Diabetes: Difference between revisions

Edit links
Source: Wikipedia, the free encyclopedia.
Browse history interactively
[pending revision][pending revision]
← Previous editNext edit →
Content deleted Content added
VisualWikitext
No edit summary
added graph
Line 14: Line 14:
| MeshNumber=C18.452.394.750|
| MeshNumber=C18.452.394.750|
}}
}}
[[Image:Suckale08 fig3 glucose insulin day.jpg|thumbnail|400px|The fluctuation of blood sugar (red) and the sugar-lowering hormone [[insulin]] (blue) in humans during the course of a day with three meals. One of the effects of a [[sucrose|sugar]]-rich vs a [[starch]]-rich meal is highlighted.]]


{{diabetes}}
{{diabetes}}

Revision as of 02:22, 2 February 2010

"Diabetes" redirects here. For For the journal, see Diabetes (journal). See also Diabetes insipidus, see Diabetes (disambiguation).
Diabetes
SpecialtyDiabetology Edit this on Wikidata
The fluctuation of blood sugar (red) and the sugar-lowering hormone insulin (blue) in humans during the course of a day with three meals. One of the effects of a sugar-rich vs a starch-rich meal is highlighted.

Diabetes mellitus (Template:Pron-en or /ˌdaɪ.əˈbiːtɨs/; /mɨˈlaɪtəs/ or /ˈmɛlɨtəs/)—often simply referred to as diabetes—is a condition in which a person has a high blood sugar (glucose) level as a result of the body either not producing enough insulin, or because body cells do not properly respond to the insulin that is produced. Insulin is a hormone produced in the pancreas which enables body cells to absorb glucose, to turn into energy. If the body cells do not absorb the glucose, the glucose accumulates in the blood (hyperglycemia), leading to various potential medical complications.[2][3]

There are many types of diabetes,[3] the most common of which are:

  • Type 1 diabetes: results from the body's failure to produce insulin, and presently requires the person to inject insulin.
  • Type 2 diabetes: results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency.
  • Gestational diabetes: is when pregnant women, who have never had diabetes before, have a high blood glucose level during pregnancy. It may precede development of type 2 DM.

Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.

All forms of diabetes have been treatable since insulin became medically available in 1921, but a cure is difficult. Pancreas transplants have been tried with limited success in type 1 DM; gastric bypass surgery has been successful in many with morbid obesity and type 2 DM; and gestational diabetes usually resolves after delivery. Diabetes without proper treatments can cause many complications. Acute complications include hypoglycemia, diabetic ketoacidosis, or nonketotic hyperosmolar coma. Serious long-term complications include cardiovascular disease, chronic renal failure, retinal damage. Adequate treatment of diabetes is thus important, as well as blood pressure control and lifestyle factors such as smoking cesation and maintaining a healthy body weight.

As of 2000 at least 171 million people worldwide suffer from diabetes, or 2.8% of the population.[4] Type 2 diabetes is by far the most common, affecting 90 to 95% of the U.S. diabetes population.[5]

Classification

Most cases of diabetes mellitus fall into the three broad categories of type 1 or type 2 and gestational diabetes. A few other types are described.

The term diabetes, without qualification, usually refers to diabetes mellitus, which roughly translates to excessive sweet urine (known as "glycosuria"). Several rare conditions are also named diabetes. The most common of these is diabetes insipidus in which large amounts of urine are produced (polyuria), which is not sweet (insipidus meaning "without taste" in Latin).

The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. Various sources have defined "type 3 diabetes" as: gestational diabetes,[6] insulin-resistant type 1 diabetes (or "double diabetes"), type 2 diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of adults (or LADA or "type 1.5" diabetes.[7])

Type 1 diabetes

Main article: Diabetes mellitus type 1

Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas leading to insulin deficiency. This type of diabetes can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, where beta cell loss is a T-cell mediated autoimmune attack.[2] There is no known preventive measure against type 1 diabetes, which causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed "juvenile diabetes" because it represents a majority of the diabetes cases in children.

Type 2 diabetes

Main article: Diabetes mellitus type 2

Type 2 diabetes mellitus is characterized by insulin resistance which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus due to a known defect are classified separately. Type 2 diabetes is the most common type.

In the early stage of type 2 diabetes, the predominant abnormality is reduced insulin sensitivity. At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses, the impairment of insulin secretion occurs, and therapeutic replacement of insulin may sometimes become necessary in certain patients.[citation needed]

Gestational diabetes

Main article: Gestational diabetes

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.

A 2008 study completed in the U.S. found that more American women are entering pregnancy with preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years.[8] This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future.

Other types

Pre-diabetes indicates a condition that occurs when a person's blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 diabetes. Many people destined to develop type 2 diabetes spend many years in a state of pre-diabetes which has been termed "America's largest healthcare epidemic,"[9]: 10–11 .

Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.[10]

Signs and symptoms

Overview of the most significant symptoms of diabetes.

The classical symptoms of DM are polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger).[11] Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes symptoms usually develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible mental fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled, although unexplained weight loss may be experienced at the onset of the disease. Final diagnosis is made by measuring the blood glucose concentration.

When the glucose concentration in the blood is raised beyond its renal threshold (about 10 mmol/L, although this may be altered in certain conditions, such as pregnancy), reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst.

Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually returns the lens to its original shape. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change, whereas with type 2 change is generally more gradual, but should still be suspected.

Patients (usually with type 1 diabetes) may also initially present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires immediate hospitalization.

A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a vicious circle in regard to the water loss.

A number of skin rashes can occur in diabetes that are collectively known as diabetic dermadromes.

Causes

Type 2 diabetes is determined primarily by lifestyle factors and genes.[12]

Lifestyle

A number of lifestyle factors are known to be important to the development of type 2 diabtetes. In one study, those who had high levels of physical activity, a healthy diet, did not smoke, and consumed alcohol in moderation had an 82% lower rate of diabetes. When a normal weight was included the rate was 89% lower. In this study a healthy diet was defined as one high in fiber, with a high polyunsaturated to saturated fat ratio, and a lower mean glycemic index.[13] Obesity has been found to contribute to approximately 55% type 2 diabetes,[14] and decreasing consumption of saturated fats and trans fatty acids while replacing them with unsaturated fats may decrease the risk.[12] The increased rate of childhood obesity in between the 1960s and 2000s is believed to have lead to the increase in type 2 diabetes in children and adolescents.[15]

Environmental toxins may contribute to recent increases in the rate of type 2 diabetes. A positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of some plastics, and the incidence of type 2 diabetes.[16]

Medical conditions

Subclinical Cushing's syndrome (cortisol excess) may be associated with DM type 2.[17] The percentage of subclinical Cushing's syndrome in the diabetic population is about 9%.[18] Diabetic patients with a pituitary microadenoma can improve insulin sensitivity by removal of these microadenomas.[19]

Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also associated with diabetes mellitus type 2,[20][21] even if the exact mechanism by which testosterone improve insulin sensitivity is still not known.

Genetics

Both type 1 and type 2 diabetes are partly inherited. Type 1 diabetes may be triggered by certain infections, with some evidence pointing at Coxsackie B4 virus. There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic "self" identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger.

There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Genes significantly associated with developing type 2 diabetes, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.[22] KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7–like 2) regulates proglucagon gene expression and thus the production of glucagon-like peptide-1.[2] Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.[23]

Monogenic forms, e.g., MODY, constitute 1–5 % of all cases.[24]

Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.[25]

Gene expression promoted by a diet of fat and glucose as well as high levels of inflammation related cytokines found in the obese results in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.[26]

Pathophysiology

Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbable glucose. The chief trigger is a rise in blood glucose levels after eating

Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.

Most of the carbohydrates in food are converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel. The most significant exceptions are fructose, most disaccharides (except sucrose and in some people lactose), and all more complex polysaccharides, with the outstanding exception of starch. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage.

Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.

Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).

If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.

Diagnosis

Main articles: Glycosylated hemoglobin and Glucose tolerance test
WHO diabetes diagnostic criteria[27][28]  edit
Condition 2-hour glucose Fasting glucose HbA1c
Unit mmol/L mg/dL mmol/L mg/dL mmol/mol DCCT %
Normal < 7.8 < 140 < 6.1 < 110 < 42 < 6.0
Impaired fasting glycaemia < 7.8 < 140 6.1–7.0 110–125 42–46 6.0–6.4
Impaired glucose tolerance ≥ 7.8 ≥ 140 < 7.0 < 126 42–46 6.0–6.4
Diabetes mellitus ≥ 11.1 ≥ 200 ≥ 7.0 ≥ 126 ≥ 48 ≥ 6.5

Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:[10]

  • Fasting plasma glucose level at or above 7.0 mmol/L (126 mg/dL).
  • Plasma glucose at or above 11.1 mmol/L (200 mg/dL) two hours after a 75 g oral glucose load as in a glucose tolerance test.
  • Symptoms of hyperglycemia and casual plasma glucose at or above 11.1 mmol/L (200 mg/dL).
  • Glycated hemoglobin (hemoglobin A1C) at or above 6.5. (This criterion was recommended by the American Diabetes Association in 2010; it has yet to be adopted by the WHO.)[29]

About a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis (a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids) by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.

A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test.[30] According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/L) is considered diagnostic for diabetes mellitus.

Patients with fasting glucose levels from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) are considered to have impaired fasting glucose. Patients with plasma glucose at or above 140 mg/dL (7.8 mmol/L), but not over 200 mg/dL (11.1 mmol/L), two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.[31]

Screening

Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. The screening test varies according to circumstances and local policy, and may be a random blood glucose test, a fasting blood glucose test, a blood glucose test two hours after 75 g of glucose, or an even more formal glucose tolerance test. Many healthcare providers recommend universal screening for adults at age 40 or 50, and often periodically thereafter. Earlier screening is typically recommended for those with risk factors such as obesity, family history of diabetes, high-risk ethnicity (Hispanic, Native American, Afro-Caribbean, Pacific Islander, or Māori).[32][33]

Many medical conditions are associated with diabetes and warrant screening. A partial list includes: subclinical Cushing's syndrome,[17] testosterone deficiency,[20] high blood pressure, elevated cholesterol levels[citation needed], coronary artery disease [citation needed], past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, fatty liver, hemochromatosis[citation needed], cystic fibrosis, several mitochondrial neuropathies and myopathies (such as MIDD), myotonic dystrophy, Friedreich's ataxia, some of the inherited forms of neonatal hyperinsulinism. The risk of diabetes is higher with chronic use of several medications, including long term corticosteroids, some chemotherapy agents (especially L-asparaginase), as well as some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics).

People with a confirmed diagnosis of diabetes are tested routinely for complications. This includes yearly urine testing for microalbuminuria and examination of the retina of the eye for retinopathy.

Prevention

Type 1

Type 1 diabetes risk is known to depend upon a genetic predisposition based on HLA types (particularly types DR3 and DR4), an unknown environmental trigger (suspected to be an infection, although none has proven definitive in all cases), and an uncontrolled autoimmune response that attacks the insulin producing beta cells.[34] Some research has suggested that breastfeeding decreased the risk in later life;[35][36] various other nutritional risk factors are being studied, but no firm evidence has been found.[37] Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes, though the causal relationship is obscure.[38]

Children with antibodies to beta cell proteins (ie at early stages of an immune reaction to them) but no overt diabetes, and treated with vitamin B-3 (niacin), had less than half the diabetes onset incidence in a 7-year time span as did the general population, and an even lower incidence relative to those with antibodies as above, but who received no vitamin B3.[39]

Type 2

Lifestyle

Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity.[40][41][42] The American Diabetes Association (ADA) recommends maintaining a healthy weight, getting at least 2½ hours of exercise per week (several brisk sustained walks appear sufficient), having a modest fat intake, and eating sufficient fiber (e.g., from whole grains). The ADA does not recommend alcohol consumption as a preventive, but it is interesting to note that moderate alcohol intake may reduce the risk (though heavy consumption absolutely and clearly increases damage to bodily systems significantly); a similarly confused connection between low dose alcohol consumption and heart disease is termed the French Paradox.[citation needed]

There is inadequate evidence that eating foods of low glycemic index is clinically helpful despite recommendations and suggested diets emphasizing this approach.[43]

Diets that are very low in saturated fats reduce the risk of becoming insulin resistant and diabetic.[44][45] Study group participants whose "physical activity level and dietary, smoking, and alcohol habits were all in the low-risk group had an 82% lower incidence of diabetes."[46] In another study of dietary practice and incidence of diabetes, "foods rich in vegetable oils, including non-hydrogenated margarines, nuts, and seeds, should replace foods rich in saturated fats from meats and fat-rich dairy products. Consumption of partially hydrogenated fats should be minimized."[47]

There are numerous studies which suggest connections between some aspects of Type II diabetes with ingestion of certain foods or with some drugs. Breastfeeding may also be associated with the prevention of type 2 of the disease in mothers.[48]

Medications

Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin,[41] rosiglitazone,[49] or valsartan.[50] In patients on hydroxychloroquine for rheumatoid arthritis, incidence of diabetes was reduced by 77% though causal mechanisms are unclear.[51] Lifestyle interventions are however more effective than metformin at preventing diabetes regardless of weightloss.[52]

Management

Main article: Diabetes management

Diabetes mellitus is a chronic disease which is difficult to cure. Management concentrates on keeping blood sugar levels as close to normal ("euglycemia") as possible without presenting undue patient danger. This can usually be with close dietary management, exercise, and use of appropriate medications (insulin only in the case of type 1 diabetes mellitus. Oral medications may be used in the case of type 2 diabetes, as well as insulin).

Lifestyle modifications

Main article: Diabetic diet

There are roles for patient education, dietetic support, sensible exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure[53] in patients with hypertension, cholesterol in those with dyslipidmia, as well as exercising more, smoking less or ideally not at all, consuming a recommended diet [citation needed]. Patients with foot problems are also recommended to wear diabetic socks [citation needed], and possibly diabetic shoes [citation needed].

Medications

Oral medications
Main article: Anti-diabetic drug
Insulin
Main article: Insulin therapy

Type 1 treatments usually include combinations of regular or NPH insulin, and/or synthetic insulin analogs.

Support

In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care of a patient in a team approach. Optometrists, podiatrists/chiropodists, dietitians, physiotherapists, nursing specialists (e.g., DSNs (Diabetic Specialist Nurse)), nurse practitioners, or Certified Diabetes Educators, may jointly provide multidisciplinary expertise. In countries where patients must provide for their own health care (e.g. in the US, and in much of the undeveloped world).

Peer support links people living with diabetes. Within peer support, people with a common illness share knowledge and experience that others, including many health workers, do not have. Peer support is frequent, ongoing, accessible and flexible and can take many forms—phone calls, text messaging, group meetings, home visits, and even grocery shopping. It complements and enhances other health care services by creating the emotional, social and practical assistance necessary for managing disease and staying healthy.

Prognosis

Main article: Prognosis of diabetes mellitus

Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-managed blood sugar levels.[54][55] Wider health problems may accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise. According to one study, women with high blood pressure (hypertension) were three times more likely to develop type 2 diabetes as compared with women with optimal BP after adjusting for various factors such as age, ethnicity, smoking, alcohol intake, body mass index (BMI), exercise, family history of diabetes, etc.[56] The study was conducted by researchers from the Brigham and Women’s Hospital, Harvard Medical School and the Harvard School of Public Health, USA, who followed over 38,000 female health professionals for ten years.

Except in the case of type 1 diabetes, which always requires insulin replacement, the way type 2 diabetes is managed may change with age. Insulin production decreases because of age-related impairment of pancreatic beta cells. Additionally, insulin resistance increases because of the loss of lean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population.[57] Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people.[58] Treatment goals for older patients with diabetes vary with the individual, and take into account health status, as well as life expectancy, level of dependence, and willingness to adhere to a treatment regimen.[59]

Epidemiology

Prevalence of diabetes worldwide in 2000 (per 1000 inhabitants). World average was 2.8%.
  no data
  ≤ 7.5
  7.5–15
  15–22.5
  22.5–30
  30–37.5
  37.5–45
  45–52.5
  52.5–60
  60–67.5
  67.5–75
  75–82.5
  ≥ 82.5
Disability-adjusted life year for diabetes mellitus per 100,000 inhabitants in 2002.[60]
  no data
  ≤ 100
  100-200
  200-300
  300-400
  400-500
  500-600
  600-700
  700-800
  800-900
  900-1000
  1000-1500
  ≥ 1500

In 2000, according to the World Health Organization, at least 171 million people worldwide suffer from diabetes, or 2.8% of the population.[4] Its incidence is increasing rapidly, and it is estimated that by the year 2030, this number will almost double.[4] Diabetes mellitus occurs throughout the world, but is more common (especially type 2) in the more developed countries. The greatest increase in prevalence is, however, expected to occur in Asia and Africa, where most patients will probably be found by 2030.[4] The increase in incidence of diabetes in developing countries follows the trend of urbanization and lifestyle changes, perhaps most importantly a "Western-style" diet. This has suggested an environmental (i.e., dietary) effect, but there is little understanding of the mechanism(s) at present, though there is much speculation, some of it most compellingly presented.[4]

For at least 20 years, diabetes rates in North America have been increasing substantially. In 2008 there were about 24 million people with diabetes in the United States alone, from those 5.7 million people remain undiagnosed. Other 57 million people are estimated to have pre-diabetes.[61]

The Centers for Disease Control has termed the change an epidemic.[62] The National Diabetes Information Clearinghouse estimates that diabetes costs $132 billion in the United States alone every year. About 5%–10% of diabetes cases in North America are type 1, with the rest being type 2. The fraction of type 1 in other parts of the world differs. Most of this difference is not currently understood. The American Diabetes Association cite the 2003 assessment of the National Center for Chronic Disease Prevention and Health Promotion (Centers for Disease Control and Prevention) that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime.[63][64]

According to the American Diabetes Association, approximately 18.3% (8.6 million) of Americans age 60 and older have diabetes.[65] Diabetes mellitus prevalence increases with age, and the numbers of older persons with diabetes are expected to grow as the elderly population increases in number. The National Health and Nutrition Examination Survey (NHANES III) demonstrated that, in the population over 65 years old, 18% to 20% have diabetes, with 40% having either diabetes or its precursor form of impaired glucose tolerance.[57]

Indigenous populations in first world countries have a higher prevalence and increasing incidence of diabetes than their corresponding non-indigenous populations. In Australia the age-standardised prevalence of self-reported diabetes in Indigenous Australians is almost 4 times that of non-indigenous Australians.[66] Preventative community health programs such as Sugar Man (diabetes education) are showing some success in tackling this problem.

History

The term diabetes (Greek: διαβήτης, diabētēs) was coined by Aretaeus of Cappadocia. It was derived from the Greek verb διαβαίνειν, diabaínein, itself formed from the prefix dia-, "across, apart," and the verb bainein, "to walk, stand." The verb diabeinein meant "to stride, walk, or stand with legs asunder"; hence, its derivative diabētēs meant "one that straddles," or specifically "a compass, siphon." The sense "siphon" gave rise to the use of diabētēs as the name for a disease involving the discharge of excessive amounts of urine. Diabetes is first recorded in English, in the form diabete, in a medical text written around 1425. In 1675, Thomas Willis added the word mellitus, from the Latin meaning "honey", a reference to the sweet taste of the urine. This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians. In 1776, Matthew Dobson confirmed that the sweet taste was because of an excess of a kind of sugar in the urine and blood of people with diabetes.[67]

Diabetes mellitus appears to have been a death sentence in the ancient era. Hippocrates makes no mention of it, which may indicate that he felt the disease was incurable. Aretaeus did attempt to treat it but could not give a good prognosis; he commented that "life (with diabetes) is short, disgusting and painful."[68]

Sushruta (6th century BCE) identified diabetes and classified it as Medhumeha.[69] He further identified it with obesity and sedentary lifestyle, advising exercises to help "cure" it.[69] The ancient Indians tested for diabetes by observing whether ants were attracted to a person's urine, and called the ailment "sweet urine disease" (Madhumeha). The Korean, Chinese, and Japanese words for diabetes are based on the same ideographs (糖尿病) which mean "sugar urine disease".

In medieval Persia, Avicenna (980–1037) provided a detailed account on diabetes mellitus in The Canon of Medicine, "describing the abnormal appetite and the collapse of sexual functions," and he documented the sweet taste of diabetic urine. Like Aretaeus before him, Avicenna recognized a primary and secondary diabetes. He also described diabetic gangrene, and treated diabetes using a mixture of lupine, trigonella (fenugreek), and zedoary seed, which produces a considerable reduction in the excretion of sugar, a treatment which is still prescribed in modern times. Avicenna also "described diabetes insipidus very precisely for the first time", though it was later Johann Peter Frank (1745–1821) who first differentiated between diabetes mellitus and diabetes insipidus.[70]

Although diabetes has been recognized since antiquity, and treatments of various efficacy have been known in various regions since the Middle Ages, and in legend for much longer, pathogenesis of diabetes has only been understood experimentally since about 1900.[71] The discovery of a role for the pancreas in diabetes is generally ascribed to Joseph von Mering and Oskar Minkowski, who in 1889 found that dogs whose pancreas was removed developed all the signs and symptoms of diabetes and died shortly afterwards.[72] In 1910, Sir Edward Albert Sharpey-Schafer suggested that people with diabetes were deficient in a single chemical that was normally produced by the pancreas—he proposed calling this substance insulin, from the Latin insula, meaning island, in reference to the insulin-producing islets of Langerhans in the pancreas.

The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not further clarified until 1921, when Sir Frederick Grant Banting and Charles Herbert Best repeated the work of Von Mering and Minkowski, and went further to demonstrate they could reverse induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs.[73] Banting, Best, and colleagues (especially the chemist Collip) went on to purify the hormone insulin from bovine pancreases at the University of Toronto. This led to the availability of an effective treatment—insulin injections—and the first patient was treated in 1922. For this, Banting and laboratory director MacLeod received the Nobel Prize in Physiology or Medicine in 1923; both shared their Prize money with others in the team who were not recognized, in particular Best and Collip. Banting and Best made the patent available without charge and did not attempt to control commercial production. Insulin production and therapy rapidly spread around the world, largely as a result of this decision. Banting is honored by World Diabetes Day which is held on his birthday, November 14.

The distinction between what is now known as type 1 diabetes and type 2 diabetes was first clearly made by Sir Harold Percival (Harry) Himsworth, and published in January 1936.[74]

Despite the availability of treatment, diabetes has remained a major cause of death. For instance, statistics reveal that the cause-specific mortality rate during 1927 amounted to about 47.7 per 100,000 population in Malta.[75]

Other landmark discoveries include:[71]

  • Identification of the first of the sulfonylureas in 1942
  • Reintroduction of the use of biguanides for Type 2 diabetes in the late 1950s. The initial phenformin was withdrawn worldwide (in the U.S. in 1977) due to its potential for sometimes fatal lactic acidosis and metformin was first marketed in France in 1979, but not until 1994 in the US.
  • The determination of the amino acid sequence of insulin (by Sir Frederick Sanger, for which he received a Nobel Prize)
  • The radioimmunoassay for insulin, as discovered by Rosalyn Yalow and Solomon Berson (gaining Yalow the 1977 Nobel Prize in Physiology or Medicine)[76]
  • The three-dimensional structure of insulin (PDB: 2INS​)
  • Dr Gerald Reaven's identification of the constellation of symptoms now called metabolic syndrome in 1988
  • Demonstration that intensive glycemic control in type 1 diabetes reduces chronic side effects more as glucose levels approach 'normal' in a large longitudinal study,[77] and also in type 2 diabetics in other large studies
  • Identification of the first thiazolidinedione as an effective insulin sensitizer during the 1990s

In 1980, U.S. biotech company Genentech developed human insulin. The insulin is isolated from genetically altered bacteria (the bacteria contain the human gene for synthesizing human insulin), which produce large quantities of insulin. Scientists then purify the insulin and distribute it to pharmacies for use by diabetes patients.

Society and culture

The 1990 "St Vincent Declaration"[78][79] was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important both in terms of quality of life and life expectancy but also economically-expenses due to diabetes have been shown to be a major drain on health-and productivity-related resources for healthcare systems and governments.

Several countries established more and less successful national diabetes programmes to improve treatment of the disease.[80]

A study shows that diabetic patients with neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.[81]

Research

Diabetics are often advised to receive regular consultation from a physician (e.g., at least every three to six months) although research is underway to develop artificial intelligence systems which may reduce the frequency of such visits.[82]

References

  1. ^ "Diabetes Blue Circle Symbol". International Diabetes Federation. 17 March 2006.
  2. ^ a b c Rother KI (2007). "Diabetes treatment—bridging the divide". The New England Journal of Medicine. 356 (15): 1499–501. doi:10.1056/NEJMp078030. PMID 17429082. {{cite journal}}: Unknown parameter |month= ignored (help)
  3. ^ a b L M Tierney, S J McPhee, M A Papadakis (2002). Current medical Diagnosis & Treatment. International edition. New York: Lange Medical Books/McGraw-Hill. pp. 1203–15. ISBN 0-07-137688-7.
  4. ^ a b c d e Wild S, Roglic G, Green A, Sicree R, King H (2004). "Global prevalence of diabetes: estimates for the year 2000 and projections for 2030". Diabetes Care. 27 (5): 1047–53. doi:10.2337/diacare.27.5.1047. PMID 15111519. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  5. ^ "Type 2 Diabetes Overview". Web MD.
  6. ^ "Other "types" of diabetes". American Diabetes Association. August 25, 2005.
  7. ^ "Diseases: Johns Hopkins Autoimmune Disease Research Center". Retrieved 2007-09-23.
  8. ^ Lawrence JM, Contreras R, Chen W, Sacks DA (2008). "Trends in the prevalence of preexisting diabetes and gestational diabetes mellitus among a racially/ethnically diverse population of pregnant women, 1999–2005". Diabetes Care. 31 (5): 899–904. doi:10.2337/dc07-2345. PMID 18223030. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ Handelsman, Yehuda, MD. "A Doctor's Diagnosis: Prediabetes." Power of Prevention, Vol 1, Issue 2, 2009.
  10. ^ a b World Health Organisation Department of Noncommunicable Disease Surveillance (1999). "Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications" (PDF).
  11. ^ Cooke DW, Plotnick L (2008). "Type 1 diabetes mellitus in pediatrics". Pediatr Rev. 29 (11): 374–84, quiz 385. doi:10.1542/pir.29-11-374. PMID 18977856. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ a b Risérus U, Willett WC, Hu FB (2009). "Dietary fats and prevention of type 2 diabetes". Progress in Lipid Research. 48 (1): 44–51. doi:10.1016/j.plipres.2008.10.002. PMC 2654180. PMID 19032965. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  13. ^ Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovick D (2009). "Lifestyle risk factors and new-onset diabetes mellitus in older adults: the cardiovascular health study". Archives of Internal Medicine. 169 (8): 798–807. doi:10.1001/archinternmed.2009.21. PMID 19398692. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  14. ^ Centers for Disease Control and Prevention (CDC) (2004). "Prevalence of overweight and obesity among adults with diagnosed diabetes—United States, 1988–1994 and 1999–2002". MMWR. Morbidity and Mortality Weekly Report. 53 (45): 1066–8. PMID 15549021. {{cite journal}}: Unknown parameter |month= ignored (help)
  15. ^ Arlan Rosenbloom, Janet H Silverstein (2003). Type 2 Diabetes in Children and Adolescents: A Clinician's Guide to Diagnosis, Epidemiology, Pathogenesis, Prevention, and Treatment. American Diabetes Association,U.S. p. 1. ISBN 978-1580401555.
  16. ^ Lang IA, Galloway TS, Scarlett A; et al. (2008). "Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults". JAMA. 300 (11): 1303–10. doi:10.1001/jama.300.11.1303. PMID 18799442. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  17. ^ a b Iwasaki Y, Takayasu S, Nishiyama M; et al. (2008). "Is the metabolic syndrome an intracellular Cushing state? Effects of multiple humoral factors on the transcriptional activity of the hepatic glucocorticoid-activating enzyme (11beta-hydroxysteroid dehydrogenase type 1) gene". Molecular and Cellular Endocrinology. 285 (1–2): 10–8. doi:10.1016/j.mce.2008.01.012. PMID 18313835. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  18. ^ Chiodini I, Torlontano M, Scillitani A; et al. (2005). "Association of subclinical hypercortisolism with type 2 diabetes mellitus: a case-control study in hospitalized patients". European Journal of Endocrinology. 153 (6): 837–44. doi:10.1530/eje.1.02045. PMID 16322389. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  19. ^ Taniguchi T, Hamasaki A, Okamoto M (2008). "Subclinical hypercortisolism in hospitalized patients with type 2 diabetes mellitus" ([dead link]). Endocrine Journal. 55 (2): 429–32. doi:10.1507/endocrj.K07E-045. PMID 18362453. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  20. ^ a b Saad F, Gooren L (2009). "The role of testosterone in the metabolic syndrome: a review". The Journal of Steroid Biochemistry and Molecular Biology. 114 (1–2): 40–3. doi:10.1016/j.jsbmb.2008.12.022. PMID 19444934. {{cite journal}}: Unknown parameter |month= ignored (help)
  21. ^ Farrell JB, Deshmukh A, Baghaie AA (2008). "Low testosterone and the association with type 2 diabetes". The Diabetes Educator. 34 (5): 799–806. doi:10.1177/0145721708323100. PMID 18832284.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. ^ Lyssenko V, Jonsson A, Almgren P; et al. (2008). "Clinical risk factors, DNA variants, and the development of type 2 diabetes". The New England Journal of Medicine. 359 (21): 2220–32. doi:10.1056/NEJMoa0801869. PMID 19020324. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  23. ^ Walley AJ, Blakemore AI, Froguel P (2006). "Genetics of obesity and the prediction of risk for health". Human Molecular Genetics. 15 Spec No 2: R124–30. doi:10.1093/hmg/ddl215. PMID 16987875. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  24. ^ "Monogenic Forms of Diabetes: Neonatal Diabetes Mellitus and Maturity-onset Diabetes of the Young". National Diabetes Information Clearinghouse (NDIC). National Institute of Diabetes and Digestive and Kidney Diseases, NIH. Retrieved 2008-08-04. {{cite news}}: Cite has empty unknown parameter: |coauthors= (help)
  25. ^ Barrett TG (2001). "Mitochondrial diabetes, DIDMOAD and other inherited diabetes syndromes". Best Practice & Research. Clinical Endocrinology & Metabolism. 15 (3): 325–43. doi:10.1053/beem.2001.0149. PMID 11554774. {{cite journal}}: Unknown parameter |month= ignored (help)
  26. ^ "The origin of diabetes Don't blame your genes They may simply be getting bad instructions—from you". Economist. 2009. {{cite news}}: Cite has empty unknown parameter: |coauthors= (help)
  27. ^ Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: Report of a WHO/IDF consultation (PDF). Geneva: World Health Organization. 2006. p. 21. ISBN 978-92-4-159493-6.
  28. ^ Vijan S (March 2010). "In the clinic. Type 2 diabetes". Annals of Internal Medicine. 152 (5): ITC31-15, quiz ITC316. doi:10.7326/0003-4819-152-5-201003020-01003. PMID 20194231.
  29. ^ ""Diabetes Care" January 2010". Retrieved 2010-01-29. {{cite web}}: Text "American Diabetes Association" ignored (help)
  30. ^ Saydah SH, Miret M, Sung J, Varas C, Gause D, Brancati FL (2001). "Postchallenge hyperglycemia and mortality in a national sample of U.S. adults". Diabetes Care. 24 (8): 1397–402. doi:10.2337/diacare.24.8.1397. PMID 11473076. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  31. ^ Santaguida PL, Balion C, Hunt D, Morrison K, Gerstein H, Raina P, Booker L, Yazdi H. "Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose". Summary of Evidence Report/Technology Assessment, No. 128. Agency for Healthcare Research and Quality. Retrieved 2008-07-20.{{cite web}}: CS1 maint: multiple names: authors list (link)
  32. ^ Lee CM, Huxley RR, Lam TH; et al. (2007). "Prevalence of diabetes mellitus and population attributable fractions for coronary heart disease and stroke mortality in the WHO South-East Asia and Western Pacific regions". Asia Pacific Journal of Clinical Nutrition. 16 (1): 187–92. PMID 17215197. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  33. ^ Seidell JC (2000). "Obesity, insulin resistance and diabetes—a worldwide epidemic". The British Journal of Nutrition. 83 Suppl 1: S5–8. doi:10.1017/S000711450000088X. PMID 10889785. {{cite journal}}: Unknown parameter |month= ignored (help)
  34. ^ Daneman D (2006). "Type 1 diabetes". Lancet. 367 (9513): 847–58. doi:10.1016/S0140-6736(06)68341-4. PMID 16530579. {{cite journal}}: Unknown parameter |month= ignored (help)
  35. ^ Borch-Johnsen K, Joner G, Mandrup-Poulsen T; et al. (1984). "Relation between breast-feeding and incidence rates of insulin-dependent diabetes mellitus. A hypothesis". Lancet. 2 (8411): 1083–6. doi:10.1016/S0140-6736(84)91517-4. PMID 6150150. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  36. ^ Naim Shehadeh, Raanan Shamir, Moshe Berant, Amos Etzioni (2001). "Insulin in human milk and the prevention of type 1 diabetes". Pediatric Diabetes. 2 (4): 175–7. doi:10.1034/j.1399-5448.2001.20406.x. PMID 15016183.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Virtanen SM, Knip M (2003). "Nutritional risk predictors of beta cell autoimmunity and type 1 diabetes at a young age". The American Journal of Clinical Nutrition. 78 (6): 1053–67. PMID 14668264. {{cite journal}}: Unknown parameter |month= ignored (help)
  38. ^ Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM (2001). "Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study". Lancet. 358 (9292): 1500–3. doi:10.1016/S0140-6736(01)06580-1. PMID 11705562. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  39. ^ Elliott RB, Pilcher CC, Fergusson DM, Stewart AW (1996). "A population based strategy to prevent insulin-dependent diabetes using nicotinamide". Journal of Pediatric Endocrinology & Metabolism. 9 (5): 501–9. PMID 8961125.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  40. ^ Lindström J, Ilanne-Parikka P, Peltonen M; et al. (2006). "Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study". Lancet. 368 (9548): 1673–9. doi:10.1016/S0140-6736(06)69701-8. PMID 17098085. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  41. ^ a b Knowler WC, Barrett-Connor E, Fowler SE; et al. (2002). "Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin". The New England Journal of Medicine. 346 (6): 393–403. doi:10.1056/NEJMoa012512. PMC 1370926. PMID 11832527. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  42. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1016/S0140-6736(09)61457-4, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1016/S0140-6736(09)61457-4 instead.
  43. ^ Bantle JP, Wylie-Rosett J, Albright AL; et al. (2006). "Nutrition recommendations and interventions for diabetes—2006: a position statement of the American Diabetes Association". Diabetes Care. 29 (9): 2140–57. doi:10.2337/dc06-9914. PMID 16936169. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  44. ^ Barnard, Neal (2007). "13". Dr. Neal Barnard's Program for Reversing Diabetes: The Scientifically Proven System for Reversing Diabetes Without Drugs. New York, NY: Rodale/Holtzbrinck Publishers. ISBN 978-1-59486-528-2. {{cite book}}: Cite has empty unknown parameter: |coauthors= (help); Unknown parameter |isbn-status= ignored (help)
  45. ^ Barnard ND, Katcher HI, Jenkins DJ, Cohen J, Turner-McGrievy G (2009). "Vegetarian and vegan diets in type 2 diabetes management". Nutrition Reviews. 67 (5): 255–63. doi:10.1111/j.1753-4887.2009.00198.x. PMID 19386029. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  46. ^ Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovick D (2009). "Lifestyle risk factors and new-onset diabetes mellitus in older adults: the cardiovascular health study". Archives of Internal Medicine. 169 (8): 798–807. doi:10.1001/archinternmed.2009.21. PMID 19398692. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  47. ^ Risérus U, Willett WC, Hu FB (2009). "Dietary fats and prevention of type 2 diabetes". Progress in Lipid Research. 48 (1): 44–51. doi:10.1016/j.plipres.2008.10.002. PMC 2654180. PMID 19032965. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  48. ^ Stuebe AM, Rich-Edwards JW, Willett WC, Manson JE, Michels KB (2005). "Duration of lactation and incidence of type 2 diabetes". JAMA. 294 (20): 2601–10. doi:10.1001/jama.294.20.2601. PMID 16304074. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  49. ^ Gerstein HC, Yusuf S, Bosch J; et al. (2006). "Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trial". Lancet. 368 (9541): 1096–105. doi:10.1016/S0140-6736(06)69420-8. PMID 16997664. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  50. ^ Kjeldsen SE, Julius S, Mancia G; et al. (2006). "Effects of valsartan compared to amlodipine on preventing type 2 diabetes in high-risk hypertensive patients: the VALUE trial". Journal of Hypertension. 24 (7): 1405–12. doi:10.1097/01.hjh.0000234122.55895.5b. PMID 16794491. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  51. ^ Wasko MC, Hubert HB, Lingala VB; et al. (2007). "Hydroxychloroquine and risk of diabetes in patients with rheumatoid arthritis". JAMA. 298 (2): 187–93. doi:10.1001/jama.298.2.187. PMID 17622600. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  52. ^ Knowler WC, Fowler SE, Hamman RF; et al. (2009). "10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study". Lancet. 374 (9702): 1677–86. doi:10.1016/S0140-6736(09)61457-4. PMID 19878986. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  53. ^ Adler AI, Stratton IM, Neil HA; et al. (2000). "Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observational study". BMJ. 321 (7258): 412–9. doi:10.1136/bmj.321.7258.412. PMC 27455. PMID 10938049. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  54. ^ Nathan DM, Cleary PA, Backlund JY; et al. (2005). "Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes". The New England Journal of Medicine. 353 (25): 2643–53. doi:10.1056/NEJMoa052187. PMC 2637991. PMID 16371630. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  55. ^ "The effect of intensive diabetes therapy on the development and progression of neuropathy. The Diabetes Control and Complications Trial Research Group". Annals of Internal Medicine. 122 (8): 561–8. 1995. doi:10.1059/0003-4819-122-8-199504150-00001. PMID 7887548. {{cite journal}}: Unknown parameter |doi_brokendate= ignored (|doi-broken-date= suggested) (help); Unknown parameter |month= ignored (help)
  56. ^ "Women with high BP at three-fold risk of developing diabetes." TopNews.in July 1, 2009. http://www.topnews.in/women-high-bp-three-fold-risk-developing-diabetes-23341
  57. ^ a b Harris MI, Flegal KM, Cowie CC; et al. (1998). "Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988–1994". Diabetes Care. 21 (4): 518–24. doi:10.2337/diacare.21.4.518. PMID 9571335. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  58. ^ Chang AM, Halter JB (2003). "Aging and insulin secretion". American Journal of Physiology. Endocrinology and Metabolism. 284 (1): E7–12. doi:10.1152/ajpendo.00366.2002. PMID 12485807. {{cite journal}}: Unknown parameter |doi_brokendate= ignored (|doi-broken-date= suggested) (help); Unknown parameter |month= ignored (help)
  59. ^ "Diabetes and Aging". Diabetes Dateline. National Institute of Diabetes and Digestive and Kidney Diseases. 2002. Retrieved 2007-05-14.
  60. ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002.
  61. ^ http://www.cdc.gov/Features/diabetesfactsheet/
  62. ^ "CDC's Diabetes Program-News and Information-Press Releases-October 26, 2000". Retrieved 2008-06-23.
  63. ^ Narayan KM, Boyle JP, Thompson TJ, Sorensen SW, Williamson DF (2003). "Lifetime risk for diabetes mellitus in the United States". JAMA. 290 (14): 1884–90. doi:10.1001/jama.290.14.1884. PMID 14532317. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  64. ^ American Diabetes Association (2005). "Total Prevalence of Diabetes & Pre-diabetes". Retrieved 2006-03-17.
  65. ^ "Seniors and Diabetes". Elderly And Diabetes-Diabetes and Seniors. LifeMed Media. 2006. Retrieved 2007-05-14.
  66. ^ Australian Institute for Health and Welfare. "Diabetes, an overview". Retrieved 2008-06-23.
  67. ^ Dobson, M. (1776). "Nature of the urine in diabetes". Medical Observations and Inquiries. 5: 298–310. {{cite journal}}: Cite has empty unknown parameter: |coauthors= (help)
  68. ^ Medvei, Victor Cornelius (1993). The history of clinical endocrinology. Carnforth, Lancs., U.K: Parthenon Pub. Group. pp. 23–34. ISBN 1-85070-427-9.
  69. ^ a b Dwivedi, Girish & Dwivedi, Shridhar (2007). History of Medicine: Sushruta – the Clinician – Teacher par Excellence. National Informatics Centre (Government of India).
  70. ^ Nabipour, I. (2003). "Clinical Endocrinology in the Islamic Civilization in Iran". International Journal of Endocrinology and Metabolism. 1: 43–45 [44–5].
  71. ^ a b Patlak M (2002). "New weapons to combat an ancient disease: treating diabetes". The FASEB Journal. 16 (14): 1853. PMID 12468446. {{cite journal}}: Unknown parameter |month= ignored (help)
  72. ^ Von Mehring J, Minkowski O. (1890). "Diabetes mellitus nach pankreasexstirpation". Arch Exp Pathol Pharmakol. 26: 371–387. doi:10.1007/BF01831214.
  73. ^ Banting FG, Best CH, Collip JB, Campbell WR, Fletcher AA (1991). "Pancreatic extracts in the treatment of diabetes mellitus: preliminary report. 1922". CMAJ. 145 (10): 1281–6. PMC 1335942. PMID 1933711. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  74. ^ Himsworth (1936). "Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types". Lancet. i: 127–30. doi:10.1016/S0140-6736(01)36134-2.
  75. ^ Department of Health (Malta), 1897–1972:Annual Reports.
  76. ^ Yalow RS, Berson SA (1960). "Immunoassay of endogenous plasma insulin in man". The Journal of Clinical Investigation. 39: 1157–75. doi:10.1172/JCI104130. PMC 441860. PMID 13846364. {{cite journal}}: Unknown parameter |month= ignored (help)
  77. ^ The Diabetes Control And Complications Trial Research Group (1993). "The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group". The New England Journal of Medicine. 329 (14): 977–86. doi:10.1056/NEJM199309303291401. PMID 8366922. {{cite journal}}: Unknown parameter |month= ignored (help)
  78. ^ Theodore H. Tulchinsky, Elena A. Varavikova (2008). The New Public Health, Second Edition. New York: Academic Press. p. 200. ISBN 0-12-370890-7.
  79. ^ Piwernetz K, Home PD, Snorgaard O, Antsiferov M, Staehr-Johansen K, Krans M (1993). "Monitoring the targets of the St Vincent Declaration and the implementation of quality management in diabetes care: the DIABCARE initiative. The DIABCARE Monitoring Group of the St Vincent Declaration Steering Committee". Diabetic Medicine. 10 (4): 371–7. doi:10.1111/j.1464-5491.1993.tb00083.x. PMID 8508624. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  80. ^ Dubois, HFW and Bankauskaite, V (2005). "Type 2 diabetes programmes in Europe" (PDF). Euro Observer. 7 (2): 5–6.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  81. ^ Stewart WF, Ricci JA, Chee E, Hirsch AG, Brandenburg NA (2007). "Lost productive time and costs due to diabetes and diabetic neuropathic pain in the US workforce". J. Occup. Environ. Med. 49 (6): 672–9. doi:10.1097/JOM.0b013e318065b83a. PMID 17563611. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  82. ^ Walker, Donald (2007). "Similarity Determination and Case Retrieval in an Intelligent Decision Support System for Diabetes Management" (PDF). Retrieved 2 October 2009. {{cite web}}: Unknown parameter |month= ignored (help)

External links

This template is no longer used; please see Template:Endocrine pathology for a suitable replacement

Template:Link FA Template:Link FA Template:Link FA

Retrieved from "https://en.wikipedia.org/w/index.php?title=Diabetes&oldid=341397890"