition), exercise, and weight loss, in any achievable combination depending on the patient. Patients who have poor diabetic control after lifestyle modifications are typically placed on oral hypoglycemics. Some Type 2 diabetics eventually fail to respond to these and must proceed to insulin therapy. Patient education and compliance with treatment is very important in managing the disease. Improper use of medications and insulin can be very dangerous causing hypo- or hyper-glycemic episodes. Insulin therapy requires close monitoring and a great deal of patient education, as improper administration is quite dangerous. For example, when food intake is reduced, less insulin is required. A previously satisfactory dosing may be too much if less food is consumed causing a hypoglycemia reaction if not intelligently adjusted. In addition, exercise decreases insulin requirements as exercise increases glucose uptake by body cells whose glucose uptake is controlled by insulin. And vice versa. In addition, there are available several types of insulin with varying times of onset and duration of action. ===Monitoring=== Optimal management of diabetes involves patients measuring and recording their own blood glucose testing at home. By keeping a diary of their own blood glucose measurements and noting the effect of food and exercise, patients can modify their lifestyle to better control their diabetes. For patients on insulin, patient involvement is important in achieving effective dosing and timing. Relying on their own perceptions of symptoms of hyperglycemia or hypoglycemia is usually unsatisfactory as mild to moderate hyperglycemia causes no obvious symptoms in nearly all patients. Other considerations include the fact that, while food takes several hours to be digested and absorbed, insulin administration can have glucose lowering effects for as little as 2 hours or 24 hours or more (depending on the nature of the insulin preparation used and individual patient reaction). In addition, the onset and duration of the effects of oral hypoglycemic agents vary from type to type and from patient to patient. A useful test that can be done in a doctor's clinic is the measurement of blood HbA1C levels. This is the ratio of glycosylated red blood cells in relation to the total number of red blood cells. Persistent raised plasma glucose levels causes the proportion of these cells to go up. This is a test that measures the average amount of diabetic control over a period originally thought to be about 3 months (the average red blood cell lifetime), but more recently thought to be about 2 to 4 weeks. In the non-diabetic, the HbA1C level ranges from 4.0-6.4%; patients with diabetes mellitus who manage to keep their HbA1C level below 7.0% are considered to have good glycaemic control. Regular blood testing especially more so in type 1 diabetics is essential to keep a tight reign on the symptoms of the disease. There are many (at least 20+) different types of blood glucose meter available on the market today; not every meter suits all patients and it is a specific matter of choice for the patient to find a meter that they personally find comfortable to use. The principle of the devices is the virtually the same, a small blood sample is collected by the patient by self-production using a lancing device (a sterile pointed needle) the blood is usually collected at the end point to a test strip. This test strip contains various chemicals which when the blood is applied creates a small electrical charge between two contacts. This charge will vary dependent on the glucose levels within the blood and its effect on the chemicals contained within the strip. In older glucose meters, the drop of blood is placed on top of a strip. A chemical reaction occurs and the strip changes color. The meter then measures the color of the strip optically. It is this level that is measured and a result in either mg/dL (milligrams per deciliter in the USA) or mmol/L (millimoles per litre in Europe) of blood. The average normal person should have a glucose level of around 4.5 to 7.0 mmol/L (80 to 125 mg/dL). In the diabetic patient, more specifically type 2 patients, it is important to maintain good glucose control, with a before meal level of <6.1 mmol/L (<110 mg/dL) and a level two hours after the start of a meal of <7.8 mmol/L (<140 mg/dL)13. A level of <3.8 mmol/L (<70 mg/dL) is usually described as a hypoglycaemic attack. Most diabetics 'know' when they're going to 'go hypo' and usually are able to eat some food or drink something sweet to raise levels. It is important to remember though, that a patient who is hyperglycemic (high glucose) can also become temporarily hypoglycemic under certain conditions (i.e. not eating regularly, or strenuous exercise, followed by fatigue). Levels greater than 13-15 mmol/L (230-270 mg/dL) should be monitored closely and the patient is advised to seek urgent medical attention as soon as possible if this continues to rise after 2-3 tests. Hyperglycemia is not as easy to detect as hypoglycemia and usually happens over a period of days rather than hours or minutes. If left untreated this can result in diabetic coma and death. Prolonged and elevated levels of glucose in the blood, which is left unchecked and untreated will, over time, result in serious diabetic complications and sometimes even death. It is therefore highly important that a diabetic patient checks their blood levels either daily or every few days to see what levels they are achieving over a given period of time. There is also computer software for the PC which is available from blood testing manufacturers which can display results and trends over time. Type 1 patients will have to check on a more regular daily basis due to insulin therapy, which is a fine art to master. The US Food and Drug Administration has also approved a non-invasive blood glucose monitoring device [http://diabetes.niddk.nih.gov/dm/pubs/glucosemonitor/index.htm]. This allows checking blood glucose levels, while puncturing the skin as little as twice a day. Once calibrated with a blood sample, it pulls body fuilds from the skin using small electrical currents, taking six readings an hour for as long as thirteen hours. It has not proven to be reliable enough, or convenient enough to be used in lieu of conventional blood monitoring. Other non-invasive methods like radiowaves, ultrasound and energy waves are also being tested. These results are especially useful for the diabetic to present to their doctor or physician in the monitoring and control of the disease. Failure to maintain a strict regimen of testing can accelerate symptoms of the condition, and it is therefore imperative that any diabetic patient strictly monitor their glucose levels regularly. ==Public health, policy and health economics== The Declaration of St Vincent was the result of international efforts to improve the care accorded to diabetics. Doing so is important if only economically. Diabetes is enormously expensive for healthcare systems and governments. In North America, it is the largest single non-traumatic cause in adults of amputation, blindness, and dialysis, all extremely expensive events. Work in the Puget Sound area of North America (by the health organization Group Health) shows that, over its large and varied patient population, specially retaining medical information on diabetic patients, keeping it up to date, and basing their continuing care on that data reduced total healthcare costs for those patients by US$1000 per year per patient for the rest of life. Recognition of this reality drove the Hawkes Bay initiative which established such a system, and resulted in various activities throughout the world including the Black Sea Telediab project which produced elements of a distributed diabetic record and management system as an open source computer program. ==History== Although diabetes has been recognized since antiquity, and treatments were known since the Middle Ages, the elucidation of the pathogenesis of diabetes occurred mainly in the 20th century7. Until 1922, when insulin was first discovered and made clinically available, a clinical diagnosis of diabetes was an invariable death sentence, more or less quickly. Non-progressing type 2 diabetics almost certainly often went undiagnosed then; many still do. The discovery of the role of the pancreas in diabetes is generally credited to Joseph Von Mering and Oskar Minkowski, two European researchers who, in 1889, found that when they completely removed the pancreas of dogs, the dogs developed all the signs and symptoms of diabetes and died shortly afterward. In 1910, Sir Edward Albert Sharpey-Schafer of Edinburgh in Scotland suggested diabetics were deficient in a single chemical that was normally produced by the pancreas - he proposed calling this substance insulin. The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not fully clarified until 1921, when Sir Frederick Grant Banting and Charles Herbert Best repeated the work of Von Mering and Minkowski but went a step further and managed to show that they could reverse the induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs8. They went on to isolate the hormone insulin from bovine pancreases at the University of Toronto in Canada. This led to the availability of an effective treatment - insulin injections - and the first clinical patient was treated in 1922. For this, Banting ''et al'' received the Nobel Prize in Physiology or Medicine in 1923. The two researchers did not patent their discovery and insulin therapy rapidly spread around the world. The distinction between what is now known as type 1 and type 2 diabetes was made by Sir Harold Percival Himsworth in 1935; he published his findings in January 1936 in The Lancet9. Other landmark discoveries7 include: * identification of sulfonylureas in 1942 * the radioimmunoassay for insulin, as discovered by Rosalyn Yalow and Solomon Berson (gaining Yalow the 1977 Nobel Prize in Physiology or Medicine); * Reaven's introduction of the metabolic syndrome in 1988 * identification of thiazolidinediones as effective antidiabetics in the 1990s. ==Etymology== "Diabetes" is a Greek language word meaning "a passer through; a siphon". "Mellitus" comes from the Greek word "sweet". Apparently, the Greeks named it thus because the excessive amounts of urine diabetics produce (when blood glucose is too high) attracted Fly and Bee because of the glucose content. The ancient China tested for diabetes by observing whether ants were attracted to a person's urine; medieval European doctors tested for it by tasting the urine themselves, a scene occasionally depicted in Gothic reliefs. It is probably important to note that passing abnormal amounts of urine is a symptom shared by several diseases (most commonly of the kidney), and the single word diabetes is applied to many of them. The most common of them are diabetes insipidus and the subject of this article, diabetes mellitus. ==References== # Diabetes Control and Complications Trial Research Group. ''The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.'' N Engl J Med 1993;329:977-86. [http://content.nejm.org/cgi/content/full/329/14/977 Fulltext]. PMID 8366922. # World Health Organisation, Department of Noncommunicable Disease Surveillance. ''Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications.'' Geneva: WHO, 1999 ([http://whqlibdoc.who.int/hq/1999/WHO_NCD_NCS_99.2.pdf PDF]) # UK Prospective Diabetes Study Group. ''Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33).'' The Lancet 1998;352:837-53. PMID 9742976. #''Conditions in Occupational Therapy: effect on occupational performance.'' Edited by Ruth A. Hansen and Ben Atchison. Baltimore: Lippincott Williams & Williams, 2000;298-309. ISBN 0-683-30417-8. # Heart Protection Study Collaborative Group. ''MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial.'' Lancet 2003;361(9374):2005-16. PMID 12814710. # Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M. ''Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.'' N Engl J Med 2001;344:1343-50. PMID 11333990. # Patlak M. ''New Weapons to Combat an Ancient Disease: Treating Diabetes.'' [http://www.fasebj.org/cgi/content/full/16/14/1853e FASEB J 2002;16:1853E]. PMID 12468446. # Banting FG, Best CH, Collip JB, Campbell WR, Fletcher AA. ''Pancreatic extracts in the treatment of diabetes mellitus.'' Canad Med Assoc J 1922;12:141-146. # Himsworth HP. ''Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types.'' Lancet 1936;i:127-130. # Colhoun HM, Betteridge DJ, Durrington PN, Hitman GA, Neil HA, Livingstone SJ, Thomason MJ, Mackness MI, Charlton-Menys V, Fuller JH on behalf of the CARDS Investigators. ''Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicenter randomized placebo-controlled trial.'' Lancet 2004; 364: 685-96. PMID 15325833 #''MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial.'' Lancet, 2002; 360: 7-22. PMID 12114036 #S Camastra, E Bonora, S DelPrato, K Rett, M Weck, E Ferrannini. Effect of obesity and insulin resistance on resting and glucose-induced thermogenesis in man. International Journal of Obesity, 1999, Vol 23, Iss 12, pp 1307-1313. PMID 10643689 # ''The American Association of Clinical Endocrinologists Medical Guidelines for the Management of Diabetes Mellitus: The AACE System of Intensive Diabetes Self-Management—2002 Update.'' [http://www.aace.com/clin/guidelines/diabetes_2002.pdf Endocrine Practice Vol. 8 (Suppl. 1) January/February 2002]. ==See also== *list of terms associated with diabetes *list of celebrities with diabetes *diabetes in cats and dogs *Pancreatic cancer ==External links== *[http://www.nlm.nih.gov/medlineplus/diabetes.html MedlinePlus Diabetes from the U.S. National Library of Medicine] *[http://www.childrenwithdiabetes.com Children with Diabetes] *[http://my.webmd.com/content/article/56/65915.htm MyWebMD Diabetes Section] *[http://www.diabetes.ca Canadian Diabetes Association] *[http://www.jdrf.org Juvenile Diabetes Research Foundation] *[http://www.diabetes.org American Diabetes Association] *[http://www.idf.org International Diabetes Federation] *[http://www.who.int/diabetes/en/ WHO - The Diabetes Programme] *[http://www.healthatoz.com/healthatoz/Atoz/dc/caz/diab/dia2/diabetescfindex2.html Health A to Z Diabetes Type 2 Section] *[http://www.hc-sc.gc.ca/pphb-dgspsp/ccdpc-cpcmc/diabetes-diabete/english/risk Health Canada Diabetes Type 2 Risk Evaluation] *[http://www.cdc.gov/diabetes Center for Disease Control Diabetes Section] *[http://www.idsoc.org The Immunology of Diabetes Society] *[http://www.uchsc.edu/misc/diabetes/books.html Informative Book on Basic and Clinical information on Type 1 Diabetes from Barbara Center for Childhood Diabetes] *[http://www.diabetes.diabetesjournals.org Journals on Basic and clinical research in Diabetes cure and care] *[http://diabetes.niddk.nih.gov/dm/pubs/riskfortype2/ Diabetes Type 2 Risks] Diabetes Nutrition fa:مرض قند ms:Kencing manis
==Foot and lower limbs need more attention== I'm really not a medical person so I'm reluctant to actually contribute to the article - but I work on creating software health interventions to help people perform self care regarding diabetes related pedal complications. This is also one of the primary concerns of Diabetes Australia this year. The prevalence of foot complication in this group is between 3-6% (in Australia at least). Common pedal complications include; foot ulcers, infections, cellulitis, peripheral vascular disease, neuropathy, fractures and the need for amputation. Lower limb complications in people with diabetes have been estimated to cost the health care system about $300 million per year in Australia. So it's a big issue - but only briefly mentioned in the article. User:Melody This page has been listed on the Wikipedia:pages needing attention list as "not up to the standards of scientific knowledge". Can you please let us know what is wrong with it, so we can correct it? -- User:Karada 22:23, 23 Sep 2003 (UTC) :several things: * reorganization of information to make more sense, removing duplicate information * verifying to ensure correctness of data * general polishing up of grammar, style, structure. I guess there might be others suggestions too, but these should do for starters. --User:Alex.tan 06:12, 24 Sep 2003 (UTC) ==Objections to diabetes mellitus article== From my (User:Karada's) talk page: Hello Karada,
You asked about diabetes mellitus article and my objections to its content.
First, it is of patchy quality. There are passages or section that are quite acceptable and other that need major rewrite.
Second, its style is inconsistent. Sometimes it uses scintific language and nomenclature and sometimes it is written in badly conceived "for patients" style. (I once proposed to make corresponding "Patient information" pages in this case "Patient information on Diabetes mellitus" linked to the scientific article Diabetes mellitus)
Third, see sections Diabetes mellitus#Diabetes treatment. Current standards - St Vincent declaration.
Presentation is also lacking and diabetic ketoacidosis is insufficient.
My ideal for a medical article would be a well researched, well referenced, scientific language, readable and state-of-the-art body of information.
User:Kpjas 06:53, 24 Sep 2003 (UTC) == Cure for Type I Diabetes == Something that seems to be not well known, is that there is a cure to Type I diabetes -- namely, pancreas transplant. I have had diabetes for 28 years, and two years ago I was diagnosed with chronic kidney disease, caused by the diabetes. As a result, in July of 2003, I received a double transplant: kidney and pancreas. This has effectively cured my diabetes. I take no medication to control my blood sugar (neither insulin nor oral medications used to control Type II diabetes). My blood sugar levels are consistantly good (i.e., normal). While this cure does not eliminate the cumulative damage caused by the 28 years of diabetes, it does prevent any additional damage (and perhaps give the body an opportunity to heal). Note that this transplant was not experimental, but a standard procedure, covered by insurance. I received the transplants at the University of Iowa Medical Centers. At that location, they will only consider pancreas transplants (at least to cure diabetes) for patients who already have or will simultaneously receive another transplanted organ (typically a kidney). I understand that other transplant centers have differing criteria, and some will transplant a pancreas by itself. Note that the donor for a pancreas must be a cadaver, as you only have one panceras and you need it to live. -rholton, 18 Nov 2003 :rholton: :Actually, there is another currently available (though so far only experimental) 'cure' for Type 1. A few years ago, researchers in Alberta Canada managed to transplant beta cells into about 10 Type 1 patients. Of those, 8 (if memory serves) succeeded. There had been sporadic attempts to do so for years, but immune system reactions (or something else) killed them not long after the transplant; the success rate was 0 in effect. The Alberta foks seem to have found a way around the problem. Getting it to clinical practice will not, it seems, be easy. Perhaps in a few years? Or perhaps figuring out how to get stem cells to produce beta cells (your very own new ones) might be an earlier answer. On the other hand, the politics surrounding stem cell research (at least in the US) may put a hold on that for a very long time. :ww ==Double diabetic ketoacidosis== This article has a section on diabetic ketoacidosis, but we have an entire article on it in the 'pedia. Wouldn't it be better to just link to it? We could have a sentence or two on the condition with a link to the article. Having a section in this article on it seems to be redundant. —User:Frecklefoot 14:40, 28 Jan 2004 (UTC) :F, I agree that a pointer would do the trick, but I would observe that a general article on DM is all some folks will ever see. Since DKA is a large and ominous looming bit for diabetics, it should be mentioned here. The details of the biochemistry (even in outline) might not need to be here, but the tricky business with absence of carbohydrate triggering inhibition of fat processing and so to DKA probably needs to be said in an era of Atkins dieters. :Altogether, as with most subjects DM, it's not easy to determine what level of coverage is needed when. My bias is to include more than less, on the general principle that people can ignore stuff, but may need stuff that's been unsaid. User:Ww 17:10, 7 Apr 2004 (UTC) == Sports and DM? == I'm curious, does sports help Diabetic people, namely Type 2? And does the dosage of metformin depend on the obesity of the person? As in, if the type 2 diabetic loses weight, does he/she stop or at least decrease the metformin dosage? Thank you :Exercise (ie, some sports -- billiards is not a good example, nor is the usual sort of 10-pin bowling) causes an increase in glucose uptake into (particularly muscle) cells that would ordinarily require insulin. Thus, all other things being equal (and they NEVER are), a brisk 45 minute hike would decrease one's need for insulin. Blood glucose levels would decrease as though more insulin had been present. Even in Type 2s with insulin resistance. :Metformin's major effect is to inhibit release of stored glucose (kept internally as glycogen in liver cells). If done incorrectly, this release will tend to keep blood glucose levels high. In nondiabetics, this is controlled by the blood insulin level which is in turn dependent on blood glucose level which is in its turn dependent on recent ingestion of carbohydrates. Low insulin level means not much recent carb intake, so disassemble some glycogen into glucose and dump into the blood. High insulin levels mean lots of recent carb intake and so don't dump glucose into the blood, but take it in and convert it to glycogen stores for later use. In Type 2's, due to insulin resistance, insulin levels are odd and somewhat decoupled from blood glucose levels (and recent carb ingestion) and so the liver's glucose release response is often inappropriate. Metformin reduces some of this inappropriateness. :For reasons which are only now becoming dimly understood, fat tissue beyond some amount (probably a proportion of body weight, varying with individual and with gender) is connected with insulin resistance and perhaps with insulin (and other hormone) secretion. Fat tissue produces several signaling chemicals (ie, hormones more or less), and a considerable amount of entirely unexpected inflammation (ie, agitated immune system cells more or less -- think disturbed wasp nest) has also been found in fat tissue. It is clinically observed that weight reduction (ie, less fat tissue mass, amputation or wasted muscles apparently doesn't count) -- even a surprisingly small reduction in some cases -- reduces cellular insulin resistance, sometimes enough to get one off diabetic medication entirely. Even metformin. Quite what going on is obscure. :On the other (athletic) hand, many diabetics have vascular damage (heart, periphery, kidneys, eyes, ...) which make them poor candidates for some kinds of sports. American or Australian football, rugby, basketball (all that jumping and abrupt starts and stops), tennis (same as basketball w/o the jumping), ... are possibilities. And nerve damage (neuropathy of various sorts) are contraindications for some kinds of things as well. For these folks, exercise may not be a good idea. Who belongs in which group is an individual matter depending on one's 'degree' of diabetes, presence of complications, response to exercise, ... :It is critical for diabetics that their medical care folk (in many places this will be a physician, but not always) be not only adequately informed about diabetes (not always, regrettably, true) and involved with the case (rather than distantly 'consulting' now and again) and available to answer such questions in an understandable to the patient way. Diabetes mellitus is rarely a problem which can be handled sensibly on a 'set something up and forget it' basis. Things change too much, and too rapidly for this. And people vary too much. The downside if such a procedure is (wrongly) followed is high. Amputation, blindness, kidney failure, ... rates are too high to accept casually without clear thought. No one should unthinkingly do something which increases their risk of any of them, if there is any alternative at all. :Sorry there's no blanket (fits all) answer to any of your questions. It's the nature of the beast, regrettably. User:Ww 15:09, 11 Jun 2004 (UTC) ---- == Diet and exercise in type-2 DM == I am a doctor recently self-diagnosed with DM, with a pretty high reading. Having controlled my own sugar levels, I found I was able to help many patients get off their medicines and control their sugar with diet and exercise alone. Note that I refer only to Type-2 diabetics. From my experience, here are some suggestions to be tested for yourself, esp if you've been struggling unsuccessfully to control your blood sugar levels: 1. Eat less. (Assuming you are not undernourished/ emaciated). Aim for a Body mass index of 21 or 22, comprising mostly muscle! 2. Eat less carbohydrate - certainly not the American diabetes assoc recommendation of 60%!! 35-40% is good enough. 3. Ideally, eat soon after exercise, when the muscles are glycogen-depleted and most responsive to glucose. the first two hours after exercise are best. 4. You may have a cup or two of tea/coffee besides the meals. Use a sugar substitute. 5. Walk twice a day, for 30 mins and 1 hr, in any order. It doesn't have to be very brisk. 6. Build some muscle - don't need to go overboard. 7. Your target is to keep the blood sugar level within 80-100 mg/dl round the clock, for the rest of your life. It is possible. If your blood sugar is very high, fast completely a day, then go on to eggs, cheese and yogurt (all sparingly) for a day. Walk a lot in this time. Take medicines which don't put a load on your pancreas - the sulfonylureas do that, so avoid them, whatever anyone says. After 2 days, get to a normal diet, eating less as suggested above. In about a week, check again, and if normal, try cutting out the medication. Check your sugar levels again in 2 days. Get a glucometer, and check your blood sugar at intervals, esp after eating different kinds of meals to see how each is affecting you. Once you get a general idea, you can check once in 2 weeks or so. Read "Diabetes solution" by Richard Bernstein, esp if you're in bad trouble. Use the book very strictly till your sugar is and has been under control for 2 months, then you can relax a bit and try things, like eating a fruit on and off, always checking to see if you're still in control. Diabetes type-2 has been called a lifestyle disease. In a nice article by the editors of Prevention magazine, they gave it the silver-lining award: a type-2 diabetic has to do what all people should be doing anyway: eating a bit less, and exercising regularly. With that, things can be completely normal - no complications, no problems. Indeed, many people (and I include myself) find themselves much happier and focused, with a major change in their lifestyle and life. Diabetes in my opinion is a mental problem - you can handle it, or you can breakdown. Depends on you entirely (with just a little know-how and a little medical help). --User:210.18.159.10 18:59, 25 Jun 2004 (UTC)AVS == Major changes == I cut a wide swath of deletion through much of this article to eliminate repetition and information which was overly technical (to the point where it obscured the topic). I slightly reorganized the article structure as well, and paraphrased some of the longer paragraphs for brevity. I think the article should strive to be a concise description of the disorder (including statistics, limited historical information, and treatment prospects), but excruciating detail on the biochemistry and modern research should be left to other sources. User:Jeeves 09:54, 12 Jul 2004 (UTC) :good on you for tackling this page Jeeves. it was indeed repetitious and needed a lot of work. BTW are you aware your editor has a nasty habit of putting carriage returns into paragraphs? (or is that just the new db server). I'm too tired to get past the intro tonight, but i've been threatening to do some damage to this article myself so I'll go have a detailed read through the dif in the next week or so. best wishes User:Erich gasboy 11:33, 12 Jul 2004 (UTC) : I think the article should not be limited to a "concise description" but good effort on removing cruft. I think some of your removed material should be brought back (with some prodigious copyediting) as it was relevant. User:Alex.tan 16:29, 12 Jul 2004 (UTC) :: Thanks. Sorry about the spurious newlines; when I copy-pasted it from my (standalone) text editor, I naively assumed that the formatting would automagically be fixed. As for bringing back deleted material, go for it. I was mostly concerned with shortening the page, so please do re-add anything that you think should have stayed. With a bit more work I think this could be a great article. User:Jeeves 00:13, 13 Jul 2004 (UTC) ::Jeeves, I am indeed impressed that you were the first to think of using Jeeves as a username. I am imagining, of course, that it is from Bertie's adventures! Anyway, I agree with Alex.tan that you've made a valient effort at removing cruft of which there remained some despite considerable recent effort (by myself and others), but I also agree with Alex that some (much, actually, in my view) of the removed material should be brought back. I take your effort as more bold than was justified by the cruft content. ::Part of the problem, not mentioned by Alex above, is that there are many misconceptions, urban legends, and other cruft in the minds of potential readers. This is a serious problem as DM is ubiquitious, uncurable, and so expensive that it is in some sense the prototypical opportunity for con artists and quacks. There has not been noticeable restraint on their part. DM is, or at least in a great many patients it is, quite dangerous, yet without attention getting symptoms. When treated on an urban legend basis, that danger is easily made manifest in death or irrecoverable damage; without attention getting recovery from obvious symptoms, such treatment is too easily credited with benefit. This article should inform readers sufficiently thoroughly (a hard line to tread, I agree) that the biggest quackish opportunities are foreclosed. That requires, regrettably from a minimalist verbiage perspective, more than you have left. ::I have also left a comment below on structure (ie, a pointer collection article) which is likely relevant. Comment? Thoughts? User:Ww 13:50, 13 Jul 2004 (UTC) :::What parts in particular do you think should be brought back from the pre-July-12th article? I can put them back, or you can, doesn't matter to me. As for a pointer collection article, I'm not so sure that's the best way to go. Putting myself in the shoes of someone who heard something about DM and is trying to look it up in WP, I think I would want to see a) a concise summary of what the disorder is b) brief explanations of the mechanisms and complications of DM, but not obscuring the summary and c) an extensive collection of links at the end, both internal and external, for if I needed more information on a particular aspect. So I think a pointer collection would be good, but following a good description. User:Jeeves 21:44, 20 Jul 2004 (UTC) == rewrite == The subject deserves an array of articles and not a single one to be comprehensive and to make a good reading. Once again we bump into the issue of "reflecting scientific knowledge" and "being understandable for general public". I'm afraid it cannot be reconciled. This page should probably be an opening portal to other articles on diabetes describing dozens of related subjects in greater detail. (see History of Poland for example). We should direct patients and interested lay public to suitable sections/separate articles. :There already exist a panapoly of supporting articles on various aspects of DM. See the links in the text, many of which have survived the recent major rewrite for some examples. This article, before Jeeves major changes, did not reflect scientific knowledge in any detail whatsoever. It included a good deal of statement, at a very high level of abstraction from the detailed scientific knowledge -- relating to curability, the known consequences of failure to treat or manage DM, and a survey of the available medications and what they do. :As an opening portal, or alternatively, an article of first reference, an article about DM should in my view address a number of issues even if not exhaustively. Among them would be to equip the Reader with a 'high abstraction level' understanding of what DM is, of the current state of treatment, of the prospects of improved treatment, and sufficient warnings about dangers (eg, of quackery) to increase the Reader's ability to detect BS. :To the extent that this results in a longer article than some would like, I think that unavoidable. DM is complex -- physically and medically across many physiological and specialty boundaries, not well understood even now, has no straighforward palliative treatment, expensive, and epidemic. No such subject is addressable succinctly. User:Ww 14:02, 13 Jul 2004 (UTC) == Featured article ... == I believe this article has failed to make it to the featured article section a couple of times. To qualify, major changes might have to be made such as separating parts to their own articles and lots of copyediting but I believe it can be accomplished soon if we beat at it a little longer. User:Alex.tan 11:52, 13 Jul 2004 (UTC) ::Alex, I agree that we can do it if we keep trying. Sigh... User:Ww 14:03, 13 Jul 2004 (UTC) ==role of insulin== I edited this section. I hope you think it slightly clearer. I corrected an apparent error (perhaps unintended). Insulin directly stimulates glycogen synthesis, but it is glucagon that stimulates glycogen breakdown to glucose (usually insulin and glucagon levels are reciprocal, so that insulin is falling while glucagon is rising, but one does not regulate the other). In diabetes, esp type 2, liver glucose output is usually excessive, rather than reduced. Does this make sense? User:Alteripse 12:27, 21 Jul 2004 (UTC) :Alterprise, I suspect that phrase was mine, and if so, it was intentional as it reflected what I understood about the details. It was my impression that low insulin levels resulted in glycogen breakdown, without necessarily requiring glucagon. I have finessed quantitative levels as I've never come across anything numeric on this. Though I was/am less clear on the mechanism: eg, default setting of the mechanism is glycogen --> glucose, inhibited in the presence of higher insulin levels, unless glucagon is present? Liver cells must be somewhat crazy listening to so many different instructions from so many different sources. In any case, I think I remember being told that many diabetics (especially after some years) have deranged glucagon secretion/control in any case. How close was/am I? User:Ww 13:41, 21 Jul 2004 (UTC) ::You are mostly right. Glycogen breakdown requires either low insulin levels or high glucagon levels. Luckily glucagon's ability to stimulate glycogenolysis exceeds insulin's ability to inhibit it or we would not be able to reverse insulin-induced hypoglycemia with glucagon. I spent 2 years of my life doing research on the nature of insulin regulation of glycogen synthesis (via the phosphatase enzymes) but that was long ago. And yes, some people w diabetes, esp type 1, lose their ability to release glucagon in response to hypoglycemia after years (mechanism complex and sometimes reversible). I added some more on this to the glycogen article. Let me know if I need to clarify further. User:Alteripse 17:28, 21 Jul 2004 (UTC) I removed new statement ''It is the chief metabolic control signal throughout the body.'' because I can't figure out how one would defend that statement to someone who wanted to say the same thing about thyroid hormone, cortisol, or growth hormone. All have sweeping multisystem effects on many metabolic pathways, and deficiency of any or excess of any lead to major changes in metabolism. It also seems excessively vague to me. Can you think of a way to refine or clarify what you meant? I wouldn't disagree with "It is an important metabolic control signal throughout the body", but I'm not sure that adds much to what we already say. What do you think? User:Alteripse 00:55, 22 Jul 2004 (UTC) :A, I was trying for something acessible (and memorable) to the layman, not precision in medical or phsiological terms. Your qualms re thyroid, cortisol, and growth hormone are apt, just off the point I was trying for. User:Ww 13:45, 22 Jul 2004 (UTC) OK, I thought about it. How about: insulin is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction. Is that understandable? Does it say what you intended? User:Alteripse 00:59, 22 Jul 2004 (UTC) :A, I would observe that, though more accurate and certainly more precise, the extra concepts make the comment less striking/memorable for those I had in mind with my original version to which you objected. A tightrope WP articles must eternally walk, I fear. I can live with this, though I'd hope someone could come up with something both accurate AND striking (I've spent 20 minutes pondering and haven't). ==units== On another point, I propose that this and related articles be subject to a rule: BOTH units are given if one is mentioned (in re mg/dl vs mmol/l). The first is almost never used in the US, and I gather the second is nearly universal in Europe. Comments from others on this? Please? User:Ww 13:45, 22 Jul 2004 (UTC) :: From a chemistry point of view, mmol/l seems to make more sense to me as that: i) measures the concentration of molecules of the stuff and, perhaps more importantly, ii) the units for the normal range are smaller and therefore easier to remember. The standard accepted units in Singapore, Malaysia and Australia are the mmol/l units, AFAIK. User:Alex.tan *Both US and systeme international are appropriate given our readership-- and I've never heard of a third system. Many glucose meters are have the ability to switch back and forth between the two systems. I put both in the diagnosis section. User:Alteripse 13:31, 24 Jul 2004 (UTC) ==reorganization due to length== The article is approaching too long and seems a bit out of balance to me in the sense that there is great disparity between amount of info on some topics compared to others which are similarly important. I suggest we concentrate in this article on defining diabetes, describing why it is so important, ways it presents (initial signs, symptoms, problems), criteria for diagnosis, goals of treatment, brief overview of methods of treatment, very brief descriptions of major acute and chronic complications, major current research directions, and briefer history. I don't want to give any of the info up, and would move the details of the shortened material into other articles, existing or new. I would suggest separate articles on type 1 and type 2 where the etiology and epidemiology are treated in more detail, separate article on uncommon forms of diabetes (a detailed classification list would now exceed 10k), diabetic hypoglycemia, diabetic ketoacidosis, hyperosmolar coma, insulin therapy, oral diabetes drugs. I am sure each of you interested in this article can come up with some more topics that warrant their own articles.User:Alteripse 13:31, 24 Jul 2004 (UTC) : hear, hear. I agree. There should be a good, short paragraph or two in this main article with links to the various sub-articles so the whole thing is still readable. User:Alex.tan 03:26, 25 Jul 2004 (UTC) :: Agreed. I proposed it some time ago in the section #rewrite above. User:Kpjas 10:28, 25 Jul 2004 (UTC) :::Before we rush off and do so, let me propose a problem with this approach. We will, under it, end up with essentially an annotated list of pointers. If well done, this would be perhaps more complete (as noted), and would have the virtue of reducing this article's length, but would condemn the Average Reader to much link chasing and mental welding thereof to achieve an adequate overview of a messy disease. Might it be better in such cases (cryptography and attack on pearl harbor are two others I've worked on in which similar considerations, if not solutions, have arisen) to tolerate a longer than usual article? Jeeves has done essentially this in his recent massive edits, and such comments as have been left seem not to be in sympathy with them for various reasons. :::I suggest that the situation is not so readily dealt with. Comments? Thoughts? Reactions? User:Ww 19:07, 26 Jul 2004 (UTC) <-- note reversion to the margin, reset : count! The ideal solution would be a 30k overview article that is coherent narrative rather than a list of pointers for someone satisfied with an overview. I would put the pointers at the end of each section (every few paragraphs) rather than as a single long list at the end or in the middle of sentences. Is this the point you are making?User:Alteripse 19:20, 26 Jul 2004 (UTC) :Alterprise, That would indeed be a reasonable resolution to the problem I note. There are probably several others, but I'd find this one perfectly livable. I like 'coherent', 'overview', 'narrative' as the Average Reader will not be well served by incoherence (too common in longish WP articles due to multiple authors), nor by lack of an oveview (this is what AR is presumably looking for anyway in an article of first resort such as this), nor by a disjointed account (we, including AR, are built to understand such things as narrative. Making sense of fragmentary semiconflicting accounts is an acquired (and rarely so) skill held by only a few). User:Ww 14:42, 27 Jul 2004 (UTC) ===Long term complications=== I changed the title of this section, I believe it was long term risks, to long term complications, and I moved it to the section after the acute complications. I reorganized along the theme of large vs small vessel disease and I changed some of the pointers to diabetes-specific articles. I made a major rewrite of diabetic neuropathy and would appreciate any feedback or amendments. user:statkit1 1715 GMT+5, 26 July 2004 ==let's get this settled! please?== On rereading the article I have again found comments (at section ketoacidosis) implying that lipids can be so processed as to generate glucose. As I have been told in authoritative terms that this is possible only for the glycerol triglyceride backbone and not for the fatty acid chains themselves, this would appear to be a limited issue. Can someone who knows the relevant biochemistry in vivo please settle this? (Alterprise, Alextan, jdwolff, ...; hint hint). In addition, both that section and the ketoacidosis article are at minimum confusing. It is my understanding that ketone body production is normal during fat metabolism, and that they are normally dealt with without causing trouble. Only when glucose is being produced from degraded protein is there a competitive inhibition with a step in the ketone metabolism chain which allows dangerous buildup of ketone bodies, leading perhaps to acidosis. At present, ketoacidosis talks about the ratio of glucagon to insulin as being the cause ??? . Again, can we have some clarification from someone who actually knows the biochemical pathways? Neither of these two claims should be permitted to remain if they are wrong. Given the prominence of Atkins diet folk, WP ought to have its factual ducks in a row on such questions. In my view anyway. User:Ww 18:04, 14 Feb 2005 (UTC) You are correct, the article is a mess, with lots of minor errors or least confusing assertions. I am removing the section you criticized and replacing it with something simpler and more accurate. Unfortunately many other sections need the same treatment. I hope to get a "round tuit" some day. This is the old section: ''In situations where there is a severe deficiency in insulin levels, the body switches to fat metabolism, a mechanism which actually exists to protect the organs during periods of starvation, as glucose is not available to be taken up due to the lack of insulin even though blood levels of glucose are high. Ketones are produced from fats, partly because the brain can utilize ketones for energy as they can pass the blood-brain barrier. As the level of ''available'' glucose for the brain (and other organs) runs low due to the persistent low levels of insulin - despite the rising levels of serum glucose as a byproduct of the fat metabolism - more and more fats are metabolized releasing more and more ketones (acetone, acetoacetate and beta-hydroxybutyrate).'' ''Runaway accumulation of these ketone bodies results in metabolic acidosis as pH buffers in the serum are used up. At the same time, as rising levels of glucose and ketones increase the osmolality of the serum, the hyperglycemic state initially encourages the patient's kidneys to produce more urine, causing the body to lose water and electrolytes such as potassium and phosphate, leading to dehydration and hypokalemia.'' ''On presentation to hospital, the patient in DKA is typically dehydrated and hypokalemic (deficient in potassium). Urgent intravenous fluid resuscitation, potassium replacement and insulin replacement should be instituted.'' Reasons for removal: first sentence is confusing because it seems to switch from describing starvation to describing insulin deficiency (glu is not high in starvation). Avoid teleological descriptions when gracefully possible ("because the brain can utilize ketones..."). The level of glucose available to the brain does not "run low" because the brain does not depend on insulin to use glucose-- which is why unconsciousness is so rare even in moderately severe dka. More Na is lost than K or PO4. At presentation most patients are NOT hypokalemic; they are K depleted. A classic managment error of the inexperienced physician is to discount the degree of K depletion because the serum levels are initially high. Anyway, I hope no one's feelings are hurt. Discussion here please if anyone has a problem with the change.User:Alteripse 19:01, 14 Feb 2005 (UTC) :Is WP great or what?! Here I gripe and within minutes an expert steps in, fixes much (A is right about more needing to be done) and leaves a long comment. Thanks and may your karma be blessed! User:Ww 21:23, 14 Feb 2005 (UTC) ==revert and rerevert== Astanhope added a pointer to a site called goldbamboo and jfdwolff removed it by reverting to the previous version. Astanhope than reverted jfdwolff's reversion. As this is back and forth has led nowhere, I investigated the site. Gold bamboo provides some not very distinguished background information, and appears to be primarily a commercial operation, with a prominent orientation toward 'alternative therapies' for various things, including diabetics. The question is thus, is this an appropriate pointer for WP. I think I would agree with jfdwolff as it adds little to the existing references and WP ought not to be pointing to commercial sites. As for the question of the value of alternative therapy approaches, that is controversial. Because it is, I think that I would suggest that Astanhope create an article on alternative therapies for diabetes in encyclopedic NPOV form and point to it from this one. The indirect endorsement is troubling as diabetes is dangerous if not effectively treated (whatever treatment that might be) and ineffective treatments (whatever they might be) ought not to survive here. Even by indirect implication. If there is not some discussion here in the next few days, I'll (try to remember to come back and) rerevert the readdition of the pointer. Comments on this? User:Ww 18:55, 28 Feb 2005 (UTC) :I thought that the juxtaposition of "Eastern" vs. "Western" on that site was valuable. I was also annoyed that JFDWOLFF simply nixed without discussion. We must choose our battles in life and in WP. Removing a link ''sans commentaire'' that was placed with forethought struck me as a poor choice of a battle. :As for your suggestion regarding creating an article on alternative diabetes therapy, I think this is an excellent idea to add to my "list." I appreciate the feedback. --User:Astanhope 19:28, 28 Feb 2005 (UTC) ::ww said "...WP ought not to be pointing to commercial sites." I'm curious what you consider WebMD to be all about? --User:Astanhope 20:27, 28 Feb 2005 (UTC) :::Good point. The unvoiced (to me at least) consensus on WebMD appears to be that it is (at base) a general information site. That is long ago became commercial what with mergers and re-purposing and all, makes your question quite to the point. I don't know what to do about pointers to it. But now that it's been brought to the foreground of my attention, I suppose I would think removing those links would be well. But I suspect others will have thoughts on this. Comment? From anyone? User:Ww 21:26, 2 Mar 2005 (UTC) :Astanhope: by adding that link you joined a large horde of editors who frequently add external links to Wikipedia. Some of these are harmless, some are hopeless. As I try to do a lot of Wikipedia maintenance, I use the revert facility open to administrators, which is almost automatic and does indeed work ''sans commentaire''. Before taking offense, perhaps you should have realised that external links is about the last thing Wikipedia needs to be informative. Google works better for web-wide resources. :Please contribute to articles by working on the text, not by fighting turf wars over mediocre outlinked resources. User:Jfdwolff | User_talk:Jfdwolff 23:05, 28 Feb 2005 (UTC) ::I can accept that. Thanks for the honesty and feedback. --User:Astanhope 23:43, 28 Feb 2005 (UTC) ==on type 2 causing obesity== User Bollar, I am not sure your sentence belongs in the cause section. Were you implying that the this fact contradicted the previous sentence on ob causing type 2 (which is a misunderstanding of your reference), or is your sentence erroneously placed and should have been put in the complications of diabetes section? Many people with both kinds of diabetes gain wt with treatment; it is a long-recognized treatment complication that can often but not always be avoided with the usual measures (exercise and eating better). This reference looks like a pretty obscure and not very important one, but if you can provide [http://en.wikipedia.org/wiki/Wikipedia:PMID PMID] link, I will look at it. I infer from your sentence and the title that they demonstrate thermogenesis is reduced in some circumstances in type 2 and that therefore it is easier to gain wt? If so, other factors such as treatment effects are quantitatively more important and this could be explained in the complications section. I haven't removed the sentence because much of the article needs a rewrite for balance, completeness, accuracy and style, but could you clarify your sentence please or move it? thanks User:Alteripse 14:14, 15 Mar 2005 (UTC) :Hi Alteripse - no problem PMID 10643689 - I'm willing to discuss where this research is placed in the article, and I'm reluctant to add lots of text to an already long article, but let me be clear that I do believe that T2 predisposes an individual to obesity. The NIDDK has done much research on the topic with the Pima Indians and I think this article, which discusses the "thrifty gene" theory is a good synopsis: [http://diabetes.niddk.nih.gov/dm/pubs/pima/obesity/obesity.htm Obesity Associated with High Rates of Diabetes in the Pima Indians]. I think this could easily become a "chicken and egg" discussion, couldn't it? Do the Pima have diabetes because they're fat, or are they fat because they have diabetes? User:Bollar 14:53, Mar 15, 2005 (UTC) ::I'm with Alteripse, you got the chicken and egg mixed up. Obesity leads to type 2 DM, not the other way around. You may or may not be predisposed to obesity or DM genetically but the relationship between obesity and DM seems clear enough. User:Alex.tan 05:10, 20 Mar 2005 (UTC) It's an interesting topic. I agree that in some circumcstances it might be difficult to determine which comes first and the research article suggests that there is an association between poorer insulin sensitivity and reduced glucose thermogenesis. We think that poorer insulin sens is a precursor to type 2 diabetes. In children and adolescents we see the obesity precede the type 2 diabetes almost always, and it can often be reversed by wt loss. It's hard to be persuaded that the main relationship isn't the conventional wisdom of ob leads to ins resistance, insulin resistance plus genetic risk for inadequate beta cell insulin response leads to hyperglycemia, chronic hyperglycemia kills off remaining beta cells. Nothing in the Pima link contradicts this paradigm. Let's leave it and elaborate the issue when we break this into a separate type 2 article. User:Alteripse 00:06, 16 Mar 2005 (UTC) Some interesting research is published in this month's ''Diabetes.'' In short, it indicates that a variant of the ENPP1 gene is much more common in people with diabetes and helps to explain why all obese people don't develop T2 and some thin people do develop T2. It also confirms why ethnic groups develop T2 at differing rates. ''Abate, N. Diabetes, April 2005; vol 54: pp 1207-1213.'' User:Bollar 21:31, Mar 28, 2005 (UTC) :Articles of this type are published at rates of 20 a month. If it's truly a breakthrough. we'll hear about it. User:Jfdwolff | User_talk:Jfdwolff 19:34, 10 Apr 2005 (UTC) == Type 3, Type4 Diabetes == Would someone care to provide a cite on the existance of Type 3 as a bonafide category? The only thing that I can find, is an article dated the 9th of this month discussing the possible need for the lable in connection with an Insulin issue involving the brain, http://www.nutraingredients-usa.com/news/news-NG.asp?n=58592-scientists-believe-new/ Scientists believe type 3 diabetes uncovered. Unless a confirming cite can be presented, that section should probably be excised. Also, I have yet to come across anybody referring to Gestational Diabetes as Type 4 , or Type 'Anything Else'. User:coro 17:13, 27 Mar 2005 PST :I'm indeed not sure what the origin of this classification is. Perhaps searching for 3A, 3B etc may uncover something. User:Jfdwolff | User_talk:Jfdwolff 19:34, 10 Apr 2005 (UTC) I just saw this article reviewed in a journal. Calling it type 3 is not likely to catch on. We already have dozens of types of diabetes beyond 1 & 2 and even the broad definitions of 1 & 2 feel like they are in flux again (e.g., it seems harder than it did in the 1980s to decide what type many people have, and we are beginning to refer to young people having "type 1.5" or "type 1+2" or "monogenic diabetes"-- I can explain what these are if you are interested). The condition described in your reference does not even involve high blood sugars so it seems silly to refer to it as any type of diabetes. The subject of intracerebral insulin is fascinating, but it isn't diabetes. User:Alteripse 13:54, 27 May 2005 (UTC) I'm still pretty undecided on how to handle the Type 3 label, but unless someone can come with a justifying reference for the Type 4 label, I intend to get rid of it after the end of the month. And just refer to it as Gestational.--User:Coro 18:08, 14 Jun 2005 (UTC) == Declaration of St Vincent == That is a red link. Who knows more about it? Was it composed by doctors, patients, busybodies or all of the above? User:Jfdwolff | User_talk:Jfdwolff 20:03, 13 Apr 2005 (UTC) It is really unobjectionable. As I recall it dates to the late 1980s and was primarily a result of an international congress that was mainly European if I recall correctly. It outlines basic health care "rights" or least minimal desires for diabetes care (like access to blood testing supplies and insulin) in a very vague and general way. I think it was mainly diabetes doctors but couldn't swear to the absence of busybodies. I will see if I can find a live link. User:Alteripse 00:31, 14 Apr 2005 (UTC) My memory is pretty good. Here: [http://www.idf.org/home/index.cfm?node=839] == too many external links == Wikipedia is not a collection of links. Would someone like to go through the external links and prune them down to relevant links? Perhaps best link in each category? Thanks. User:Alex.tan 17:06, 27 Apr 2005 (UTC) ==Something that might be possible=== Hey this is what I want to do: Add ''Diabetis Type 1'' to the Autoimmune disease category, but only type one and it needs to say ''Daibetis Type 1'' on the Category page, also the link on the page should take you to the daibetis type 1 section of the diabetis page. Also it would be good if the category of Atoimmune diseases did not appear at the foot of the diabetis page as not all of diabetis belongs to that category. Some of this might be possible or not, anyone?, this is User:mexaguil User:219.88.206.183 11:14, 27 May 2005 (UTC) :I think the time is coming that we need to split this article anyway. The article ''as a whole'' should be about diabetic emergencies and end-organ damage, with subarticles on DMI and DMII that emphasise on pathogenesis and specific therapies (e.g. islet transplants for DMI). 13:34, 27 May 2005 (UTC) *I have been toying with a better structure and division of topics. Please look at User:Alteripse/diabetes_workshop and feel free to leave comments. Especially I would appreciate it if you would list diabetes-related titles I have missed. Thanks. User:Alteripse 14:06, 27 May 2005 (UTC) == Yet another style/content complaint... :-) == In reading through this piece tonight, I note the uneven style that others have commented on here on the talk page... but I believe that I discern another more fundamental problem. Some of the phrasing in this page leads me to wonder if parts of it have been copied wholesale from other sources ("These symptoms may also manifest in Type 2 diabetes in patients who present with frank poorly controlled diabetes."?), and what those sources might be. Now, if *I* can write "believe that I discern" on a talk page, clearly someone else can write "who present with frank poorly controlled diabetes"... but there seems a thread of that sort of uncommonly precise medical language woven through the article. Am I the only one who noticed this?
--User:Baylink 23:59, 13 Jun 2005 (UTC) :That's because this article is being edited by laypeople and MDs at the same time. When Alteripse, myself and other docs write, we may gravitate towards medical jargon. I don't think anything on this page is from other sources - it's been edited too heavily. User:Jfdwolff | User_talk:Jfdwolff 22:42, 14 Jun 2005 (UTC) == The reasoning behind including Pancreatic cancer link. == I noticed that the link for Pancreatic cancer in the diabetics article under the See Also section is removed. The reason why i included it was that a distant relative of mine was infected with pancreatic cancer and it seems he later had diabetes. I was initially confused and the doctors later told me that pancreatic cancer generally leads to diabetes and occasionally vice versa, since both diseases affect the pancreas. So I decided to add a link to a disease closely related to the organ that it affects to the article. Here are some reports and links on the matter. [http://www.cancersupportivecare.com/pancreas.html] [http://www.molecular-cancer.com/content/2/1/4] Hope this clarifies. --User:Idleguy 08:30, Jun 23, 2005 (UTC)
See other meanings of words starting from letter:
Words begining with Diabetes_Mellitus:
Diabetes_Mellitus
Diabetes_mellitus
Diabetes_mellitus
Diabetes_Mellitus_Type_1
Diabetes_mellitus_type_1
Diabetes_Mellitus_Type_2
Diabetes_mellitus_type_2
Diabetes_mellitus_type_2
Diabetes Mellitus
#REDIRECT Diabetes mellitus
Diabetes mellitus
Diabetes mellitus is a medical disorder characterized by varying or persistent hyperglycemia (elevated blood sugar levels), especially after eating. All types of diabetes mellitus share similar symptoms and complications at advanced stages. Hyperglycemia itself can lead to dehydration and ketoacidosis. Longer-term complications include cardiovascular disease (doubled risk), chronic renal failure (it is the main cause for renal dialysis), diabetic retinopathy with eventual blindness, diabetic neuropathy and eventual gangrene with risk of amputation of toes, feet, and even legs. The most important forms of diabetes are due to decreased production of insulin (diabetes mellitus type 1, the first recognized form), or insulin resistance of body tissues to insulin (diabetes mellitus type 2, the more common form). The former requires insulin injections, while the latter is generally managed with oral medication and only requires insulin if the tablets are ineffective. Patient understanding and participation is vital as blood glucose levels change continuously, while successfully keeping blood sugar within normal limits has been compellingly shown to reduce or prevent development of some of the complications of diabetes. Other risk factors that can require addressing to reduce complications are: cessation of tobacco smoking, optimizing cholesterol levels, maintaining a stable human weight, controlling arterial hypertension and engaging in regular exercise. ==Statistics== In 2004, according to the World Health Organization, more than 150 million people worldwide suffer from diabetes. Its incidence is increasing rapidly, and it is estimated that by the year 2025 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 rate is, however, expected to occur in Asia and Africa, where most of the diabetic patients will be seen by 2025. The increase in incidence of diabetes in the developing countries follows the trend of urbanisation and life style changes. 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 (see big killers). For at least 20 years, diabetes rates in North America have been increasing substantially. In 2002 there were about 18.2 million diabetics in the United States alone. 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. ==Causes and types== ===The role of insulin=== Since insulin is the principal hormone that regulates uptake of glucose into cells (primarily muscle and fat cells) from the blood, deficiency of insulin or its action plays a central role in all forms of diabetes. Most of the carbohydrates in food are rapidly digested to glucose, the principal sugar in blood. Insulin is produced by beta cells in the pancreas in response to rising levels of glucose in the blood, as occurs after a meal. Insulin makes it possible for most body tissues to remove 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 (the basic sugar unit) to glycogen for storage in liver and muscle cells. Lowered insulin levels result in the reverse conversion of glycogen to glucose when glucose levels fall -- though only in the liver not muscle tissue. Higher insulin level increase many anabolic ("building up") processes such as cell growth, cellular protein synthesis, and fat storage. Insulin is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction. If the amount of insulin produced is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or insulin resistance), or if the insulin itself is defective, glucose is not handled properly by body cells (about 2/3 require it) nor stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements. ===Type 1 diabetes mellitus=== Type 1 diabetes is most commonly diagnosed in children and adolescents, but can occur in adults as well. It is an autoimmune disorder, in which the body's own immune system attacks the beta cells in the Islets of Langerhans of the pancreas, destroying them or damaging them sufficiently to reduce insulin production. The autoimmune attack may be triggered by reaction to an infection, for example by one of the viruses of the Coxsackie virus family. A subtype of type 1 (identifiable by the presence of antibodies against beta cells) develops slowly and so is often confused with Type 2. In addition, a small proportion of type 1 cases has the hereditary condition maturity onset diabetes of the young (MODY). Some poisons (e.g. certain rat poisons) work by selectively destroying certain types of cells, including pancreatic beta cells, thus producing "artificial" type 1 diabetes. Other pancreatic problems including trauma, pancreatitis or tumors (either malignant or benign) can also lead to loss of insulin production. As of 2004, type 1 is treated with insulin injections, lifestyle adjustments, and careful monitoring of blood glucose levels using blood test kits. Insulin delivery is also available by an insulin pump, which allows the infusion of insulin 24 hours a day at preset levels, and the ability to program push doses (bolus) of insulin as needed at meal times. The treatment must be continued indefinitely. Experimental replacement of beta cells (by transplant) is being investigated in several research programs and may become clinically available in the future. About 5-10% of all North American cases of diabetes are Type 1 diabetics. The fraction of type 1 diabetics 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. Formerly, type 1 diabetes was called "childhood" or "juvenile" diabetes or "insulin dependent" diabetes. Each term is a misnomer, especially since the obesity epidemic in recent years has led to increased incidence of type 2 diabetes in children and adolescents in the USA, and insulin is used in some type 2 cases. ===Type 2 diabetes mellitus=== Type 2 diabetes is characterized by "insulin resistance" as body cells do not respond appropriately when insulin is present. This is a more complex problem than type 1, but is sometimes easier to treat, since insulin is still produced, especially in the initial years. Type 2 may go unnoticed for years in a patient before diagnosis, since the symptoms are typically milder (no ketoacidosis) and can be sporadic. However, severe complications can result from unnoticed type 2 diabetes, including renal failure, and coronary artery disease. Type 2 diabetes was formerly known by a variety of partially misleading names, including "adult-onset diabetes", "obesity-related diabetes", "insulin-resistant diabetes", or "non-insulin-dependent diabetes" (NIDDM). It may be caused by a number of diseases, such as hemochromatosis and polycystic ovary syndrome, and can also be caused by certain types of medications (e.g. long-term steroid use). About 90-95% of all North American cases of diabetes are type 2, and about 20% of the population over the age of 65 is a type 2 diabetic. The fraction of type 2 diabetics in other parts of the world varies substantially, almost certainly for environmental and lifestyle reasons. There is also a strong inheritable genetics connection in type 2 diabetes: having relatives (especially first degree) with type 2 is a considerable risk factor for developing type 2 diabetes. The majority of patients with type 2 diabetes mellitus are obesity - chronic obesity leads to increased insulin resistance that can develop into diabetes, most likely because adipose tissue is a (recently identified) source of chemical signals (hormones and cytokines). Other research shows that type 2 diabetes causes obesity.12 Type 2 is initially treated by changes in diet and through weight loss. This can restore insulin sensitivity, even when the weight lost is modest e.g. around 5 kg (10 to 15 lb). The next step, if necessary, is treatment with oral antidiabetic drugs: the sulphonylureas, metformin, or (if these are insufficient) thiazolidinediones. When these have failed, insulin therapy may be necessary to maintain normal glucose levels. ===Type 3 diabetes mellitus=== All other specific forms of diabetes, accounting for up to 5% of all diagnosed cases of diabetes, are termed Type 3: * Type 3A: genetic defect in beta cells. * Type 3B: genetically related insulin resistance. * Type 3C: diseases of the pancreas. * Type 3D: caused by hormonal defects. * Type 3E: caused by chemicals or drugs. ===Type 4 diabetes mellitus=== ''Main article: Gestational diabetes'' Type 4 or ''gestational diabetes mellitus'' appears in about 2-5% of all pregnancy. It is temporary and fully treatable, but if untreated it may cause problems with the pregnancy, including macrosomia (high birth weight) of the child. It requires careful medical supervision during the pregnancy. In addition, about 20-50% of these women go on to develop type 2 diabetes. ===Genetics=== Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by infection, stress, or environmental factors (e.g. exposure to a causative agent). There is a genetic element in the susceptibility of individuals to some of these triggers which has been traced to particular HLA genotypes (i.e. genetic "self" identifiers used 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 type 1 diabetics carry a mutation that causes maturity onset diabetes of the young (MODY). There is an even stronger inheritance pattern for Type 2 diabetes; those with type 2 ancestors or relatives have very much higher chances of developing Type 2. It is also often connected to obesity, which is found in approximately 85% of (North American) patients diagnosed with that form of the disease, so inheriting a tendency toward obesity seems also to contribute. Age is also thought to be a contributing factor, as most type 2 patients in the past were older. The exact reasons for these connections are unknown. ==Diagnosis== ===Signs and symptoms=== Type 2 diabetes almost always has a slow onset (often years), but in type 1, particularly in children, onset may be quite fast (weeks or months). Early symptoms of type 1 diabetes are often polyuria (frequent urination) and polydipsia (increased thirst, and consequent increased fluid intake). There may also be weight loss (despite normal or increased eating), increased appetite, and irreduceable fatigue. These symptoms may also manifest in Type 2 diabetes in patients who present with frank poorly controlled diabetes. Thirst develops because of osmosis effects — sufficiently high glucose (above the 'renal threshold') in the blood is excreted by the kidneys but this requires water to carry it and causes increased fluid loss, which must be replaced. The lost blood volume will be replaced from water held inside body cells, causing dehydration. Another common presenting symptom is altered vision. Prolonged high blood glucose causes changes in the shape of the lens in the eye, leading to blurred vision and, perhaps, a visit to an optometry. All unexplained quick changes in eyesight should force a fasting blood glucose test. These are now quick (less than 5 minutes total), inexpensive (materials less than US$1), and can be safely performed by almost anyone with trivial training. Especially dangerous symptoms in diabetics include the smell of acetone on the patient's breath (a sign of Diabetic ketoacidosis), Kussmaul breathing (a rapid, deep breathing), and any altered state of consciousness or arousal (hostility and mania are both possible, as is confusion and lethargy). The most dangerous form of altered consciousness is the so-called "diabetic coma" which produces unconsciousness. Early symptoms of impending diabetic coma include polyuria, nausea, vomiting and abdominal pain, with lethargy and somnolence a later development, progressing to unconsciousness and death if untreated. ===Diagnostic approach=== 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 25% of people with new type 1 diabetes have developed a degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is made in many other ways. The most common are (1) health screening, (2) detection of hyperglycemia when a doctor is investigating a complication of longstanding, unrecognized diabetes, and less commonly (3) new signs and symptoms attributable to the diabetes. # Diabetes screening is recommended for many types of people at various stages of life or with several different risk factors. The screening test varies according to circumstances and local policy and may be a random glucose, a fasting glucose and insulin, a glucose 2 hours after 75 g of glucose, or a formal glucose tolerance test. Many health care recommendations for adults recommend universal screening at age 40 or 50 years, and sometimes occasionally thereafter. Earlier screening is recommended for those with risk factors such as obesity, family history of diabetes, high risk ethnicity (Hispanic [Latin American], American Indian, African American, Pacific Island, and South Asian ancestry). # Many medical conditions are associated with a higher risk of various types of diabetes and warrant screening. A partial list includes: arterial hypertension, dyslipidemia, coronary artery disease, past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, hepatic steatosis (fatty liver), cystic fibrosis, several mitochondrial neuropathies and myopathies, myotonic dystrophy, Friedreich's ataxia, some of the inherited forms of neonatal hyperinsulinism and many others. Risk of diabetes is higher with chronic use of several medications, including high dose glucocorticoids, some chemotherapy agents (especially L-asparaginase), and some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics). # Diabetes is often detected when a person suffers a problem 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. ===Criteria for diagnosis=== Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of # two fasting plasma glucose levels above 7 mmol/l (125 mg/dl) on different days; # plasma glucose above 11.1 mmol/l (200 mg/dl) two hours after a 75 g glucose load; or # symptoms of diabetes and a random glucose above 11 mmol/l (200 mg/dl). While not used for diagnosis, an elevated glucose bound to hemoglobin, HbA1c, of 6.0% or higher (2003 revised US standard); is a screening and treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). ===Diabetic ketoacidosis and coma=== ''See also the more detailed articles diabetic ketoacidosis and diabetic coma'' Diabetic ketoacidosis (DKA) is an acute, dangerous complication and is always a ''medical emergency''. Without prompt proper treatment, diabetic ketoacidosis leads to death. DKA occurs more commonly in type 1 diabetes because the insulin deficiency is more severe, though it can occur rarely in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, the insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. When a person is known to have diabetes and is being adequately treated, DKA usually results from omission of insulin, mismanagement of acute gastroenteritis (the "flu"), or an overwhelming new health problem (e.g., bacterial infection, myocardial infarction). Insulin deficiency switches many aspects of metabolic balance in a catabolic direction. The liver becomes a net producer of glucose by way of gluconeogenesis and glycogenolysis. Fat in adipose tissue is reduced to triglycerides and fatty acids by lipolysis. Muscle is degraded to release amino acids for gluconeogenesis. The rise of fatty acid levels is accompanied by a rise of ketones (acetone, acetoacetate and beta-hydroxybutyrate). As the ketosis worsens, it produces a metabolic acidosis, with anorexia, abdominal distress, and eventually vomiting. The rising level of glucose increases the volume of urine produced by the kidneys (an ''osmolar diuresis''). The high volume of urination (polyuria) also produces increased losses of electrolytes, especially sodium, potassium, chloride, phosphate, and magnesium. Reduced fluid intake from vomiting combined with amplified urination produce dehydration. As the metabolic acidosis worsens, it induces obvious hyperventilation (termed Kussmaul respiration). On presentation to hospital, the patient in DKA is typically dehydrated and breathing both fast and deeply. Abdominal pain is common and may be severe. The level of consciousness is normal until late in the process, when obtundation may progress to coma. The dehydration can become severe enough to cause shock. Laboratory tests typically show hyperglycemia, metabolic acidosis, normal or hyperkalemia, and severe ketosis. Many other tests can be affected. At this point the patient is urgently in need of intravenous fluids. The basic principles of DKA treatment are #Rapid restoration of adequate circulation and perfusion with isotonic intravenous fluids #Gradual rehydration and restoration of depleted electrolytes (especially sodium and potassium) #Insulin to reverse the ketosis and lower the glucose #Careful monitoring to detect and treat complications Treatment usually results in full recovery, though death can result from inadequate treatment or a variety of complications. ===Hyperosmotic diabetic coma=== Hyperosmotic diabetic coma is another acute problem associated with improper management of diabetes mellitus. It has some symptoms in common with DKA, but a different cause, and requires different treatment. In anyone with very high blood glucose levels (usually considered to be above 300 mg/dl) water will be osmotically driven out of cells into the blood. The kidneys will also be "dumping" glucose into the urine, resulting in concomitant loss of water, causing an increase in blood osmolality. The osmotic effect of high glucose levels combined with the loss of water will eventually result in such a high serum osmolality that the body's cells may become directly affected as water is drawn out from them. Electrolyte imbalances are also common. This combination of changes, especially if prolonged, will result in symptoms similar to ketoacidosis, including loss of consciousness. As with DKA, urgent medical treatment is necessary. This is the diabetic coma to which type 2 diabetics are prone; it is less common in type 1 diabetics. ===Hypoglycemia=== Hypoglycemia in diabetic patients almost always arises as a result of poor management of the disease either from too much or poorly timed insulin or oral hypoglycemics or too much exercise, not enough food, or poor timing of either. If blood glucose levels are low enough, the patient may become agitated, sweaty, and have many symptoms of Autonomic nervous system activation of the autonomic nervous system - they may experience feelings similar to dread and immobilized panic. Consciousness can be altered, or even lost, in extreme cases, leading to coma and/or seizures or even death and brain damage. Experienced diabetics can often recognise the symptoms early on - all diabetics should always carry something sugary to eat or drink as these symptoms can be rapidly reduced if treated early enough. In the case of children, this can be a type of candy disliked by the patient, to prevent concerns about unnecessary use. Other ways of treating hypoglycemia include an injection of glucagon which causes the liver to convert its internal stores of glycogen to be released as glucose into the blood. Oral or intravenous dextrose can also be given. In most cases, recovery is rapid and troublefree. Longstanding hypoglycemia may require hospital admission to allow supervised recovery and adjustment of diabetic medications. ==Long-term complications== Among the major risks of the disorder are chronic problems affecting multiple organ systems which will eventually arise in patients with poor glycemic control. Many of these arise from damage to the blood vessels. These illnesses can be divided into those arising from large blood vessel diseases, macroangiopathy, and those arising from small blood vessel disease, microangiopathy. Interestingly, small vessel disease is minimized by tight blood glucose control, but large vessel disease is unaffected by tight blood glucose control. *Small vessel disease complications: **proliferative diabetic retinopathy which can lead to blindness; **peripheral diabetic neuropathy which, particularly when combined with damaged blood vessesls, can lead to foot ulcers, and possibly progressing to necrosis, infection and gangrene, sometimes requiring limb amputation, see below **diabetic nephropathy (due to microangiopathy) which can lead to renal failure *Large vessel disease complications: **ischemic heart disease caused by both large and small vessel disease **stroke **peripheral vascular disease which contributes to foot ulcers and the risk of amputation Diabetes mellitus is the most common cause of adult renal failure worldwide. It also the most common cause of amputation in the US, usually toes and feet, often as a result of gangrene, and almost always as a result of peripheral vascular disease. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US. ==Management of the disease== Diabetes is a chronic disease with no cure (except experimentally in type 1 diabetics) as of 2004. Management of this disease may include lifestyle modifications such as achieving and maintaining proper weight, diet, exercise and foot care. The most important is the hypoglycemic treatment with either oral hypoglycemics and/or insulin therapy. Nowadays, the goal for diabetics is to avoid or minimize chronic diabetic complications, as well as to avoid acute problems of hyperglycemia or hypoglycemia. Adequate control of diabetes leads to a lower risk of the complications of uncontrolled diabetes which include kidney failure (requiring dialysis or transplant), blindness, heart disease and limb amputation. Recent studies show that use of statins might be needed in primary and secondary prevention of cardiovascular complications and mortality. Ideal control of hypertension plays a pivotal role in preventing both diabetic nephropathy and cardiovascular disease. There is emerging solid evidence that full-blown diabetes mellitus type 2 can be evaded in those with only mildly impaired glucose tolerance6. Patients with type 1 diabetes mellitus require direct injection of insulin as their bodies cannot produce enough (or even any) insulin. As of 2004, there is no other clinically available form of insulin administration other than injection for patients with type 1: injection can be done by insulin pump, by jet injector, or any of several forms of hypodermic needle. There are several insulin application mechanisms under experimental development as of 2004. There have also been proposed vaccines for type I using glutamic acid decarboxylase (GAD), but these are currently not being tested by the pharmaceutical companies that have sublicensed the patents to them. For type 2 diabetics, diabetic management consists of a combination of diet (nutrition), exercise, and weight loss, in any achievable combination depending on the patient. Patients who have poor diabetic control after lifestyle modifications are typically placed on oral hypoglycemics. Some Type 2 diabetics eventually fail to respond to these and must proceed to insulin therapy. Patient education and compliance with treatment is very important in managing the disease. Improper use of medications and insulin can be very dangerous causing hypo- or hyper-glycemic episodes. Insulin therapy requires close monitoring and a great deal of patient education, as improper administration is quite dangerous. For example, when food intake is reduced, less insulin is required. A previously satisfactory dosing may be too much if less food is consumed causing a hypoglycemia reaction if not intelligently adjusted. In addition, exercise decreases insulin requirements as exercise increases glucose uptake by body cells whose glucose uptake is controlled by insulin. And vice versa. In addition, there are available several types of insulin with varying times of onset and duration of action. ===Monitoring=== Optimal management of diabetes involves patients measuring and recording their own blood glucose testing at home. By keeping a diary of their own blood glucose measurements and noting the effect of food and exercise, patients can modify their lifestyle to better control their diabetes. For patients on insulin, patient involvement is important in achieving effective dosing and timing. Relying on their own perceptions of symptoms of hyperglycemia or hypoglycemia is usually unsatisfactory as mild to moderate hyperglycemia causes no obvious symptoms in nearly all patients. Other considerations include the fact that, while food takes several hours to be digested and absorbed, insulin administration can have glucose lowering effects for as little as 2 hours or 24 hours or more (depending on the nature of the insulin preparation used and individual patient reaction). In addition, the onset and duration of the effects of oral hypoglycemic agents vary from type to type and from patient to patient. A useful test that can be done in a doctor's clinic is the measurement of blood HbA1C levels. This is the ratio of glycosylated red blood cells in relation to the total number of red blood cells. Persistent raised plasma glucose levels causes the proportion of these cells to go up. This is a test that measures the average amount of diabetic control over a period originally thought to be about 3 months (the average red blood cell lifetime), but more recently thought to be about 2 to 4 weeks. In the non-diabetic, the HbA1C level ranges from 4.0-6.4%; patients with diabetes mellitus who manage to keep their HbA1C level below 7.0% are considered to have good glycaemic control. Regular blood testing especially more so in type 1 diabetics is essential to keep a tight reign on the symptoms of the disease. There are many (at least 20+) different types of blood glucose meter available on the market today; not every meter suits all patients and it is a specific matter of choice for the patient to find a meter that they personally find comfortable to use. The principle of the devices is the virtually the same, a small blood sample is collected by the patient by self-production using a lancing device (a sterile pointed needle) the blood is usually collected at the end point to a test strip. This test strip contains various chemicals which when the blood is applied creates a small electrical charge between two contacts. This charge will vary dependent on the glucose levels within the blood and its effect on the chemicals contained within the strip. In older glucose meters, the drop of blood is placed on top of a strip. A chemical reaction occurs and the strip changes color. The meter then measures the color of the strip optically. It is this level that is measured and a result in either mg/dL (milligrams per deciliter in the USA) or mmol/L (millimoles per litre in Europe) of blood. The average normal person should have a glucose level of around 4.5 to 7.0 mmol/L (80 to 125 mg/dL). In the diabetic patient, more specifically type 2 patients, it is important to maintain good glucose control, with a before meal level of <6.1 mmol/L (<110 mg/dL) and a level two hours after the start of a meal of <7.8 mmol/L (<140 mg/dL)13. A level of <3.8 mmol/L (<70 mg/dL) is usually described as a hypoglycaemic attack. Most diabetics 'know' when they're going to 'go hypo' and usually are able to eat some food or drink something sweet to raise levels. It is important to remember though, that a patient who is hyperglycemic (high glucose) can also become temporarily hypoglycemic under certain conditions (i.e. not eating regularly, or strenuous exercise, followed by fatigue). Levels greater than 13-15 mmol/L (230-270 mg/dL) should be monitored closely and the patient is advised to seek urgent medical attention as soon as possible if this continues to rise after 2-3 tests. Hyperglycemia is not as easy to detect as hypoglycemia and usually happens over a period of days rather than hours or minutes. If left untreated this can result in diabetic coma and death. Prolonged and elevated levels of glucose in the blood, which is left unchecked and untreated will, over time, result in serious diabetic complications and sometimes even death. It is therefore highly important that a diabetic patient checks their blood levels either daily or every few days to see what levels they are achieving over a given period of time. There is also computer software for the PC which is available from blood testing manufacturers which can display results and trends over time. Type 1 patients will have to check on a more regular daily basis due to insulin therapy, which is a fine art to master. The US Food and Drug Administration has also approved a non-invasive blood glucose monitoring device [http://diabetes.niddk.nih.gov/dm/pubs/glucosemonitor/index.htm]. This allows checking blood glucose levels, while puncturing the skin as little as twice a day. Once calibrated with a blood sample, it pulls body fuilds from the skin using small electrical currents, taking six readings an hour for as long as thirteen hours. It has not proven to be reliable enough, or convenient enough to be used in lieu of conventional blood monitoring. Other non-invasive methods like radiowaves, ultrasound and energy waves are also being tested. These results are especially useful for the diabetic to present to their doctor or physician in the monitoring and control of the disease. Failure to maintain a strict regimen of testing can accelerate symptoms of the condition, and it is therefore imperative that any diabetic patient strictly monitor their glucose levels regularly. ==Public health, policy and health economics== The Declaration of St Vincent was the result of international efforts to improve the care accorded to diabetics. Doing so is important if only economically. Diabetes is enormously expensive for healthcare systems and governments. In North America, it is the largest single non-traumatic cause in adults of amputation, blindness, and dialysis, all extremely expensive events. Work in the Puget Sound area of North America (by the health organization Group Health) shows that, over its large and varied patient population, specially retaining medical information on diabetic patients, keeping it up to date, and basing their continuing care on that data reduced total healthcare costs for those patients by US$1000 per year per patient for the rest of life. Recognition of this reality drove the Hawkes Bay initiative which established such a system, and resulted in various activities throughout the world including the Black Sea Telediab project which produced elements of a distributed diabetic record and management system as an open source computer program. ==History== Although diabetes has been recognized since antiquity, and treatments were known since the Middle Ages, the elucidation of the pathogenesis of diabetes occurred mainly in the 20th century7. Until 1922, when insulin was first discovered and made clinically available, a clinical diagnosis of diabetes was an invariable death sentence, more or less quickly. Non-progressing type 2 diabetics almost certainly often went undiagnosed then; many still do. The discovery of the role of the pancreas in diabetes is generally credited to Joseph Von Mering and Oskar Minkowski, two European researchers who, in 1889, found that when they completely removed the pancreas of dogs, the dogs developed all the signs and symptoms of diabetes and died shortly afterward. In 1910, Sir Edward Albert Sharpey-Schafer of Edinburgh in Scotland suggested diabetics were deficient in a single chemical that was normally produced by the pancreas - he proposed calling this substance insulin. The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not fully clarified until 1921, when Sir Frederick Grant Banting and Charles Herbert Best repeated the work of Von Mering and Minkowski but went a step further and managed to show that they could reverse the induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs8. They went on to isolate the hormone insulin from bovine pancreases at the University of Toronto in Canada. This led to the availability of an effective treatment - insulin injections - and the first clinical patient was treated in 1922. For this, Banting ''et al'' received the Nobel Prize in Physiology or Medicine in 1923. The two researchers did not patent their discovery and insulin therapy rapidly spread around the world. The distinction between what is now known as type 1 and type 2 diabetes was made by Sir Harold Percival Himsworth in 1935; he published his findings in January 1936 in The Lancet9. Other landmark discoveries7 include: * identification of sulfonylureas in 1942 * the radioimmunoassay for insulin, as discovered by Rosalyn Yalow and Solomon Berson (gaining Yalow the 1977 Nobel Prize in Physiology or Medicine); * Reaven's introduction of the metabolic syndrome in 1988 * identification of thiazolidinediones as effective antidiabetics in the 1990s. ==Etymology== "Diabetes" is a Greek language word meaning "a passer through; a siphon". "Mellitus" comes from the Greek word "sweet". Apparently, the Greeks named it thus because the excessive amounts of urine diabetics produce (when blood glucose is too high) attracted Fly and Bee because of the glucose content. The ancient China tested for diabetes by observing whether ants were attracted to a person's urine; medieval European doctors tested for it by tasting the urine themselves, a scene occasionally depicted in Gothic reliefs. It is probably important to note that passing abnormal amounts of urine is a symptom shared by several diseases (most commonly of the kidney), and the single word diabetes is applied to many of them. The most common of them are diabetes insipidus and the subject of this article, diabetes mellitus. ==References== # Diabetes Control and Complications Trial Research Group. ''The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.'' N Engl J Med 1993;329:977-86. [http://content.nejm.org/cgi/content/full/329/14/977 Fulltext]. PMID 8366922. # World Health Organisation, Department of Noncommunicable Disease Surveillance. ''Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications.'' Geneva: WHO, 1999 ([http://whqlibdoc.who.int/hq/1999/WHO_NCD_NCS_99.2.pdf PDF]) # UK Prospective Diabetes Study Group. ''Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33).'' The Lancet 1998;352:837-53. PMID 9742976. #''Conditions in Occupational Therapy: effect on occupational performance.'' Edited by Ruth A. Hansen and Ben Atchison. Baltimore: Lippincott Williams & Williams, 2000;298-309. ISBN 0-683-30417-8. # Heart Protection Study Collaborative Group. ''MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial.'' Lancet 2003;361(9374):2005-16. PMID 12814710. # Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M. ''Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.'' N Engl J Med 2001;344:1343-50. PMID 11333990. # Patlak M. ''New Weapons to Combat an Ancient Disease: Treating Diabetes.'' [http://www.fasebj.org/cgi/content/full/16/14/1853e FASEB J 2002;16:1853E]. PMID 12468446. # Banting FG, Best CH, Collip JB, Campbell WR, Fletcher AA. ''Pancreatic extracts in the treatment of diabetes mellitus.'' Canad Med Assoc J 1922;12:141-146. # Himsworth HP. ''Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types.'' Lancet 1936;i:127-130. # Colhoun HM, Betteridge DJ, Durrington PN, Hitman GA, Neil HA, Livingstone SJ, Thomason MJ, Mackness MI, Charlton-Menys V, Fuller JH on behalf of the CARDS Investigators. ''Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicenter randomized placebo-controlled trial.'' Lancet 2004; 364: 685-96. PMID 15325833 #''MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial.'' Lancet, 2002; 360: 7-22. PMID 12114036 #S Camastra, E Bonora, S DelPrato, K Rett, M Weck, E Ferrannini. Effect of obesity and insulin resistance on resting and glucose-induced thermogenesis in man. International Journal of Obesity, 1999, Vol 23, Iss 12, pp 1307-1313. PMID 10643689 # ''The American Association of Clinical Endocrinologists Medical Guidelines for the Management of Diabetes Mellitus: The AACE System of Intensive Diabetes Self-Management—2002 Update.'' [http://www.aace.com/clin/guidelines/diabetes_2002.pdf Endocrine Practice Vol. 8 (Suppl. 1) January/February 2002]. ==See also== *list of terms associated with diabetes *list of celebrities with diabetes *diabetes in cats and dogs *Pancreatic cancer ==External links== *[http://www.nlm.nih.gov/medlineplus/diabetes.html MedlinePlus Diabetes from the U.S. National Library of Medicine] *[http://www.childrenwithdiabetes.com Children with Diabetes] *[http://my.webmd.com/content/article/56/65915.htm MyWebMD Diabetes Section] *[http://www.diabetes.ca Canadian Diabetes Association] *[http://www.jdrf.org Juvenile Diabetes Research Foundation] *[http://www.diabetes.org American Diabetes Association] *[http://www.idf.org International Diabetes Federation] *[http://www.who.int/diabetes/en/ WHO - The Diabetes Programme] *[http://www.healthatoz.com/healthatoz/Atoz/dc/caz/diab/dia2/diabetescfindex2.html Health A to Z Diabetes Type 2 Section] *[http://www.hc-sc.gc.ca/pphb-dgspsp/ccdpc-cpcmc/diabetes-diabete/english/risk Health Canada Diabetes Type 2 Risk Evaluation] *[http://www.cdc.gov/diabetes Center for Disease Control Diabetes Section] *[http://www.idsoc.org The Immunology of Diabetes Society] *[http://www.uchsc.edu/misc/diabetes/books.html Informative Book on Basic and Clinical information on Type 1 Diabetes from Barbara Center for Childhood Diabetes] *[http://www.diabetes.diabetesjournals.org Journals on Basic and clinical research in Diabetes cure and care] *[http://diabetes.niddk.nih.gov/dm/pubs/riskfortype2/ Diabetes Type 2 Risks] Diabetes Nutrition fa:مرض قند ms:Kencing manis
Diabetes mellitus
==Foot and lower limbs need more attention== I'm really not a medical person so I'm reluctant to actually contribute to the article - but I work on creating software health interventions to help people perform self care regarding diabetes related pedal complications. This is also one of the primary concerns of Diabetes Australia this year. The prevalence of foot complication in this group is between 3-6% (in Australia at least). Common pedal complications include; foot ulcers, infections, cellulitis, peripheral vascular disease, neuropathy, fractures and the need for amputation. Lower limb complications in people with diabetes have been estimated to cost the health care system about $300 million per year in Australia. So it's a big issue - but only briefly mentioned in the article. User:Melody This page has been listed on the Wikipedia:pages needing attention list as "not up to the standards of scientific knowledge". Can you please let us know what is wrong with it, so we can correct it? -- User:Karada 22:23, 23 Sep 2003 (UTC) :several things: * reorganization of information to make more sense, removing duplicate information * verifying to ensure correctness of data * general polishing up of grammar, style, structure. I guess there might be others suggestions too, but these should do for starters. --User:Alex.tan 06:12, 24 Sep 2003 (UTC) ==Objections to diabetes mellitus article== From my (User:Karada's) talk page: Hello Karada,
You asked about diabetes mellitus article and my objections to its content.
First, it is of patchy quality. There are passages or section that are quite acceptable and other that need major rewrite.
Second, its style is inconsistent. Sometimes it uses scintific language and nomenclature and sometimes it is written in badly conceived "for patients" style. (I once proposed to make corresponding "Patient information" pages in this case "Patient information on Diabetes mellitus" linked to the scientific article Diabetes mellitus)
Third, see sections Diabetes mellitus#Diabetes treatment. Current standards - St Vincent declaration.
Presentation is also lacking and diabetic ketoacidosis is insufficient.
My ideal for a medical article would be a well researched, well referenced, scientific language, readable and state-of-the-art body of information.
User:Kpjas 06:53, 24 Sep 2003 (UTC) == Cure for Type I Diabetes == Something that seems to be not well known, is that there is a cure to Type I diabetes -- namely, pancreas transplant. I have had diabetes for 28 years, and two years ago I was diagnosed with chronic kidney disease, caused by the diabetes. As a result, in July of 2003, I received a double transplant: kidney and pancreas. This has effectively cured my diabetes. I take no medication to control my blood sugar (neither insulin nor oral medications used to control Type II diabetes). My blood sugar levels are consistantly good (i.e., normal). While this cure does not eliminate the cumulative damage caused by the 28 years of diabetes, it does prevent any additional damage (and perhaps give the body an opportunity to heal). Note that this transplant was not experimental, but a standard procedure, covered by insurance. I received the transplants at the University of Iowa Medical Centers. At that location, they will only consider pancreas transplants (at least to cure diabetes) for patients who already have or will simultaneously receive another transplanted organ (typically a kidney). I understand that other transplant centers have differing criteria, and some will transplant a pancreas by itself. Note that the donor for a pancreas must be a cadaver, as you only have one panceras and you need it to live. -rholton, 18 Nov 2003 :rholton: :Actually, there is another currently available (though so far only experimental) 'cure' for Type 1. A few years ago, researchers in Alberta Canada managed to transplant beta cells into about 10 Type 1 patients. Of those, 8 (if memory serves) succeeded. There had been sporadic attempts to do so for years, but immune system reactions (or something else) killed them not long after the transplant; the success rate was 0 in effect. The Alberta foks seem to have found a way around the problem. Getting it to clinical practice will not, it seems, be easy. Perhaps in a few years? Or perhaps figuring out how to get stem cells to produce beta cells (your very own new ones) might be an earlier answer. On the other hand, the politics surrounding stem cell research (at least in the US) may put a hold on that for a very long time. :ww ==Double diabetic ketoacidosis== This article has a section on diabetic ketoacidosis, but we have an entire article on it in the 'pedia. Wouldn't it be better to just link to it? We could have a sentence or two on the condition with a link to the article. Having a section in this article on it seems to be redundant. —User:Frecklefoot 14:40, 28 Jan 2004 (UTC) :F, I agree that a pointer would do the trick, but I would observe that a general article on DM is all some folks will ever see. Since DKA is a large and ominous looming bit for diabetics, it should be mentioned here. The details of the biochemistry (even in outline) might not need to be here, but the tricky business with absence of carbohydrate triggering inhibition of fat processing and so to DKA probably needs to be said in an era of Atkins dieters. :Altogether, as with most subjects DM, it's not easy to determine what level of coverage is needed when. My bias is to include more than less, on the general principle that people can ignore stuff, but may need stuff that's been unsaid. User:Ww 17:10, 7 Apr 2004 (UTC) == Sports and DM? == I'm curious, does sports help Diabetic people, namely Type 2? And does the dosage of metformin depend on the obesity of the person? As in, if the type 2 diabetic loses weight, does he/she stop or at least decrease the metformin dosage? Thank you :Exercise (ie, some sports -- billiards is not a good example, nor is the usual sort of 10-pin bowling) causes an increase in glucose uptake into (particularly muscle) cells that would ordinarily require insulin. Thus, all other things being equal (and they NEVER are), a brisk 45 minute hike would decrease one's need for insulin. Blood glucose levels would decrease as though more insulin had been present. Even in Type 2s with insulin resistance. :Metformin's major effect is to inhibit release of stored glucose (kept internally as glycogen in liver cells). If done incorrectly, this release will tend to keep blood glucose levels high. In nondiabetics, this is controlled by the blood insulin level which is in turn dependent on blood glucose level which is in its turn dependent on recent ingestion of carbohydrates. Low insulin level means not much recent carb intake, so disassemble some glycogen into glucose and dump into the blood. High insulin levels mean lots of recent carb intake and so don't dump glucose into the blood, but take it in and convert it to glycogen stores for later use. In Type 2's, due to insulin resistance, insulin levels are odd and somewhat decoupled from blood glucose levels (and recent carb ingestion) and so the liver's glucose release response is often inappropriate. Metformin reduces some of this inappropriateness. :For reasons which are only now becoming dimly understood, fat tissue beyond some amount (probably a proportion of body weight, varying with individual and with gender) is connected with insulin resistance and perhaps with insulin (and other hormone) secretion. Fat tissue produces several signaling chemicals (ie, hormones more or less), and a considerable amount of entirely unexpected inflammation (ie, agitated immune system cells more or less -- think disturbed wasp nest) has also been found in fat tissue. It is clinically observed that weight reduction (ie, less fat tissue mass, amputation or wasted muscles apparently doesn't count) -- even a surprisingly small reduction in some cases -- reduces cellular insulin resistance, sometimes enough to get one off diabetic medication entirely. Even metformin. Quite what going on is obscure. :On the other (athletic) hand, many diabetics have vascular damage (heart, periphery, kidneys, eyes, ...) which make them poor candidates for some kinds of sports. American or Australian football, rugby, basketball (all that jumping and abrupt starts and stops), tennis (same as basketball w/o the jumping), ... are possibilities. And nerve damage (neuropathy of various sorts) are contraindications for some kinds of things as well. For these folks, exercise may not be a good idea. Who belongs in which group is an individual matter depending on one's 'degree' of diabetes, presence of complications, response to exercise, ... :It is critical for diabetics that their medical care folk (in many places this will be a physician, but not always) be not only adequately informed about diabetes (not always, regrettably, true) and involved with the case (rather than distantly 'consulting' now and again) and available to answer such questions in an understandable to the patient way. Diabetes mellitus is rarely a problem which can be handled sensibly on a 'set something up and forget it' basis. Things change too much, and too rapidly for this. And people vary too much. The downside if such a procedure is (wrongly) followed is high. Amputation, blindness, kidney failure, ... rates are too high to accept casually without clear thought. No one should unthinkingly do something which increases their risk of any of them, if there is any alternative at all. :Sorry there's no blanket (fits all) answer to any of your questions. It's the nature of the beast, regrettably. User:Ww 15:09, 11 Jun 2004 (UTC) ---- == Diet and exercise in type-2 DM == I am a doctor recently self-diagnosed with DM, with a pretty high reading. Having controlled my own sugar levels, I found I was able to help many patients get off their medicines and control their sugar with diet and exercise alone. Note that I refer only to Type-2 diabetics. From my experience, here are some suggestions to be tested for yourself, esp if you've been struggling unsuccessfully to control your blood sugar levels: 1. Eat less. (Assuming you are not undernourished/ emaciated). Aim for a Body mass index of 21 or 22, comprising mostly muscle! 2. Eat less carbohydrate - certainly not the American diabetes assoc recommendation of 60%!! 35-40% is good enough. 3. Ideally, eat soon after exercise, when the muscles are glycogen-depleted and most responsive to glucose. the first two hours after exercise are best. 4. You may have a cup or two of tea/coffee besides the meals. Use a sugar substitute. 5. Walk twice a day, for 30 mins and 1 hr, in any order. It doesn't have to be very brisk. 6. Build some muscle - don't need to go overboard. 7. Your target is to keep the blood sugar level within 80-100 mg/dl round the clock, for the rest of your life. It is possible. If your blood sugar is very high, fast completely a day, then go on to eggs, cheese and yogurt (all sparingly) for a day. Walk a lot in this time. Take medicines which don't put a load on your pancreas - the sulfonylureas do that, so avoid them, whatever anyone says. After 2 days, get to a normal diet, eating less as suggested above. In about a week, check again, and if normal, try cutting out the medication. Check your sugar levels again in 2 days. Get a glucometer, and check your blood sugar at intervals, esp after eating different kinds of meals to see how each is affecting you. Once you get a general idea, you can check once in 2 weeks or so. Read "Diabetes solution" by Richard Bernstein, esp if you're in bad trouble. Use the book very strictly till your sugar is and has been under control for 2 months, then you can relax a bit and try things, like eating a fruit on and off, always checking to see if you're still in control. Diabetes type-2 has been called a lifestyle disease. In a nice article by the editors of Prevention magazine, they gave it the silver-lining award: a type-2 diabetic has to do what all people should be doing anyway: eating a bit less, and exercising regularly. With that, things can be completely normal - no complications, no problems. Indeed, many people (and I include myself) find themselves much happier and focused, with a major change in their lifestyle and life. Diabetes in my opinion is a mental problem - you can handle it, or you can breakdown. Depends on you entirely (with just a little know-how and a little medical help). --User:210.18.159.10 18:59, 25 Jun 2004 (UTC)AVS == Major changes == I cut a wide swath of deletion through much of this article to eliminate repetition and information which was overly technical (to the point where it obscured the topic). I slightly reorganized the article structure as well, and paraphrased some of the longer paragraphs for brevity. I think the article should strive to be a concise description of the disorder (including statistics, limited historical information, and treatment prospects), but excruciating detail on the biochemistry and modern research should be left to other sources. User:Jeeves 09:54, 12 Jul 2004 (UTC) :good on you for tackling this page Jeeves. it was indeed repetitious and needed a lot of work. BTW are you aware your editor has a nasty habit of putting carriage returns into paragraphs? (or is that just the new db server). I'm too tired to get past the intro tonight, but i've been threatening to do some damage to this article myself so I'll go have a detailed read through the dif in the next week or so. best wishes User:Erich gasboy 11:33, 12 Jul 2004 (UTC) : I think the article should not be limited to a "concise description" but good effort on removing cruft. I think some of your removed material should be brought back (with some prodigious copyediting) as it was relevant. User:Alex.tan 16:29, 12 Jul 2004 (UTC) :: Thanks. Sorry about the spurious newlines; when I copy-pasted it from my (standalone) text editor, I naively assumed that the formatting would automagically be fixed. As for bringing back deleted material, go for it. I was mostly concerned with shortening the page, so please do re-add anything that you think should have stayed. With a bit more work I think this could be a great article. User:Jeeves 00:13, 13 Jul 2004 (UTC) ::Jeeves, I am indeed impressed that you were the first to think of using Jeeves as a username. I am imagining, of course, that it is from Bertie's adventures! Anyway, I agree with Alex.tan that you've made a valient effort at removing cruft of which there remained some despite considerable recent effort (by myself and others), but I also agree with Alex that some (much, actually, in my view) of the removed material should be brought back. I take your effort as more bold than was justified by the cruft content. ::Part of the problem, not mentioned by Alex above, is that there are many misconceptions, urban legends, and other cruft in the minds of potential readers. This is a serious problem as DM is ubiquitious, uncurable, and so expensive that it is in some sense the prototypical opportunity for con artists and quacks. There has not been noticeable restraint on their part. DM is, or at least in a great many patients it is, quite dangerous, yet without attention getting symptoms. When treated on an urban legend basis, that danger is easily made manifest in death or irrecoverable damage; without attention getting recovery from obvious symptoms, such treatment is too easily credited with benefit. This article should inform readers sufficiently thoroughly (a hard line to tread, I agree) that the biggest quackish opportunities are foreclosed. That requires, regrettably from a minimalist verbiage perspective, more than you have left. ::I have also left a comment below on structure (ie, a pointer collection article) which is likely relevant. Comment? Thoughts? User:Ww 13:50, 13 Jul 2004 (UTC) :::What parts in particular do you think should be brought back from the pre-July-12th article? I can put them back, or you can, doesn't matter to me. As for a pointer collection article, I'm not so sure that's the best way to go. Putting myself in the shoes of someone who heard something about DM and is trying to look it up in WP, I think I would want to see a) a concise summary of what the disorder is b) brief explanations of the mechanisms and complications of DM, but not obscuring the summary and c) an extensive collection of links at the end, both internal and external, for if I needed more information on a particular aspect. So I think a pointer collection would be good, but following a good description. User:Jeeves 21:44, 20 Jul 2004 (UTC) == rewrite == The subject deserves an array of articles and not a single one to be comprehensive and to make a good reading. Once again we bump into the issue of "reflecting scientific knowledge" and "being understandable for general public". I'm afraid it cannot be reconciled. This page should probably be an opening portal to other articles on diabetes describing dozens of related subjects in greater detail. (see History of Poland for example). We should direct patients and interested lay public to suitable sections/separate articles. :There already exist a panapoly of supporting articles on various aspects of DM. See the links in the text, many of which have survived the recent major rewrite for some examples. This article, before Jeeves major changes, did not reflect scientific knowledge in any detail whatsoever. It included a good deal of statement, at a very high level of abstraction from the detailed scientific knowledge -- relating to curability, the known consequences of failure to treat or manage DM, and a survey of the available medications and what they do. :As an opening portal, or alternatively, an article of first reference, an article about DM should in my view address a number of issues even if not exhaustively. Among them would be to equip the Reader with a 'high abstraction level' understanding of what DM is, of the current state of treatment, of the prospects of improved treatment, and sufficient warnings about dangers (eg, of quackery) to increase the Reader's ability to detect BS. :To the extent that this results in a longer article than some would like, I think that unavoidable. DM is complex -- physically and medically across many physiological and specialty boundaries, not well understood even now, has no straighforward palliative treatment, expensive, and epidemic. No such subject is addressable succinctly. User:Ww 14:02, 13 Jul 2004 (UTC) == Featured article ... == I believe this article has failed to make it to the featured article section a couple of times. To qualify, major changes might have to be made such as separating parts to their own articles and lots of copyediting but I believe it can be accomplished soon if we beat at it a little longer. User:Alex.tan 11:52, 13 Jul 2004 (UTC) ::Alex, I agree that we can do it if we keep trying. Sigh... User:Ww 14:03, 13 Jul 2004 (UTC) ==role of insulin== I edited this section. I hope you think it slightly clearer. I corrected an apparent error (perhaps unintended). Insulin directly stimulates glycogen synthesis, but it is glucagon that stimulates glycogen breakdown to glucose (usually insulin and glucagon levels are reciprocal, so that insulin is falling while glucagon is rising, but one does not regulate the other). In diabetes, esp type 2, liver glucose output is usually excessive, rather than reduced. Does this make sense? User:Alteripse 12:27, 21 Jul 2004 (UTC) :Alterprise, I suspect that phrase was mine, and if so, it was intentional as it reflected what I understood about the details. It was my impression that low insulin levels resulted in glycogen breakdown, without necessarily requiring glucagon. I have finessed quantitative levels as I've never come across anything numeric on this. Though I was/am less clear on the mechanism: eg, default setting of the mechanism is glycogen --> glucose, inhibited in the presence of higher insulin levels, unless glucagon is present? Liver cells must be somewhat crazy listening to so many different instructions from so many different sources. In any case, I think I remember being told that many diabetics (especially after some years) have deranged glucagon secretion/control in any case. How close was/am I? User:Ww 13:41, 21 Jul 2004 (UTC) ::You are mostly right. Glycogen breakdown requires either low insulin levels or high glucagon levels. Luckily glucagon's ability to stimulate glycogenolysis exceeds insulin's ability to inhibit it or we would not be able to reverse insulin-induced hypoglycemia with glucagon. I spent 2 years of my life doing research on the nature of insulin regulation of glycogen synthesis (via the phosphatase enzymes) but that was long ago. And yes, some people w diabetes, esp type 1, lose their ability to release glucagon in response to hypoglycemia after years (mechanism complex and sometimes reversible). I added some more on this to the glycogen article. Let me know if I need to clarify further. User:Alteripse 17:28, 21 Jul 2004 (UTC) I removed new statement ''It is the chief metabolic control signal throughout the body.'' because I can't figure out how one would defend that statement to someone who wanted to say the same thing about thyroid hormone, cortisol, or growth hormone. All have sweeping multisystem effects on many metabolic pathways, and deficiency of any or excess of any lead to major changes in metabolism. It also seems excessively vague to me. Can you think of a way to refine or clarify what you meant? I wouldn't disagree with "It is an important metabolic control signal throughout the body", but I'm not sure that adds much to what we already say. What do you think? User:Alteripse 00:55, 22 Jul 2004 (UTC) :A, I was trying for something acessible (and memorable) to the layman, not precision in medical or phsiological terms. Your qualms re thyroid, cortisol, and growth hormone are apt, just off the point I was trying for. User:Ww 13:45, 22 Jul 2004 (UTC) OK, I thought about it. How about: insulin is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction. Is that understandable? Does it say what you intended? User:Alteripse 00:59, 22 Jul 2004 (UTC) :A, I would observe that, though more accurate and certainly more precise, the extra concepts make the comment less striking/memorable for those I had in mind with my original version to which you objected. A tightrope WP articles must eternally walk, I fear. I can live with this, though I'd hope someone could come up with something both accurate AND striking (I've spent 20 minutes pondering and haven't). ==units== On another point, I propose that this and related articles be subject to a rule: BOTH units are given if one is mentioned (in re mg/dl vs mmol/l). The first is almost never used in the US, and I gather the second is nearly universal in Europe. Comments from others on this? Please? User:Ww 13:45, 22 Jul 2004 (UTC) :: From a chemistry point of view, mmol/l seems to make more sense to me as that: i) measures the concentration of molecules of the stuff and, perhaps more importantly, ii) the units for the normal range are smaller and therefore easier to remember. The standard accepted units in Singapore, Malaysia and Australia are the mmol/l units, AFAIK. User:Alex.tan *Both US and systeme international are appropriate given our readership-- and I've never heard of a third system. Many glucose meters are have the ability to switch back and forth between the two systems. I put both in the diagnosis section. User:Alteripse 13:31, 24 Jul 2004 (UTC) ==reorganization due to length== The article is approaching too long and seems a bit out of balance to me in the sense that there is great disparity between amount of info on some topics compared to others which are similarly important. I suggest we concentrate in this article on defining diabetes, describing why it is so important, ways it presents (initial signs, symptoms, problems), criteria for diagnosis, goals of treatment, brief overview of methods of treatment, very brief descriptions of major acute and chronic complications, major current research directions, and briefer history. I don't want to give any of the info up, and would move the details of the shortened material into other articles, existing or new. I would suggest separate articles on type 1 and type 2 where the etiology and epidemiology are treated in more detail, separate article on uncommon forms of diabetes (a detailed classification list would now exceed 10k), diabetic hypoglycemia, diabetic ketoacidosis, hyperosmolar coma, insulin therapy, oral diabetes drugs. I am sure each of you interested in this article can come up with some more topics that warrant their own articles.User:Alteripse 13:31, 24 Jul 2004 (UTC) : hear, hear. I agree. There should be a good, short paragraph or two in this main article with links to the various sub-articles so the whole thing is still readable. User:Alex.tan 03:26, 25 Jul 2004 (UTC) :: Agreed. I proposed it some time ago in the section #rewrite above. User:Kpjas 10:28, 25 Jul 2004 (UTC) :::Before we rush off and do so, let me propose a problem with this approach. We will, under it, end up with essentially an annotated list of pointers. If well done, this would be perhaps more complete (as noted), and would have the virtue of reducing this article's length, but would condemn the Average Reader to much link chasing and mental welding thereof to achieve an adequate overview of a messy disease. Might it be better in such cases (cryptography and attack on pearl harbor are two others I've worked on in which similar considerations, if not solutions, have arisen) to tolerate a longer than usual article? Jeeves has done essentially this in his recent massive edits, and such comments as have been left seem not to be in sympathy with them for various reasons. :::I suggest that the situation is not so readily dealt with. Comments? Thoughts? Reactions? User:Ww 19:07, 26 Jul 2004 (UTC) <-- note reversion to the margin, reset : count! The ideal solution would be a 30k overview article that is coherent narrative rather than a list of pointers for someone satisfied with an overview. I would put the pointers at the end of each section (every few paragraphs) rather than as a single long list at the end or in the middle of sentences. Is this the point you are making?User:Alteripse 19:20, 26 Jul 2004 (UTC) :Alterprise, That would indeed be a reasonable resolution to the problem I note. There are probably several others, but I'd find this one perfectly livable. I like 'coherent', 'overview', 'narrative' as the Average Reader will not be well served by incoherence (too common in longish WP articles due to multiple authors), nor by lack of an oveview (this is what AR is presumably looking for anyway in an article of first resort such as this), nor by a disjointed account (we, including AR, are built to understand such things as narrative. Making sense of fragmentary semiconflicting accounts is an acquired (and rarely so) skill held by only a few). User:Ww 14:42, 27 Jul 2004 (UTC) ===Long term complications=== I changed the title of this section, I believe it was long term risks, to long term complications, and I moved it to the section after the acute complications. I reorganized along the theme of large vs small vessel disease and I changed some of the pointers to diabetes-specific articles. I made a major rewrite of diabetic neuropathy and would appreciate any feedback or amendments. user:statkit1 1715 GMT+5, 26 July 2004 ==let's get this settled! please?== On rereading the article I have again found comments (at section ketoacidosis) implying that lipids can be so processed as to generate glucose. As I have been told in authoritative terms that this is possible only for the glycerol triglyceride backbone and not for the fatty acid chains themselves, this would appear to be a limited issue. Can someone who knows the relevant biochemistry in vivo please settle this? (Alterprise, Alextan, jdwolff, ...; hint hint). In addition, both that section and the ketoacidosis article are at minimum confusing. It is my understanding that ketone body production is normal during fat metabolism, and that they are normally dealt with without causing trouble. Only when glucose is being produced from degraded protein is there a competitive inhibition with a step in the ketone metabolism chain which allows dangerous buildup of ketone bodies, leading perhaps to acidosis. At present, ketoacidosis talks about the ratio of glucagon to insulin as being the cause ??? . Again, can we have some clarification from someone who actually knows the biochemical pathways? Neither of these two claims should be permitted to remain if they are wrong. Given the prominence of Atkins diet folk, WP ought to have its factual ducks in a row on such questions. In my view anyway. User:Ww 18:04, 14 Feb 2005 (UTC) You are correct, the article is a mess, with lots of minor errors or least confusing assertions. I am removing the section you criticized and replacing it with something simpler and more accurate. Unfortunately many other sections need the same treatment. I hope to get a "round tuit" some day. This is the old section: ''In situations where there is a severe deficiency in insulin levels, the body switches to fat metabolism, a mechanism which actually exists to protect the organs during periods of starvation, as glucose is not available to be taken up due to the lack of insulin even though blood levels of glucose are high. Ketones are produced from fats, partly because the brain can utilize ketones for energy as they can pass the blood-brain barrier. As the level of ''available'' glucose for the brain (and other organs) runs low due to the persistent low levels of insulin - despite the rising levels of serum glucose as a byproduct of the fat metabolism - more and more fats are metabolized releasing more and more ketones (acetone, acetoacetate and beta-hydroxybutyrate).'' ''Runaway accumulation of these ketone bodies results in metabolic acidosis as pH buffers in the serum are used up. At the same time, as rising levels of glucose and ketones increase the osmolality of the serum, the hyperglycemic state initially encourages the patient's kidneys to produce more urine, causing the body to lose water and electrolytes such as potassium and phosphate, leading to dehydration and hypokalemia.'' ''On presentation to hospital, the patient in DKA is typically dehydrated and hypokalemic (deficient in potassium). Urgent intravenous fluid resuscitation, potassium replacement and insulin replacement should be instituted.'' Reasons for removal: first sentence is confusing because it seems to switch from describing starvation to describing insulin deficiency (glu is not high in starvation). Avoid teleological descriptions when gracefully possible ("because the brain can utilize ketones..."). The level of glucose available to the brain does not "run low" because the brain does not depend on insulin to use glucose-- which is why unconsciousness is so rare even in moderately severe dka. More Na is lost than K or PO4. At presentation most patients are NOT hypokalemic; they are K depleted. A classic managment error of the inexperienced physician is to discount the degree of K depletion because the serum levels are initially high. Anyway, I hope no one's feelings are hurt. Discussion here please if anyone has a problem with the change.User:Alteripse 19:01, 14 Feb 2005 (UTC) :Is WP great or what?! Here I gripe and within minutes an expert steps in, fixes much (A is right about more needing to be done) and leaves a long comment. Thanks and may your karma be blessed! User:Ww 21:23, 14 Feb 2005 (UTC) ==revert and rerevert== Astanhope added a pointer to a site called goldbamboo and jfdwolff removed it by reverting to the previous version. Astanhope than reverted jfdwolff's reversion. As this is back and forth has led nowhere, I investigated the site. Gold bamboo provides some not very distinguished background information, and appears to be primarily a commercial operation, with a prominent orientation toward 'alternative therapies' for various things, including diabetics. The question is thus, is this an appropriate pointer for WP. I think I would agree with jfdwolff as it adds little to the existing references and WP ought not to be pointing to commercial sites. As for the question of the value of alternative therapy approaches, that is controversial. Because it is, I think that I would suggest that Astanhope create an article on alternative therapies for diabetes in encyclopedic NPOV form and point to it from this one. The indirect endorsement is troubling as diabetes is dangerous if not effectively treated (whatever treatment that might be) and ineffective treatments (whatever they might be) ought not to survive here. Even by indirect implication. If there is not some discussion here in the next few days, I'll (try to remember to come back and) rerevert the readdition of the pointer. Comments on this? User:Ww 18:55, 28 Feb 2005 (UTC) :I thought that the juxtaposition of "Eastern" vs. "Western" on that site was valuable. I was also annoyed that JFDWOLFF simply nixed without discussion. We must choose our battles in life and in WP. Removing a link ''sans commentaire'' that was placed with forethought struck me as a poor choice of a battle. :As for your suggestion regarding creating an article on alternative diabetes therapy, I think this is an excellent idea to add to my "list." I appreciate the feedback. --User:Astanhope 19:28, 28 Feb 2005 (UTC) ::ww said "...WP ought not to be pointing to commercial sites." I'm curious what you consider WebMD to be all about? --User:Astanhope 20:27, 28 Feb 2005 (UTC) :::Good point. The unvoiced (to me at least) consensus on WebMD appears to be that it is (at base) a general information site. That is long ago became commercial what with mergers and re-purposing and all, makes your question quite to the point. I don't know what to do about pointers to it. But now that it's been brought to the foreground of my attention, I suppose I would think removing those links would be well. But I suspect others will have thoughts on this. Comment? From anyone? User:Ww 21:26, 2 Mar 2005 (UTC) :Astanhope: by adding that link you joined a large horde of editors who frequently add external links to Wikipedia. Some of these are harmless, some are hopeless. As I try to do a lot of Wikipedia maintenance, I use the revert facility open to administrators, which is almost automatic and does indeed work ''sans commentaire''. Before taking offense, perhaps you should have realised that external links is about the last thing Wikipedia needs to be informative. Google works better for web-wide resources. :Please contribute to articles by working on the text, not by fighting turf wars over mediocre outlinked resources. User:Jfdwolff | User_talk:Jfdwolff 23:05, 28 Feb 2005 (UTC) ::I can accept that. Thanks for the honesty and feedback. --User:Astanhope 23:43, 28 Feb 2005 (UTC) ==on type 2 causing obesity== User Bollar, I am not sure your sentence belongs in the cause section. Were you implying that the this fact contradicted the previous sentence on ob causing type 2 (which is a misunderstanding of your reference), or is your sentence erroneously placed and should have been put in the complications of diabetes section? Many people with both kinds of diabetes gain wt with treatment; it is a long-recognized treatment complication that can often but not always be avoided with the usual measures (exercise and eating better). This reference looks like a pretty obscure and not very important one, but if you can provide [http://en.wikipedia.org/wiki/Wikipedia:PMID PMID] link, I will look at it. I infer from your sentence and the title that they demonstrate thermogenesis is reduced in some circumstances in type 2 and that therefore it is easier to gain wt? If so, other factors such as treatment effects are quantitatively more important and this could be explained in the complications section. I haven't removed the sentence because much of the article needs a rewrite for balance, completeness, accuracy and style, but could you clarify your sentence please or move it? thanks User:Alteripse 14:14, 15 Mar 2005 (UTC) :Hi Alteripse - no problem PMID 10643689 - I'm willing to discuss where this research is placed in the article, and I'm reluctant to add lots of text to an already long article, but let me be clear that I do believe that T2 predisposes an individual to obesity. The NIDDK has done much research on the topic with the Pima Indians and I think this article, which discusses the "thrifty gene" theory is a good synopsis: [http://diabetes.niddk.nih.gov/dm/pubs/pima/obesity/obesity.htm Obesity Associated with High Rates of Diabetes in the Pima Indians]. I think this could easily become a "chicken and egg" discussion, couldn't it? Do the Pima have diabetes because they're fat, or are they fat because they have diabetes? User:Bollar 14:53, Mar 15, 2005 (UTC) ::I'm with Alteripse, you got the chicken and egg mixed up. Obesity leads to type 2 DM, not the other way around. You may or may not be predisposed to obesity or DM genetically but the relationship between obesity and DM seems clear enough. User:Alex.tan 05:10, 20 Mar 2005 (UTC) It's an interesting topic. I agree that in some circumcstances it might be difficult to determine which comes first and the research article suggests that there is an association between poorer insulin sensitivity and reduced glucose thermogenesis. We think that poorer insulin sens is a precursor to type 2 diabetes. In children and adolescents we see the obesity precede the type 2 diabetes almost always, and it can often be reversed by wt loss. It's hard to be persuaded that the main relationship isn't the conventional wisdom of ob leads to ins resistance, insulin resistance plus genetic risk for inadequate beta cell insulin response leads to hyperglycemia, chronic hyperglycemia kills off remaining beta cells. Nothing in the Pima link contradicts this paradigm. Let's leave it and elaborate the issue when we break this into a separate type 2 article. User:Alteripse 00:06, 16 Mar 2005 (UTC) Some interesting research is published in this month's ''Diabetes.'' In short, it indicates that a variant of the ENPP1 gene is much more common in people with diabetes and helps to explain why all obese people don't develop T2 and some thin people do develop T2. It also confirms why ethnic groups develop T2 at differing rates. ''Abate, N. Diabetes, April 2005; vol 54: pp 1207-1213.'' User:Bollar 21:31, Mar 28, 2005 (UTC) :Articles of this type are published at rates of 20 a month. If it's truly a breakthrough. we'll hear about it. User:Jfdwolff | User_talk:Jfdwolff 19:34, 10 Apr 2005 (UTC) == Type 3, Type4 Diabetes == Would someone care to provide a cite on the existance of Type 3 as a bonafide category? The only thing that I can find, is an article dated the 9th of this month discussing the possible need for the lable in connection with an Insulin issue involving the brain, http://www.nutraingredients-usa.com/news/news-NG.asp?n=58592-scientists-believe-new/ Scientists believe type 3 diabetes uncovered. Unless a confirming cite can be presented, that section should probably be excised. Also, I have yet to come across anybody referring to Gestational Diabetes as Type 4 , or Type 'Anything Else'. User:coro 17:13, 27 Mar 2005 PST :I'm indeed not sure what the origin of this classification is. Perhaps searching for 3A, 3B etc may uncover something. User:Jfdwolff | User_talk:Jfdwolff 19:34, 10 Apr 2005 (UTC) I just saw this article reviewed in a journal. Calling it type 3 is not likely to catch on. We already have dozens of types of diabetes beyond 1 & 2 and even the broad definitions of 1 & 2 feel like they are in flux again (e.g., it seems harder than it did in the 1980s to decide what type many people have, and we are beginning to refer to young people having "type 1.5" or "type 1+2" or "monogenic diabetes"-- I can explain what these are if you are interested). The condition described in your reference does not even involve high blood sugars so it seems silly to refer to it as any type of diabetes. The subject of intracerebral insulin is fascinating, but it isn't diabetes. User:Alteripse 13:54, 27 May 2005 (UTC) I'm still pretty undecided on how to handle the Type 3 label, but unless someone can come with a justifying reference for the Type 4 label, I intend to get rid of it after the end of the month. And just refer to it as Gestational.--User:Coro 18:08, 14 Jun 2005 (UTC) == Declaration of St Vincent == That is a red link. Who knows more about it? Was it composed by doctors, patients, busybodies or all of the above? User:Jfdwolff | User_talk:Jfdwolff 20:03, 13 Apr 2005 (UTC) It is really unobjectionable. As I recall it dates to the late 1980s and was primarily a result of an international congress that was mainly European if I recall correctly. It outlines basic health care "rights" or least minimal desires for diabetes care (like access to blood testing supplies and insulin) in a very vague and general way. I think it was mainly diabetes doctors but couldn't swear to the absence of busybodies. I will see if I can find a live link. User:Alteripse 00:31, 14 Apr 2005 (UTC) My memory is pretty good. Here: [http://www.idf.org/home/index.cfm?node=839] == too many external links == Wikipedia is not a collection of links. Would someone like to go through the external links and prune them down to relevant links? Perhaps best link in each category? Thanks. User:Alex.tan 17:06, 27 Apr 2005 (UTC) ==Something that might be possible=== Hey this is what I want to do: Add ''Diabetis Type 1'' to the Autoimmune disease category, but only type one and it needs to say ''Daibetis Type 1'' on the Category page, also the link on the page should take you to the daibetis type 1 section of the diabetis page. Also it would be good if the category of Atoimmune diseases did not appear at the foot of the diabetis page as not all of diabetis belongs to that category. Some of this might be possible or not, anyone?, this is User:mexaguil User:219.88.206.183 11:14, 27 May 2005 (UTC) :I think the time is coming that we need to split this article anyway. The article ''as a whole'' should be about diabetic emergencies and end-organ damage, with subarticles on DMI and DMII that emphasise on pathogenesis and specific therapies (e.g. islet transplants for DMI). 13:34, 27 May 2005 (UTC) *I have been toying with a better structure and division of topics. Please look at User:Alteripse/diabetes_workshop and feel free to leave comments. Especially I would appreciate it if you would list diabetes-related titles I have missed. Thanks. User:Alteripse 14:06, 27 May 2005 (UTC) == Yet another style/content complaint... :-) == In reading through this piece tonight, I note the uneven style that others have commented on here on the talk page... but I believe that I discern another more fundamental problem. Some of the phrasing in this page leads me to wonder if parts of it have been copied wholesale from other sources ("These symptoms may also manifest in Type 2 diabetes in patients who present with frank poorly controlled diabetes."?), and what those sources might be. Now, if *I* can write "believe that I discern" on a talk page, clearly someone else can write "who present with frank poorly controlled diabetes"... but there seems a thread of that sort of uncommonly precise medical language woven through the article. Am I the only one who noticed this?
--User:Baylink 23:59, 13 Jun 2005 (UTC) :That's because this article is being edited by laypeople and MDs at the same time. When Alteripse, myself and other docs write, we may gravitate towards medical jargon. I don't think anything on this page is from other sources - it's been edited too heavily. User:Jfdwolff | User_talk:Jfdwolff 22:42, 14 Jun 2005 (UTC) == The reasoning behind including Pancreatic cancer link. == I noticed that the link for Pancreatic cancer in the diabetics article under the See Also section is removed. The reason why i included it was that a distant relative of mine was infected with pancreatic cancer and it seems he later had diabetes. I was initially confused and the doctors later told me that pancreatic cancer generally leads to diabetes and occasionally vice versa, since both diseases affect the pancreas. So I decided to add a link to a disease closely related to the organ that it affects to the article. Here are some reports and links on the matter. [http://www.cancersupportivecare.com/pancreas.html] [http://www.molecular-cancer.com/content/2/1/4] Hope this clarifies. --User:Idleguy 08:30, Jun 23, 2005 (UTC)
See other meanings of words starting from letter:
D
DA | DB | DC | DE | DF | DG | DH | DI | DJ | DK | DL | DM | DN | DO | DP | DR | DS | DT | DU | DW | DX | DY | DZ |Words begining with Diabetes_Mellitus:
Diabetes_Mellitus
Diabetes_mellitus
Diabetes_mellitus
Diabetes_Mellitus_Type_1
Diabetes_mellitus_type_1
Diabetes_Mellitus_Type_2
Diabetes_mellitus_type_2
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