Diabetes

Last updated

Diabetes mellitus
Blue circle for diabetes.svg
Universal blue circle symbol for diabetes [1]
Pronunciation
Specialty Endocrinology
Symptoms
Complications
  • Metabolic imbalances
  • Cardiovascular diseases
  • Nerve and brain damage
  • Kidney failure
  • Gastrointestinal changes [2] [3] [4] [5]
DurationRemission may occur, but diabetes is often life-long
Types
  • Type 1 diabetes
  • Type 2 diabetes
  • Gestational diabetes
CausesInsulin insufficiency or gradual resistance
Risk factors
Diagnostic method
Treatment
Medication
Frequency463 million (8.8%) [10]
Deaths4.2 million (2019) [10]

Diabetes mellitus, often known simply as diabetes, is a group of common endocrine diseases characterized by sustained high blood sugar levels. [11] [12] Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body becoming unresponsive to the hormone's effects. [13] Classic symptoms include thirst, polyuria, weight loss, and blurred vision. If left untreated, the disease can lead to various health complications, including disorders of the cardiovascular system, eye, kidney, and nerves. [3] Untreated or poorly treated diabetes accounts for approximately 1.5 million deaths every year. [11]

Contents

The major types of diabetes are type 1 and type 2, though other forms also exist. The most common treatment for type 1 is insulin replacement therapy (insulin injections), while anti-diabetic medications (such as metformin and semaglutide) and lifestyle modifications can be used to manage type 2. Gestational diabetes, a form that arises during pregnancy in some women, normally resolves shortly after delivery.

As of 2021, an estimated 537 million people had diabetes worldwide accounting for 10.5% of the adult population, with type 2 making up about 90% of all cases. It is estimated that by 2045, approximately 783 million adults, or 1 in 8, will be living with diabetes, representing a 46% increase from the current figures. [14] The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations. [15] Rates are similar in women and men, with diabetes being the seventh leading cause of death globally. [16] [17] The global expenditure on diabetes-related healthcare is an estimated US$760 billion a year. [18]

Signs and symptoms

Overview of the most significant symptoms of diabetes Main symptoms of diabetes.svg
Overview of the most significant symptoms of diabetes
Retinopathy, nephropathy, and neuropathy are potential complications of diabetes Diabetes complications.jpg
Retinopathy, nephropathy, and neuropathy are potential complications of diabetes

The classic symptoms of untreated diabetes are polyuria, thirst, and weight loss. [19] Several other non-specific signs and symptoms may also occur, including fatigue, blurred vision, and genital itchiness due to Candida infection. [19] About half of affected individuals may also be asymptomatic. [19] Type 1 presents abruptly following a pre-clinical phase, while type 2 has a more insidious onset; patients may remain asymptomatic for many years. [20]

Diabetic ketoacidosis is a medical emergency that occurs most commonly in type 1, but may also occur in type 2 if it has been longstanding or if the individual has significant β-cell dysfunction. [21] Excessive production of ketone bodies leads to signs and symptoms including nausea, vomiting, abdominal pain, the smell of acetone in the breath, deep breathing known as Kussmaul breathing, and in severe cases decreased level of consciousness. [21] Hyperosmolar hyperglycemic state is another emergency characterised by dehydration secondary to severe hyperglycaemia, with resultant hypernatremia leading to an altered mental state and possibly coma. [22]

Hypoglycaemia is a recognised complication of insulin treatment used in diabetes. [23] An acute presentation can include mild symptoms such as sweating, trembling, and palpitations, to more serious effects including impaired cognition, confusion, seizures, coma, and rarely death. [23] Recurrent hypoglycaemic episodes may lower the glycaemic threshold at which symptoms occur, meaning mild symptoms may not appear before cognitive deterioration begins to occur. [23]

Long-term complications

The major long-term complications of diabetes relate to damage to blood vessels at both macrovascular and microvascular levels. [24] [25] Diabetes doubles the risk of cardiovascular disease, and about 75% of deaths in people with diabetes are due to coronary artery disease. [26] Other macrovascular morbidities include stroke and peripheral artery disease. [27]

Microvascular disease affects the eyes, kidneys, and nerves. [24] Damage to the retina, known as diabetic retinopathy, is the most common cause of blindness in people of working age. [19] The eyes can also be affected in other ways, including development of cataract and glaucoma. [19] It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year. [28]

Diabetic nephropathy is a major cause of chronic kidney disease, accounting for over 50% of patients on dialysis in the United States. [29] Diabetic neuropathy, damage to nerves, manifests in various ways, including sensory loss, neuropathic pain, and autonomic dysfunction (such as postural hypotension, diarrhoea, and erectile dysfunction). [19] Loss of pain sensation predisposes to trauma that can lead to diabetic foot problems (such as ulceration), the most common cause of non-traumatic lower-limb amputation. [19]

Based on extensive data and numerous cases of gallstone disease, it appears that a causal link might exist between type 2 diabetes and gallstones. People with diabetes are at a higher risk of developing gallstones compared to those without diabetes. [30]

There is a link between cognitive deficit and diabetes; studies have shown that diabetic individuals are at a greater risk of cognitive decline, and have a greater rate of decline compared to those without the disease. [31] The condition also predisposes to falls in the elderly, especially those treated with insulin. [32]

Causes

Comparison of type 1 and 2 diabetes [33]
FeatureType 1 diabetesType 2 diabetes
OnsetSuddenGradual
Age at onsetMostly in childrenMostly in adults
Body sizeThin or normal [34] Often obese
Ketoacidosis CommonRare
Autoantibodies Usually presentAbsent
Endogenous insulinLow or absentNormal, decreased
or increased
Heritability0.69 to 0.88 [35] [36] [37] 0.47 to 0.77 [38]
Prevalence

(age standardized)

<2 per 1,000 [39] ~6% (men), ~5% (women) [40]

Diabetes is classified by the World Health Organization into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes (including slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes), hyperglycemia first detected during pregnancy, "other specific types", and "unclassified diabetes". [41] Diabetes is a more variable disease than once thought, and individuals may have a combination of forms. [42]

Type 1

Type 1 accounts for 5 to 10% of diabetes cases and is the most common type diagnosed in patients under 20 years; [43] however, the older term "juvenile-onset diabetes" is no longer used as the disease not uncommonly has onset in adulthood. [29] The disease is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to severe insulin deficiency, and can be further classified as immune-mediated or idiopathic (without known cause). [43] The majority of cases are immune-mediated, in which a T cell-mediated autoimmune attack causes loss of beta cells and thus insulin deficiency. [44] Patients often have irregular and unpredictable blood sugar levels due to very low insulin and an impaired counter-response to hypoglycaemia. [45]

Autoimmune attack in type 1 diabetes. Type 1 Diabetes Mellitus.jpg
Autoimmune attack in type 1 diabetes.

Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, [46] such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans. [46] [47]

Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause. [48] LADA leaves adults with higher levels of insulin production than type 1 diabetes, but not enough insulin production for healthy blood sugar levels. [49] [50]

Type 2

Reduced insulin secretion or weaker effect of insulin on its receptor leads to high glucose content in the blood. Type 2 Diabetes Mellitus.jpg
Reduced insulin secretion or weaker effect of insulin on its receptor leads to high glucose content in the blood.

Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. [13] The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor [51] . However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes. [2] Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes. [52] The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production. [53]

Type 2 diabetes is primarily due to lifestyle factors and genetics. [54] A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. [33] [55] Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. [13] Even those who are not obese may have a high waist–hip ratio. [13]

Dietary factors such as sugar-sweetened drinks are associated with an increased risk. [56] [57] The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. [54] Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people. [58] Lack of physical activity may increase the risk of diabetes in some people. [59]

Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect. [60]

Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) and unhealthy lifestyles (including poor diet and decreased physical activity), are potential risk factors. [61]

Gestational diabetes

Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. [62] It is recommended that all pregnant women get tested starting around 24–28 weeks gestation. [63] It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time. [63] However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2. [62] Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required. [64]

Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress [65] or an increased risk of injury associated with macrosomia, such as shoulder dystocia. [66]

Other types

Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. [67] It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin. [68]

Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999. [69] Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes. [70] It was first discovered in 1990 or 1991.

The following is a list of disorders that may increase the risk of diabetes: [71]

Pathophysiology

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. Suckale08 fig3 glucose insulin day.png
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.
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells. Its release is triggered by food, chiefly food containing absorbable glucose. Glucose-insulin-release.svg
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells. Its release is triggered by food, chiefly food containing absorbable glucose.

Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1.[ citation needed ] Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus. [73]

The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. [74] Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen. [74]

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. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin. [75]

If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency. [74]

When there is too much glucose in the blood for a long time, the kidneys cannot absorb it all (reach a threshold of reabsorption) and the extra glucose gets passed out of the body through urine (glycosuria). [76] 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 is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia). [74] In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia). [77]

Diagnosis

Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following: [69]

WHO diabetes diagnostic criteria [79] [80]   edit
Condition2-hour glucoseFasting glucoseHbA1c
Unitmmol/Lmg/dLmmol/Lmg/dLmmol/molDCCT %
Normal< 7.8< 140< 6.1< 110< 42< 6.0
Impaired fasting glycaemia < 7.8< 1406.1–7.0110–12542–466.0–6.4
Impaired glucose tolerance ≥ 7.8≥ 140< 7.0< 12642–466.0–6.4
Diabetes mellitus ≥ 11.1≥ 200≥ 7.0≥ 126≥ 48≥ 6.5

A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable 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. [81] According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.

Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. [82] People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. [83] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL). [84]

Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause. [85]

Prevention

There is no known preventive measure for type 1 diabetes. [2] However, islet autoimmunity and multiple antibodies can be a strong predictor of the onset of type 1 diabetes. [86] Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed [87] by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet. [2] Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. [88] Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. [89] Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. [89] Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well. [90]

The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment. [91]

Management

Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar. [92] This can usually be accomplished with dietary changes, [93] exercise, weight loss, and use of appropriate medications (insulin, oral medications). [92]

Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. [92] [94] The goal of treatment is an A1C level below 7%. [95] [96] Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise. [92] [97] Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot. [98] [99] [100] Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure. [101]

Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population. [102]

Lifestyle

People with diabetes can benefit from education about the disease and treatment, dietary changes, and 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. [103] [104]

Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes. [105] [106] No single dietary pattern is best for all people with diabetes. [107] Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others. [105] [106] According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach. [106] For overweight people with type 2 diabetes, any diet that achieves weight loss is effective. [107] [108]

A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events. [109] The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects. [109]

Medications

Glucose control

Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems. [110] [111] There is however debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant. [112]

There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals. [113] Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists. [114]

Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. [8] It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue. [115] Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors). [115] When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications. [8]

Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached. [8] [116]

Blood pressure lowering

Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes. [117] However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg, [118] and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events. [119]

2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death. [120] There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs), [121] or aliskiren in preventing cardiovascular disease. [122] Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes. [123] There is no evidence that combining ACEIs and ARBs provides additional benefits. [123]

Aspirin

The use of aspirin to prevent cardiovascular disease in diabetes is controversial. [120] Aspirin is recommended by some in people at high risk of cardiovascular disease, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes. [124] 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%). [120] National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease. [113] [114]

Surgery

Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure. [125] Many are able to maintain normal blood sugar levels with little or no medications following surgery [126] and long-term mortality is decreased. [127] There is, however, a short-term mortality risk of less than 1% from the surgery. [128] The body mass index cutoffs for when surgery is appropriate are not yet clear. [127] It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control. [129]

A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation. [130]

Self-management and 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 in a team approach. Evidence has shown that social prescribing led to slight improvements in blood sugar control for people with type 2 diabetes. [131] Home telehealth support can be an effective management technique. [132]

The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management. [133] There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes. [133] [134]

Epidemiology

Rates of diabetes worldwide in 2014. The worldwide prevalence was 9.2%. Prevalence of Diabetes by Percent of Country Population (2014) Gradient Map.png
Rates of diabetes worldwide in 2014. The worldwide prevalence was 9.2%.
Mortality rate of diabetes worldwide in 2012 per million inhabitants
.mw-parser-output .div-col{margin-top:0.3em;column-width:30em}.mw-parser-output .div-col-small{font-size:90%}.mw-parser-output .div-col-rules{column-rule:1px solid #aaa}.mw-parser-output .div-col dl,.mw-parser-output .div-col ol,.mw-parser-output .div-col ul{margin-top:0}.mw-parser-output .div-col li,.mw-parser-output .div-col dd{page-break-inside:avoid;break-inside:avoid-column}
.mw-parser-output .legend{page-break-inside:avoid;break-inside:avoid-column}.mw-parser-output .legend-color{display:inline-block;min-width:1.25em;height:1.25em;line-height:1.25;margin:1px 0;text-align:center;border:1px solid black;background-color:transparent;color:black}.mw-parser-output .legend-text{}
28-91
92-114
115-141
142-163
164-184
185-209
210-247
248-309
310-404
405-1879 Diabetes mellitus world map-Deaths per million persons-WHO2012.svg
Mortality rate of diabetes worldwide in 2012 per million inhabitants
  28–91
  92–114
  115–141
  142–163
  164–184
  185–209
  210–247
  248–309
  310–404
  405–1879

In 2017, 425 million people had diabetes worldwide, [135] up from an estimated 382 million people in 2013 [136] and from 108 million in 1980. [137] Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980. [135] [137] Type 2 makes up about 90% of the cases. [16] [33] Some data indicate rates are roughly equal in women and men, [16] but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake. [138] [139]

The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death. [140] [137] However another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes. [137] [141] For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide, [135] using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes. [135]

Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, [137] where more than 80% of diabetic deaths occur. [142] The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. [143] The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). [137] [143] The global number of diabetes cases might increase by 48% between 2017 and 2045. [135]

As of 2020, 38% of all US adults had prediabetes. [144] Prediabetes is an early stage of diabetes.

History

Diabetes was one of the first diseases described, [145] with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." [146] The Ebers papyrus includes a recommendation for a drink to take in such cases. [147] The first described cases are believed to have been type 1 diabetes. [146] Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants. [146] [147]

The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis. [146] The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career. [146] This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa). [148]

The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice. [148]

Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight. [146] Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Best isolated and purified insulin in 1921 and 1922. [146] This was followed by the development of the long-acting insulin NPH in the 1940s. [146]

Etymology

The word diabetes ( /ˌd.əˈbtz/ or /ˌd.əˈbtɪs/ ) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon". [149] Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. [150] [151] Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through", [149] which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go". [150] The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.

The word mellitus ( /məˈltəs/ or /ˈmɛlɪtəs/ ) comes from the classical Latin word mellītus, meaning "mellite" [152] (i.e. sweetened with honey; [152] honey-sweet [153] ). The Latin word comes from mell-, which comes from mel, meaning "honey"; [152] [153] sweetness; [153] pleasant thing, [153] and the suffix -ītus, [152] whose meaning is the same as that of the English suffix "-ite". [154] It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians [ citation needed ].

Society and culture

The 1989 "St. Vincent Declaration" [155] [156] was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only 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. [157]

Diabetes stigma

Diabetes stigma describes the negative attitudes, judgment, discrimination, or prejudice against people with diabetes. Often, the stigma stems from the idea that diabetes (particularly Type 2 diabetes) resulted from poor lifestyle and unhealthy food choices rather than other causal factors like genetics and social determinants of health. [158] Manifestation of stigma can be seen throughout different cultures and contexts. Scenarios include diabetes statuses affecting marriage proposals, workplace-employment, and social standing in communities. [159]

Stigma is also seen internally, as people with diabetes can also have negative beliefs about themselves. Often these cases of self-stigma are associated with higher diabetes-specific distress, lower self-efficacy, and poorer provider-patient interactions during diabetes care. [160]

Racial and economic inequalities

Racial and ethnic minorities are disproportionately affected with higher prevalence of diabetes compared to non-minority individuals. [161] While US adults overall have a 40% chance of developing type 2 diabetes, Hispanic/Latino adults chance is more than 50%. [162] African Americans also are much more likely to be diagnosed with diabetes compared to White Americans. Asians have increased risk of diabetes as diabetes can develop at lower BMI due to differences in visceral fat compared to other races. For Asians, diabetes can develop at a younger age and lower body fat compared to other groups. Additionally, diabetes is highly underreported in Asian American people, as 1 in 3 cases are diagnosed compared to the average 1 in 5 for the nation. [163]

People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms. [164]

In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured. [165]

Naming

The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature. [166]

Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus. [167]

Other animals

Diabetes can occur in mammals or reptiles. [168] [169] Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels. [170]

In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles. [171]

Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk. [172]

The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans. [171]

See also

Related Research Articles

<span class="mw-page-title-main">Diabetic ketoacidosis</span> Medical condition

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific "fruity" smell. The onset of symptoms is usually rapid. People without a previous diagnosis of diabetes may develop DKA as the first obvious symptom.

<span class="mw-page-title-main">Blood glucose monitoring</span> Use of a glucose monitor for testing the concentration of glucose in the blood

Blood glucose monitoring is the use of a glucose meter for testing the concentration of glucose in the blood (glycemia). Particularly important in diabetes management, a blood glucose test is typically performed by piercing the skin to draw blood, then applying the blood to a chemically active disposable 'test-strip'. The other main option is continuous glucose monitoring (CGM). Different manufacturers use different technology, but most systems measure an electrical characteristic and use this to determine the glucose level in the blood. Skin-prick methods measure capillary blood glucose, whereas CGM correlates interstitial fluid glucose level to blood glucose level. Measurements may occur after fasting or at random nonfasting intervals, each of which informs diagnosis or monitoring in different ways.

<span class="mw-page-title-main">Hyperglycemia</span> Too much blood sugar, usually because of diabetes

Hyperglycemia is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/L (200 mg/dL), but symptoms may not start to become noticeable until even higher values such as 13.9–16.7 mmol/L (~250–300 mg/dL). A subject with a consistent fasting blood glucose range between ~5.6 and ~7 mmol/L is considered slightly hyperglycemic, and above 7 mmol/L is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average, however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time.

<span class="mw-page-title-main">Type 2 diabetes</span> Type of diabetes mellitus with high blood sugar and insulin resistance

Type 2 diabetes (T2D), formerly known as adult-onset diabetes, is a form of diabetes mellitus that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. Common symptoms include increased thirst, frequent urination, fatigue and unexplained weight loss. Symptoms may also include increased hunger, having a sensation of pins and needles, and sores (wounds) that do not heal. Often symptoms come on slowly. Long-term complications from high blood sugar include heart disease, strokes, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations. The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon.

Drugs used in diabetes treat diabetes mellitus by decreasing the glucose level in the blood. With the exception of insulin, most GLP receptor agonists, and pramlintide, all are administered orally and are thus also called oral hypoglycemic agents or oral antihyperglycemic agents. There are different classes of hypoglycemic drugs, and their selection depends on the nature of diabetes, age, and situation of the person, as well as other factors.

<span class="mw-page-title-main">Gestational diabetes</span> Medical condition

Gestational diabetes is a condition in which a woman without diabetes develops high blood sugar levels during pregnancy. Gestational diabetes generally results in few symptoms; however, it increases the risk of pre-eclampsia, depression, and of needing a Caesarean section. Babies born to mothers with poorly treated gestational diabetes are at increased risk of macrosomia, of having hypoglycemia after birth, and of jaundice. If untreated, diabetes can also result in stillbirth. Long term, children are at higher risk of being overweight and of developing type 2 diabetes.

Glycated hemoglobin is a form of hemoglobin (Hb) that is chemically linked to a sugar. Most monosaccharides, including glucose, galactose and fructose, spontaneously bond with hemoglobin when present in the bloodstream. However, glucose is only 21% as likely to do so as galactose and 13% as likely to do so as fructose, which may explain why glucose is used as the primary metabolic fuel in humans.

<span class="mw-page-title-main">Type 1 diabetes</span> Form of diabetes mellitus

Type 1 diabetes (T1D), formerly known as juvenile diabetes, is an autoimmune disease that originates when cells that make insulin are destroyed by the immune system. Insulin is a hormone required for the cells to use blood sugar for energy and it helps regulate glucose levels in the bloodstream. Before treatment this results in high blood sugar levels in the body. The common symptoms of this elevated blood sugar are frequent urination, increased thirst, increased hunger, weight loss, and other serious complications. Additional symptoms may include blurry vision, tiredness, and slow wound healing. Symptoms typically develop over a short period of time, often a matter of weeks if not months.

The term diabetes includes several different metabolic disorders that all, if left untreated, result in abnormally high concentrations of a sugar called glucose in the blood. Diabetes mellitus type 1 results when the pancreas no longer produces significant amounts of the hormone insulin, usually owing to the autoimmune destruction of the insulin-producing beta cells of the pancreas. Diabetes mellitus type 2, in contrast, is now thought to result from autoimmune attacks on the pancreas and/or insulin resistance. The pancreas of a person with type 2 diabetes may be producing normal or even abnormally large amounts of insulin. Other forms of diabetes mellitus, such as the various forms of maturity-onset diabetes of the young, may represent some combination of insufficient insulin production and insulin resistance. Some degree of insulin resistance may also be present in a person with type 1 diabetes.

<span class="mw-page-title-main">Diabetes and pregnancy</span> Effects of pre-existing diabetes upon pregnancy

For pregnant women with diabetes, some particular challenges exist for both mother and fetus. If the pregnant woman has diabetes as a pre-existing disorder, it can cause early labor, birth defects, and larger than average infants. Therefore, experts advise diabetics to maintain blood sugar level close to normal range about 3 months before planning for pregnancy.

Slowly evolving immune-mediated diabetes, or latent autoimmune diabetes in adults (LADA), is a form of diabetes that exhibits clinical features similar to both type 1 diabetes (T1D) and type 2 diabetes (T2D), and is sometimes referred to as type 1.5 diabetes. It is an autoimmune form of diabetes, similar to T1D, but patients with LADA often show insulin resistance, similar to T2D, and share some risk factors for the disease with T2D. Studies have shown that LADA patients have certain types of antibodies against the insulin-producing cells, and that these cells stop producing insulin more slowly than in T1D patients. Since many people develop the disease later in life, it is often misdiagnosed as type 2 diabetes.

A diabetic diet is a diet that is used by people with diabetes mellitus or high blood sugar to minimize symptoms and dangerous complications of long-term elevations in blood sugar.

<span class="mw-page-title-main">Dapagliflozin</span> Diabetes medication

Dapagliflozin, sold under the brand names Farxiga (US) and Forxiga (EU) among others, is a medication used to treat type 2 diabetes. It is also used to treat adults with heart failure and chronic kidney disease. It reversibly inhibits sodium-glucose co-transporter 2 (SGLT2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

<span class="mw-page-title-main">Prediabetes</span> Predisease state of hyperglycemia with high risk for diabetes

Prediabetes is a component of metabolic syndrome and is characterized by elevated blood sugar levels that fall below the threshold to diagnose diabetes mellitus. It usually does not cause symptoms but people with prediabetes often have obesity, dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertension. It is also associated with increased risk for cardiovascular disease (CVD). Prediabetes is more accurately considered an early stage of diabetes as health complications associated with type 2 diabetes often occur before the diagnosis of diabetes.

<span class="mw-page-title-main">Canagliflozin</span> Chemical compound

Canagliflozin, sold under the brand name Invokana among others, is a medication used to treat type 2 diabetes. It is used together with exercise and diet. It is not recommended in type 1 diabetes. It is taken by mouth.

Complications of diabetes are secondary diseases that are a result of elevated blood glucose levels that occur in diabetic patients. These complications can be divided into two types: acute and chronic. Acute complications are complications that develop rapidly and can be exemplified as diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), lactic acidosis (LA), and hypoglycemia. Chronic complications develop over time and are generally classified in two categories: microvascular and macrovascular. Microvascular complications include neuropathy, nephropathy, and retinopathy; while cardiovascular disease, stroke, and peripheral vascular disease are included in the macrovascular complications.

Prevention of type 2 diabetes can be achieved with both lifestyle changes and use of medication. The American Diabetes Association categorizes people with prediabetes, who have glycemic levels higher than normal but do not meet criteria for diabetes, as a high-risk group. Without intervention, people with prediabetes progress to type 2 diabetes with a 5% to 10% rate. Diabetes prevention is achieved through weight loss and increased physical activity, which can reduce the risk of diabetes by 50% to 60%.

Empagliflozin, sold under the brand name Jardiance, among others, is an antidiabetic medication used to improve glucose control in people with type 2 diabetes. It is not recommended for type 1 diabetes. It is taken by mouth.

<span class="mw-page-title-main">Dulaglutide</span> Diabetes medication

Dulaglutide, sold under the brand name Trulicity among others, is a medication used for the treatment of type 2 diabetes in combination with diet and exercise. It is also approved in the United States for the reduction of major adverse cardiovascular events in adults with type 2 diabetes who have established cardiovascular disease or multiple cardiovascular risk factors. It is a once-weekly injection.

This article describes the influence of exercise on the persons who suffer from diabetes.

References

  1. "Diabetes Blue Circle Symbol". International Diabetes Federation. 17 March 2006. Archived from the original on 5 August 2007.
  2. 1 2 3 4 5 6 7 8 "Diabetes". www.who.int. Retrieved 1 October 2022.
  3. 1 2 Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (July 2009). "Hyperglycemic crises in adult patients with diabetes". Diabetes Care. 32 (7): 1335–1343. doi:10.2337/dc09-9032. PMC   2699725 . PMID   19564476. Archived from the original on 2016-06-25.
  4. Krishnasamy S, Abell TL (July 2018). "Diabetic Gastroparesis: Principles and Current Trends in Management". Diabetes Therapy. 9 (Suppl 1): 1–42. doi:10.1007/s13300-018-0454-9. PMC   6028327 . PMID   29934758.
  5. Saedi E, Gheini MR, Faiz F, Arami MA (September 2016). "Diabetes mellitus and cognitive impairments". World Journal of Diabetes. 7 (17): 412–422. doi: 10.4239/wjd.v7.i17.412 . PMC   5027005 . PMID   27660698.
  6. "Causes of Diabetes". National Institute of Diabetes and Digestive and Kidney Diseases. June 2014. Archived from the original on 2 February 2016. Retrieved 10 February 2016.
  7. Heinrich J, Yang BY (January 2020). "Ambient air pollution and diabetes: a systematic review and meta-analysis". Environmental Research. 180: 108817. Bibcode:2020ER....180j8817Y. doi:10.1016/j.envres.2019.108817. PMID   31627156. S2CID   204787461 . Retrieved 21 April 2022.
  8. 1 2 3 4 Ripsin CM, Kang H, Urban RJ (January 2009). "Management of blood glucose in type 2 diabetes mellitus" (PDF). American Family Physician. 79 (1): 29–36. PMID   19145963. Archived (PDF) from the original on 2013-05-05.
  9. Brutsaert EF (February 2017). "Drug Treatment of Diabetes Mellitus". MSDManuals.com. Retrieved 12 October 2018.
  10. 1 2 "IDF DIABETES ATLAS Ninth Edition 2019" (PDF). www.diabetesatlas.org. Retrieved 18 May 2020.
  11. 1 2 "Diabetes". World Health Organization . Archived from the original on 29 January 2023. Retrieved 29 January 2023.
  12. "Diabetes Mellitus (DM) - Hormonal and Metabolic Disorders". MSD Manual Consumer Version. Retrieved 1 October 2022.
  13. 1 2 3 4 Shoback DG, Gardner D, eds. (2011). "Chapter 17". Greenspan's basic & clinical endocrinology (9th ed.). New York: McGraw-Hill Medical. ISBN   978-0-07-162243-1.
  14. "Facts & figures". International Diabetes Federation. Retrieved 2023-08-10.
  15. De Silva AP, De Silva SH, Haniffa R, Liyanage IK, Jayasinghe S, Katulanda P, et al. (April 2018). "Inequalities in the prevalence of diabetes mellitus and its risk factors in Sri Lanka: a lower middle income country". International Journal for Equity in Health. 17 (1): 45. doi: 10.1186/s12939-018-0759-3 . PMC   5905173 . PMID   29665834.
  16. 1 2 3 Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al. (December 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–2196. doi:10.1016/S0140-6736(12)61729-2. PMC   6350784 . PMID   23245607.
  17. "The top 10 causes of death". www.who.int. Retrieved 18 May 2020.
  18. Bommer C, Sagalova V, Heesemann E, Manne-Goehler J, Atun R, Bärnighausen T, et al. (May 2018). "Global Economic Burden of Diabetes in Adults: Projections From 2015 to 2030". Diabetes Care. 41 (5): 963–970. doi: 10.2337/dc17-1962 . PMID   29475843. S2CID   3538441.
  19. 1 2 3 4 5 6 7 Feather, Adam; Randall, David; Waterhouse, Mona (2021). Kumar and Clark's Clinical Medicine (10th ed.). Elsevier. pp. 699–741. ISBN   978-0-7020-7868-2.
  20. Goldman, Lee; Schafer, Andrew (2020). Goldman-Cecil Medicine (26th ed.). Elsevier. pp. 1490–1510. ISBN   978-0-323-53266-2.
  21. 1 2 Penman, Ian; Ralston, Stuart; Strachan, Mark; Hobson, Richard (2023). Davidson's Principles and Practice of Medicine (24th ed.). Elsevier. pp. 703–753. ISBN   978-0-7020-8348-8.
  22. Willix, Clare; Griffiths, Emma; Singleton, Sally (May 2019). "Hyperglycaemic presentations in type 2 diabetes". Australian Journal of General Practice. 48 (5): 263–267. doi: 10.31128/AJGP-12-18-4785 . PMID   31129935. S2CID   167207067.
  23. 1 2 3 Amiel, Stephanie A. (2021-05-01). "The consequences of hypoglycaemia". Diabetologia. 64 (5): 963–970. doi:10.1007/s00125-020-05366-3. ISSN   1432-0428. PMC   8012317 . PMID   33550443.
  24. 1 2 "Diabetes - long-term effects". Better Health Channel. Victoria: Department of Health. Retrieved 2023-08-12.
  25. Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, et al. (June 2010). "Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies". Lancet. 375 (9733): 2215–2222. doi:10.1016/S0140-6736(10)60484-9. PMC   2904878 . PMID   20609967.
  26. O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA, et al. (January 2013). "2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. 127 (4): e368. doi: 10.1161/CIR.0b013e3182742cf6 . PMID   23247304.
  27. Papatheodorou K, Banach M, Bekiari E, Rizzo M, Edmonds M (11 March 2018). "Complications of Diabetes 2017". Journal of Diabetes Research. 2018: 3086167. doi: 10.1155/2018/3086167 . PMC   5866895 . PMID   29713648.
  28. "Diabetes eye care". MedlinePlus. Maryland: National Library of Medicine. Retrieved 2018-03-27.
  29. 1 2 Wing, Edward J; Schiffman, Fred (2022). Cecil Essentials of Medicine (10th ed.). Pennsylvania: Elsevier. pp. 282–297, 662–677. ISBN   978-0-323-72271-1.
  30. Yuan, Shuai; Gill, Dipender; Giovannucci, Edward L.; Larsson, Susanna C. (March 2022). "Obesity, Type 2 Diabetes, Lifestyle Factors, and Risk of Gallstone Disease: A Mendelian Randomization Investigation". Clinical Gastroenterology and Hepatology. 20 (3): e529–e537. doi: 10.1016/j.cgh.2020.12.034 . hdl: 10044/1/86461 . PMID   33418132.
  31. Cukierman T, Gerstein HC, Williamson JD (December 2005). "Cognitive decline and dementia in diabetes--systematic overview of prospective observational studies". Diabetologia. 48 (12): 2460–2469. doi: 10.1007/s00125-005-0023-4 . PMID   16283246.
  32. Yang Y, Hu X, Zhang Q, Zou R (November 2016). "Diabetes mellitus and risk of falls in older adults: a systematic review and meta-analysis". Age and Ageing. 45 (6): 761–767. doi: 10.1093/ageing/afw140 . PMID   27515679.
  33. 1 2 3 Williams textbook of endocrinology (12th ed.). Elsevier/Saunders. 2011. pp. 1371–1435. ISBN   978-1-4377-0324-5.
  34. Lambert P, Bingley PJ (2002). "What is Type 1 Diabetes?". Medicine. 30: 1–5. doi:10.1383/medc.30.1.1.28264.
  35. Skov J, Eriksson D, Kuja-Halkola R, Höijer J, Gudbjörnsdottir S, Svensson AM, et al. (May 2020). "Co-aggregation and heritability of organ-specific autoimmunity: a population-based twin study". European Journal of Endocrinology. 182 (5): 473–480. doi:10.1530/EJE-20-0049. PMC   7182094 . PMID   32229696.
  36. Hyttinen V, Kaprio J, Kinnunen L, Koskenvuo M, Tuomilehto J (April 2003). "Genetic liability of type 1 diabetes and the onset age among 22,650 young Finnish twin pairs: a nationwide follow-up study". Diabetes. 52 (4): 1052–1055. doi: 10.2337/diabetes.52.4.1052 . PMID   12663480.
  37. Condon J, Shaw JE, Luciano M, Kyvik KO, Martin NG, Duffy DL (February 2008). "A study of diabetes mellitus within a large sample of Australian twins" (PDF). Twin Research and Human Genetics. 11 (1): 28–40. doi:10.1375/twin.11.1.28. PMID   18251672. S2CID   18072879.
  38. Willemsen G, Ward KJ, Bell CG, Christensen K, Bowden J, Dalgård C, et al. (December 2015). "The Concordance and Heritability of Type 2 Diabetes in 34,166 Twin Pairs From International Twin Registers: The Discordant Twin (DISCOTWIN) Consortium". Twin Research and Human Genetics. 18 (6): 762–771. doi: 10.1017/thg.2015.83 . PMID   26678054. S2CID   17854531.
  39. Lin X, Xu Y, Pan X, Xu J, Ding Y, Sun X, et al. (September 2020). "Global, regional, and national burden and trend of diabetes in 195 countries and territories: an analysis from 1990 to 2025". Scientific Reports. 10 (1): 14790. Bibcode:2020NatSR..1014790L. doi:10.1038/s41598-020-71908-9. PMC   7478957 . PMID   32901098.
  40. Tinajero MG, Malik VS (September 2021). "An Update on the Epidemiology of Type 2 Diabetes: A Global Perspective". Endocrinology and Metabolism Clinics of North America. 50 (3): 337–355. doi:10.1016/j.ecl.2021.05.013. PMID   34399949.
  41. Classification of diabetes mellitus 2019 (Report). Geneva: World Health Organisation. 2019. ISBN   978-92-4-151570-2 . Retrieved 2023-08-15.
  42. Tuomi T, Santoro N, Caprio S, Cai M, Weng J, Groop L (March 2014). "The many faces of diabetes: a disease with increasing heterogeneity". Lancet. 383 (9922): 1084–1094. doi:10.1016/S0140-6736(13)62219-9. PMID   24315621. S2CID   12679248.
  43. 1 2 Kumar, V; Abbas, A; Aster, J (2021). Robbins & Cotran Pathologic Basis of Disease (10th ed.). Pennsylvania: Elsevier. pp. 1065–1132. ISBN   978-0-323-60992-0.
  44. Rother KI (April 2007). "Diabetes treatment--bridging the divide". The New England Journal of Medicine. 356 (15): 1499–1501. doi:10.1056/NEJMp078030. PMC   4152979 . PMID   17429082.
  45. Brutsaert, EF (September 2022). "Diabetes Mellitus (DM)". MSD Manual Professional Version. Merck Publishing . Retrieved 2023-08-15.
  46. 1 2 Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC   4539350 . PMID   26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
  47. Butalia S, Kaplan GG, Khokhar B, Rabi DM (December 2016). "Environmental Risk Factors and Type 1 Diabetes: Past, Present, and Future". Canadian Journal of Diabetes (Review). 40 (6): 586–593. doi:10.1016/j.jcjd.2016.05.002. PMID   27545597.
  48. Laugesen E, Østergaard JA, Leslie RD (July 2015). "Latent autoimmune diabetes of the adult: current knowledge and uncertainty". Diabetic Medicine. 32 (7): 843–852. doi:10.1111/dme.12700. PMC   4676295 . PMID   25601320.
  49. "What Is Diabetes?". Diabetes Daily. Retrieved 2023-09-10.
  50. Nolasco-Rosales, Germán Alberto; Ramírez-González, Dania; Rodríguez-Sánchez, Ester; Ávila-Fernandez, Ángela; Villar-Juarez, Guillermo Efrén; González-Castro, Thelma Beatriz; Tovilla-Zárate, Carlos Alfonso; Guzmán-Priego, Crystell Guadalupe; Genis-Mendoza, Alma Delia; Ble-Castillo, Jorge Luis; Marín-Medina, Alejandro; Juárez-Rojop, Isela Esther (2023-04-29). "Identification and phenotypic characterization of patients with LADA in a population of southeast Mexico". Scientific Reports. 13 (1): 7029. Bibcode:2023NatSR..13.7029N. doi:10.1038/s41598-023-34171-2. ISSN   2045-2322. PMC   10148806 . PMID   37120620.
  51. Freeman, Andrew M.; Acevedo, Luis A.; Pennings, Nicholas (2024), "Insulin Resistance", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29939616 , retrieved 2024-02-13
  52. American Diabetes Association (January 2017). "2. Classification and Diagnosis of Diabetes". Diabetes Care. 40 (Suppl 1): S11–S24. doi: 10.2337/dc17-S005 . PMID   27979889.
  53. Carris NW, Magness RR, Labovitz AJ (February 2019). "Prevention of Diabetes Mellitus in Patients With Prediabetes". The American Journal of Cardiology. 123 (3): 507–512. doi:10.1016/j.amjcard.2018.10.032. PMC   6350898 . PMID   30528418.
  54. 1 2 Risérus U, Willett WC, Hu FB (January 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.
  55. Fletcher, Barbara; Gulanick, Meg; Lamendola, Cindy (January 2002). "Risk factors for type 2 diabetes mellitus". The Journal of Cardiovascular Nursing. 16 (2): 17–23. doi:10.1097/00005082-200201000-00003. ISSN   0889-4655. PMID   11800065.
  56. Malik VS, Popkin BM, Bray GA, Després JP, Hu FB (March 2010). "Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk". Circulation. 121 (11): 1356–1364. doi:10.1161/CIRCULATIONAHA.109.876185. PMC   2862465 . PMID   20308626.
  57. Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB (November 2010). "Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis". Diabetes Care. 33 (11): 2477–2483. doi:10.2337/dc10-1079. PMC   2963518 . PMID   20693348.
  58. Hu EA, Pan A, Malik V, Sun Q (March 2012). "White rice consumption and risk of type 2 diabetes: meta-analysis and systematic review". BMJ. 344: e1454. doi:10.1136/bmj.e1454. PMC   3307808 . PMID   22422870.
  59. Lee IM, Shiroma EJ, Lobelo F, Puska P, Blair SN, Katzmarzyk PT (July 2012). "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". Lancet. 380 (9838): 219–229. doi:10.1016/S0140-6736(12)61031-9. PMC   3645500 . PMID   22818936.
  60. Huang H, Yan P, Shan Z, Chen S, Li M, Luo C, et al. (November 2015). "Adverse childhood experiences and risk of type 2 diabetes: A systematic review and meta-analysis". Metabolism. 64 (11): 1408–1418. doi:10.1016/j.metabol.2015.08.019. PMID   26404480.
  61. Zhang Y, Liu Y, Su Y, You Y, Ma Y, Yang G, et al. (November 2017). "The metabolic side effects of 12 antipsychotic drugs used for the treatment of schizophrenia on glucose: a network meta-analysis". BMC Psychiatry. 17 (1): 373. doi: 10.1186/s12888-017-1539-0 . PMC   5698995 . PMID   29162032.
  62. 1 2 "National Diabetes Clearinghouse (NDIC): National Diabetes Statistics 2011". U.S. Department of Health and Human Services. Archived from the original on 17 April 2014. Retrieved 22 April 2014.
  63. 1 2 Soldavini J (November 2019). "Krause's Food & The Nutrition Care Process". Journal of Nutrition Education and Behavior. 51 (10): 1225. doi:10.1016/j.jneb.2019.06.022. ISSN   1499-4046. S2CID   209272489.
  64. "Managing & Treating Gestational Diabetes | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 2019-05-06.
  65. Tarvonen M, Hovi P, Sainio S, Vuorela P, Andersson S, Teramo K (November 2021). "Intrapartal cardiotocographic patterns and hypoxia-related perinatal outcomes in pregnancies complicated by gestational diabetes mellitus". Acta Diabetologica. 58 (11): 1563–1573. doi: 10.1007/s00592-021-01756-0 . PMC   8505288 . PMID   34151398. S2CID   235487220.
  66. National Collaborating Centre for Women's and Children's Health (February 2015). "Intrapartum care". Diabetes in Pregnancy: Management of diabetes and its complications from preconception to the postnatal period. National Institute for Health and Care Excellence (UK).
  67. "Monogenic Forms of Diabetes". National institute of diabetes and digestive and kidney diseases. US NIH. Archived from the original on 12 March 2017. Retrieved 12 March 2017.
  68. Thanabalasingham G, Owen KR (October 2011). "Diagnosis and management of maturity onset diabetes of the young (MODY)". BMJ. 343 (oct19 3): d6044. doi:10.1136/bmj.d6044. PMID   22012810. S2CID   44891167.
  69. 1 2 "Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications" (PDF). World Health Organization. 1999. Archived (PDF) from the original on 2003-03-08.
  70. Cleland SJ, Fisher BM, Colhoun HM, Sattar N, Petrie JR (July 2013). "Insulin resistance in type 1 diabetes: what is 'double diabetes' and what are the risks?". Diabetologia. National Library of Medicine. 56 (7): 1462–1470. doi:10.1007/s00125-013-2904-2. PMC   3671104 . PMID   23613085.
  71. Unless otherwise specified, reference is: Table 20-5 in Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN   978-1-4160-2973-1.
  72. Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, et al. (February 2010). "Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials". Lancet. 375 (9716): 735–742. doi:10.1016/S0140-6736(09)61965-6. PMID   20167359. S2CID   11544414.
  73. "Insulin Basics". American Diabetes Association. Archived from the original on 21 June 2023. Retrieved 25 June 2023.
  74. 1 2 3 4 Shoback DG, Gardner D, eds. (2011). Greenspan's basic & clinical endocrinology (9th ed.). McGraw-Hill Medical. ISBN   978-0-07-162243-1.
  75. Barrett KE, et al. (2012). Ganong's review of medical physiology (24th ed.). McGraw-Hill Medical. ISBN   978-0-07-178003-2.
  76. Murray RK, et al. (2012). Harper's illustrated biochemistry (29th ed.). McGraw-Hill Medical. ISBN   978-0-07-176576-3.
  77. Mogotlane S (2013). Juta's Complete Textbook of Medical Surgical Nursing. Cape Town: Juta. p. 839.
  78. "Summary of revisions for the 2010 Clinical Practice Recommendations". Diabetes Care. 33 (Suppl 1): S3. January 2010. doi:10.2337/dc10-S003. PMC   2797388 . PMID   20042773. Archived from the original on 13 January 2010. Retrieved 29 January 2010.
  79. 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.
  80. 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.
  81. Saydah SH, Miret M, Sung J, Varas C, Gause D, Brancati FL (August 2001). "Postchallenge hyperglycemia and mortality in a national sample of U.S. adults". Diabetes Care. 24 (8): 1397–1402. doi: 10.2337/diacare.24.8.1397 . PMID   11473076.
  82. Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: report of a WHO/IDF consultation (PDF). World Health Organization. 2006. p. 21. ISBN   978-92-4-159493-6. Archived (PDF) from the original on 11 May 2012.
  83. Santaguida PL, Balion C, Hunt D, Morrison K, Gerstein H, Raina P, et al. (August 2005). "Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose". Evidence Report/Technology Assessment. Agency for Healthcare Research and Quality (128): 1–11. PMC   4780988 . PMID   16194123. Archived from the original on 16 September 2008. Retrieved 20 July 2008.
  84. Bartoli E, Fra GP, Carnevale Schianca GP (February 2011). "The oral glucose tolerance test (OGTT) revisited". European Journal of Internal Medicine. 22 (1): 8–12. doi:10.1016/j.ejim.2010.07.008. PMID   21238885.
  85. Selvin E, Steffes MW, Zhu H, Matsushita K, Wagenknecht L, Pankow J, et al. (March 2010). "Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults". The New England Journal of Medicine. 362 (9): 800–811. CiteSeerX   10.1.1.589.1658 . doi:10.1056/NEJMoa0908359. PMC   2872990 . PMID   20200384.
  86. Jacobsen, Laura M.; Haller, Michael J.; Schatz, Desmond A. (2018-03-06). "Understanding Pre-Type 1 Diabetes: The Key to Prevention". Frontiers in Endocrinology. 9: 70. doi: 10.3389/fendo.2018.00070 . PMC   5845548 . PMID   29559955.
  87. "Tackling risk factors for type 2 diabetes in adolescents: PRE-STARt study in Euskadi". Anales de Pediatria. Anales de Pediatría. 95 (3): 186–196. 2020. doi: 10.1016/j.anpedi.2020.11.001 . PMID   33388268.
  88. Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, et al. (August 2016). "Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013". BMJ. 354: i3857. doi:10.1136/bmj.i3857. PMC   4979358 . PMID   27510511.
  89. 1 2 "Simple Steps to Preventing Diabetes". The Nutrition Source. Harvard T.H. Chan School of Public Health. 18 September 2012. Archived from the original on 25 April 2014.
  90. Willi C, Bodenmann P, Ghali WA, Faris PD, Cornuz J (December 2007). "Active smoking and the risk of type 2 diabetes: a systematic review and meta-analysis". JAMA. 298 (22): 2654–2664. doi:10.1001/jama.298.22.2654. PMID   18073361. S2CID   30550981.
  91. "Chronic diseases and their common risk factors" (PDF). World Health Organization. 2005. Archived (PDF) from the original on 2016-10-17. Retrieved 30 August 2016.
  92. 1 2 3 4 "Managing diabetes". National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 1 December 2016. Retrieved 4 February 2023.
  93. Toumpanakis A, Turnbull T, Alba-Barba I (2018-10-30). "Effectiveness of plant-based diets in promoting well-being in the management of type 2 diabetes: a systematic review". BMJ Open Diabetes Research & Care. 6 (1): e000534. doi:10.1136/bmjdrc-2018-000534. PMC   6235058 . PMID   30487971.
  94. The Diabetes Control and Complications Trial Research Group (April 1995). "The effect of intensive diabetes therapy on the development and progression of neuropathy". Annals of Internal Medicine. 122 (8): 561–568. doi:10.7326/0003-4819-122-8-199504150-00001. PMID   7887548. S2CID   24754081.
  95. "The A1C test and diabetes". National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 1 April 2018. Retrieved 4 February 2023.
  96. Qaseem A, Wilt TJ, Kansagara D, et al. (April 2018). "Hemoglobin A1c Targets for Glycemic Control With Pharmacologic Therapy for Nonpregnant Adults With Type 2 Diabetes Mellitus: A Guidance Statement Update From the American College of Physicians". Annals of Internal Medicine. 168 (8): 569–576. doi: 10.7326/M17-0939 . PMID   29507945.
  97. National Institute for Health and Clinical Excellence . Clinical guideline 66: Type 2 diabetes . London, 2008.
  98. Bus SA, van Deursen RW, Armstrong DG, Lewis JE, Caravaggi CF, Cavanagh PR (January 2016). "Footwear and offloading interventions to prevent and heal foot ulcers and reduce plantar pressure in patients with diabetes: a systematic review". Diabetes/Metabolism Research and Reviews. 32 (Suppl 1): 99–118. doi: 10.1002/dmrr.2702 . PMID   26342178. S2CID   24862853.
  99. Heuch L, Streak Gomersall J (July 2016). "Effectiveness of offloading methods in preventing primary diabetic foot ulcers in adults with diabetes: a systematic review". JBI Database of Systematic Reviews and Implementation Reports. 14 (7): 236–265. doi:10.11124/JBISRIR-2016-003013. PMID   27532798. S2CID   12012686.
  100. van Netten JJ, Raspovic A, Lavery LA, Monteiro-Soares M, Rasmussen A, Sacco IC, Bus SA (March 2020). "Prevention of foot ulcers in the at-risk patient with diabetes: a systematic review" (PDF). Diabetes/Metabolism Research and Reviews. 36 (S1 Suppl 1): e3270. doi:10.1002/dmrr.3270. PMID   31957213. S2CID   210830578.
  101. Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM (January 2004). "Preventive foot care in diabetes". Diabetes Care. 27 (suppl_1): S63–S64. doi: 10.2337/diacare.27.2007.S63 . PMID   14693928.
  102. McBain H, Mulligan K, Haddad M, Flood C, Jones J, Simpson A, et al. (Cochrane Metabolic and Endocrine Disorders Group) (April 2016). "Self management interventions for type 2 diabetes in adult people with severe mental illness". The Cochrane Database of Systematic Reviews. 2016 (4): CD011361. doi:10.1002/14651858.CD011361.pub2. PMC   10201333 . PMID   27120555.
  103. Haw JS, Galaviz KI, Straus AN, et al. (December 2017). "Long-term Sustainability of Diabetes Prevention Approaches: A Systematic Review and Meta-analysis of Randomized Clinical Trials". JAMA Internal Medicine. 177 (12): 1808–1817. doi:10.1001/jamainternmed.2017.6040. PMC   5820728 . PMID   29114778.
  104. Mottalib A, Kasetty M, Mar JY, Elseaidy T, Ashrafzadeh S, Hamdy O (August 2017). "Weight Management in Patients with Type 1 Diabetes and Obesity". Current Diabetes Reports. 17 (10): 92. doi:10.1007/s11892-017-0918-8. PMC   5569154 . PMID   28836234.
  105. 1 2 American Diabetes Association (January 2019). "5. Lifestyle Management: Standards of Medical Care in Diabetes-2019". Diabetes Care. 42 (Suppl 1): S46–S60. doi: 10.2337/dc19-S005 . PMID   30559231.
  106. 1 2 3 Evert AB, Dennison M, Gardner CD, et al. (May 2019). "Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report". Diabetes Care (Professional society guidelines). 42 (5): 731–754. doi: 10.2337/dci19-0014 . PMC   7011201 . PMID   31000505.
  107. 1 2 Emadian A, Andrews RC, England CY, Wallace V, Thompson JL (November 2015). "The effect of macronutrients on glycaemic control: a systematic review of dietary randomised controlled trials in overweight and obese adults with type 2 diabetes in which there was no difference in weight loss between treatment groups". The British Journal of Nutrition. 114 (10): 1656–1666. doi:10.1017/S0007114515003475. PMC   4657029 . PMID   26411958.
  108. Grams J, Garvey WT (June 2015). "Weight Loss and the Prevention and Treatment of Type 2 Diabetes Using Lifestyle Therapy, Pharmacotherapy, and Bariatric Surgery: Mechanisms of Action". Current Obesity Reports. 4 (2): 287–302. doi:10.1007/s13679-015-0155-x. PMID   26627223. S2CID   207474124.
  109. 1 2 Lohner, Szimonetta; Kuellenberg de Gaudry, Daniela; Toews, Ingrid; Ferenci, Tamas; Meerpohl, Joerg J (2020-05-25). Cochrane Metabolic and Endocrine Disorders Group (ed.). "Non-nutritive sweeteners for diabetes mellitus". Cochrane Database of Systematic Reviews. 2020 (5): CD012885. doi:10.1002/14651858.CD012885.pub2. PMC   7387865 . PMID   32449201.
  110. Rosberger DF (December 2013). "Diabetic retinopathy: current concepts and emerging therapy". Endocrinology and Metabolism Clinics of North America. 42 (4): 721–745. doi:10.1016/j.ecl.2013.08.001. PMID   24286948.
  111. MacIsaac RJ, Jerums G, Ekinci EI (March 2018). "Glycemic Control as Primary Prevention for Diabetic Kidney Disease". Advances in Chronic Kidney Disease. 25 (2): 141–148. doi:10.1053/j.ackd.2017.11.003. PMID   29580578.
  112. Pozzilli P, Strollo R, Bonora E (March 2014). "One size does not fit all glycemic targets for type 2 diabetes". Journal of Diabetes Investigation. 5 (2): 134–141. doi:10.1111/jdi.12206. PMC   4023573 . PMID   24843750.
  113. 1 2 "Type 1 diabetes in adults: diagnosis and management". www.nice.org.uk. National Institute for Health and Care Excellence. 26 August 2015. Retrieved 25 December 2020.
  114. 1 2 "Type 2 diabetes in adults: management". www.nice.org.uk. National Institute for Health and Care Excellence. 2 December 2015. Retrieved 25 December 2020.
  115. 1 2 Krentz AJ, Bailey CJ (2005). "Oral antidiabetic agents: current role in type 2 diabetes mellitus". Drugs. 65 (3): 385–411. doi:10.2165/00003495-200565030-00005. PMID   15669880. S2CID   29670619.
  116. Consumer Reports; American College of Physicians (April 2012), "Choosing a type 2 diabetes drug – Why the best first choice is often the oldest drug" (PDF), High Value Care, Consumer Reports, archived (PDF) from the original on July 2, 2014, retrieved August 14, 2012
  117. Mitchell S, Malanda B, Damasceno A, et al. (September 2019). "A Roadmap on the Prevention of Cardiovascular Disease Among People Living With Diabetes". Global Heart. 14 (3): 215–240. doi: 10.1016/j.gheart.2019.07.009 . PMID   31451236.
  118. Brunström M, Carlberg B (February 2016). "Effect of antihypertensive treatment at different blood pressure levels in patients with diabetes mellitus: systematic review and meta-analyses". BMJ. 352: i717. doi:10.1136/bmj.i717. PMC   4770818 . PMID   26920333.
  119. Brunström M, Carlberg B (September 2019). "Benefits and harms of lower blood pressure treatment targets: systematic review and meta-analysis of randomised placebo-controlled trials". BMJ Open. 9 (9): e026686. doi:10.1136/bmjopen-2018-026686. PMC   6773352 . PMID   31575567.
  120. 1 2 3 Fox CS, Golden SH, Anderson C, et al. (September 2015). "Update on Prevention of Cardiovascular Disease in Adults With Type 2 Diabetes Mellitus in Light of Recent Evidence: A Scientific Statement From the American Heart Association and the American Diabetes Association". Diabetes Care. 38 (9): 1777–1803. doi:10.2337/dci15-0012. PMC   4876675 . PMID   26246459.
  121. Cheng J, Zhang W, Zhang X, et al. (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–785. doi: 10.1001/jamainternmed.2014.348 . PMID   24687000.
  122. Zheng SL, Roddick AJ, Ayis S (September 2017). "Effects of aliskiren on mortality, cardiovascular outcomes and adverse events in patients with diabetes and cardiovascular disease or risk: A systematic review and meta-analysis of 13,395 patients". Diabetes & Vascular Disease Research. 14 (5): 400–406. doi:10.1177/1479164117715854. PMC   5600262 . PMID   28844155.
  123. 1 2 Catalá-López F, Macías Saint-Gerons D, González-Bermejo D, et al. (March 2016). "Cardiovascular and Renal Outcomes of Renin-Angiotensin System Blockade in Adult Patients with Diabetes Mellitus: A Systematic Review with Network Meta-Analyses". PLOS Medicine. 13 (3): e1001971. doi: 10.1371/journal.pmed.1001971 . PMC   4783064 . PMID   26954482.
  124. Pignone M, Alberts MJ, Colwell JA, et al. (June 2010). "Aspirin for primary prevention of cardiovascular events in people with diabetes: a position statement of the American Diabetes Association, a scientific statement of the American Heart Association, and an expert consensus document of the American College of Cardiology Foundation". Diabetes Care. 33 (6): 1395–1402. doi:10.2337/dc10-0555. PMC   2875463 . PMID   20508233.
  125. Picot J, Jones J, Colquitt JL, Gospodarevskaya E, Loveman E, Baxter L, Clegg AJ (September 2009). "The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation". Health Technology Assessment. 13 (41): 1–190, 215–357, iii–iv. doi: 10.3310/hta13410 . hdl: 10536/DRO/DU:30064294 . PMID   19726018.
  126. Frachetti KJ, Goldfine AB (April 2009). "Bariatric surgery for diabetes management". Current Opinion in Endocrinology, Diabetes and Obesity. 16 (2): 119–124. doi: 10.1097/MED.0b013e32832912e7 . PMID   19276974. S2CID   31797748.
  127. 1 2 Schulman AP, del Genio F, Sinha N, Rubino F (September–October 2009). ""Metabolic" surgery for treatment of type 2 diabetes mellitus". Endocrine Practice. 15 (6): 624–631. doi:10.4158/EP09170.RAR. PMID   19625245.
  128. Colucci RA (January 2011). "Bariatric surgery in patients with type 2 diabetes: a viable option". Postgraduate Medicine. 123 (1): 24–33. doi:10.3810/pgm.2011.01.2242. PMID   21293081. S2CID   207551737.
  129. Dixon JB, le Roux CW, Rubino F, Zimmet P (June 2012). "Bariatric surgery for type 2 diabetes". Lancet. 379 (9833): 2300–2311. doi:10.1016/S0140-6736(12)60401-2. PMID   22683132. S2CID   5198462.
  130. "Pancreas Transplantation". American Diabetes Association. Archived from the original on 13 April 2014. Retrieved 9 April 2014.
  131. "Can social prescribing improve the health of people with diabetes?". National Institute for Health and Care Research - NIHR Evidence. 2024. doi:10.3310/nihrevidence_61876. S2CID   267264134 . Retrieved 26 January 2024.
  132. Polisena J, Tran K, Cimon K, Hutton B, McGill S, Palmer K (October 2009). "Home telehealth for diabetes management: a systematic review and meta-analysis". Diabetes, Obesity & Metabolism. 11 (10): 913–930. doi:10.1111/j.1463-1326.2009.01057.x. PMID   19531058. S2CID   44260857.
  133. 1 2 Pal K, Eastwood SV, Michie S, et al. (Cochrane Metabolic and Endocrine Disorders Group) (March 2013). "Computer-based diabetes self-management interventions for adults with type 2 diabetes mellitus". The Cochrane Database of Systematic Reviews. 2013 (3): CD008776. doi:10.1002/14651858.CD008776.pub2. PMC   6486319 . PMID   23543567.
  134. Wei I, Pappas Y, Car J, Sheikh A, Majeed A, et al. (Cochrane Metabolic and Endocrine Disorders Group) (December 2011). "Computer-assisted versus oral-and-written dietary history taking for diabetes mellitus". The Cochrane Database of Systematic Reviews. 2011 (12): CD008488. doi:10.1002/14651858.CD008488.pub2. PMC   6486022 . PMID   22161430.
  135. 1 2 3 4 5 Elflein J (10 December 2019). Estimated number diabetics worldwide.
  136. Shi Y, Hu FB (June 2014). "The global implications of diabetes and cancer". Lancet. 383 (9933): 1947–1948. doi:10.1016/S0140-6736(14)60886-2. PMID   24910221. S2CID   7496891.
  137. 1 2 3 4 5 6 "Global Report on Diabetes" (PDF). World Health Organization. 2016. Retrieved 20 September 2018.
  138. Gale EA, Gillespie KM (January 2001). "Diabetes and gender". Diabetologia. 44 (1): 3–15. doi: 10.1007/s001250051573 . PMID   11206408.
  139. Meisinger C, Thorand B, Schneider A, Stieber J, Döring A, Löwel H (January 2002). "Sex differences in risk factors for incident type 2 diabetes mellitus: the MONICA Augsburg cohort study". Archives of Internal Medicine. 162 (1): 82–89. doi: 10.1001/archinte.162.1.82 . PMID   11784224.
  140. "The top 10 causes of death Fact sheet N°310". World Health Organization. October 2013. Archived from the original on 30 May 2017.
  141. Public Health Agency of Canada, Diabetes in Canada: Facts and figures from a public health perspective. Ottawa, 2011.
  142. Mathers CD, Loncar D (November 2006). "Projections of global mortality and burden of disease from 2002 to 2030". PLOS Medicine. 3 (11): e442. doi: 10.1371/journal.pmed.0030442 . PMC   1664601 . PMID   17132052.
  143. 1 2 Wild S, Roglic G, Green A, Sicree R, King H (May 2004). "Global prevalence of diabetes: estimates for the year 2000 and projections for 2030". Diabetes Care. 27 (5): 1047–1053. doi: 10.2337/diacare.27.5.1047 . PMID   15111519.
  144. "Prevalence of Prediabetes Among Adults - Diabetes". CDC. 2018-03-13. Retrieved 2022-12-15.
  145. Ripoll BC, Leutholtz I (2011-04-25). Exercise and disease management (2nd ed.). Boca Raton: CRC Press. p. 25. ISBN   978-1-4398-2759-8. Archived from the original on 2016-04-03.
  146. 1 2 3 4 5 6 7 8 Poretsky L, ed. (2009). Principles of diabetes mellitus (2nd ed.). New York: Springer. p. 3. ISBN   978-0-387-09840-1. Archived from the original on 2016-04-04.
  147. 1 2 Roberts J (2015). "Sickening sweet". Distillations. Vol. 1, no. 4. pp. 12–15. Retrieved 20 March 2018.
  148. 1 2 Laios K, Karamanou M, Saridaki Z, Androutsos G (2012). "Aretaeus of Cappadocia and the first description of diabetes" (PDF). Hormones. 11 (1): 109–113. doi:10.1007/BF03401545. PMID   22450352. S2CID   4730719. Archived (PDF) from the original on 2017-01-04.
  149. 1 2 Oxford English Dictionary. diabetes. Retrieved 2011-06-10.
  150. 1 2 Harper D (2001–2010). "Online Etymology Dictionary. diabetes.". Archived from the original on 2012-01-13. Retrieved 2011-06-10.
  151. Aretaeus, De causis et signis acutorum morborum (lib. 2), Κεφ. β. περὶ Διαβήτεω (Chapter 2, On Diabetes, Greek original) Archived 2014-07-02 at the Wayback Machine , on Perseus
  152. 1 2 3 4 Oxford English Dictionary. mellite. Retrieved 2011-06-10.
  153. 1 2 3 4 "MyEtimology. mellitus.". Archived from the original on 2011-03-16. Retrieved 2011-06-10.{{cite web}}: CS1 maint: unfit URL (link)
  154. Oxford English Dictionary. -ite. Retrieved 2011-06-10.
  155. Tulchinsky TH, Varavikova EA (2008). The New Public Health, Second Edition. New York: Academic Press. p. 200. ISBN   978-0-12-370890-8.
  156. Piwernetz K, Home PD, Snorgaard O, Antsiferov M, Staehr-Johansen K, Krans M (May 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): 371–377. doi:10.1111/j.1464-5491.1993.tb00083.x. PMID   8508624. S2CID   9931183.
  157. Dubois H, Bankauskaite V (2005). "Type 2 diabetes programmes in Europe" (PDF). Euro Observer. 7 (2): 5–6. Archived (PDF) from the original on 2012-10-24.
  158. CDC (2022-11-03). "Diabetes Stigma: Learn About It, Recognize It, Reduce It". Centers for Disease Control and Prevention. Retrieved 2023-10-31.
  159. Schabert, Jasmin; Browne, Jessica L.; Mosely, Kylie; Speight, Jane (2013-03-01). "Social Stigma in Diabetes". The Patient - Patient-Centered Outcomes Research. 6 (1): 1–10. doi: 10.1007/s40271-012-0001-0 . ISSN   1178-1661. PMID   23322536. S2CID   207490680.
  160. Puhl, Rebecca M.; Himmelstein, Mary S.; Hateley-Browne, Jessica L.; Speight, Jane (October 2020). "Weight stigma and diabetes stigma in U.S. adults with type 2 diabetes: Associations with diabetes self-care behaviors and perceptions of health care". Diabetes Research and Clinical Practice. 168: 108387. doi:10.1016/j.diabres.2020.108387. ISSN   0168-8227. PMID   32858100. S2CID   221366068.
  161. Spanakis, Elias K.; Golden, Sherita Hill (December 2013). "Race/Ethnic Difference in Diabetes and Diabetic Complications". Current Diabetes Reports. 13 (6): 10.1007/s11892–013–0421–9. doi:10.1007/s11892-013-0421-9. ISSN   1534-4827. PMC   3830901 . PMID   24037313.
  162. CDC (2022-04-04). "Hispanic/Latino Americans and Type 2 Diabetes". Centers for Disease Control and Prevention. Retrieved 2023-10-31.
  163. CDC (2022-11-21). "Diabetes and Asian American People". Centers for Disease Control and Prevention. Retrieved 2023-10-31.
  164. Stewart WF, Ricci JA, Chee E, Hirsch AG, Brandenburg NA (June 2007). "Lost productive time and costs due to diabetes and diabetic neuropathic pain in the US workforce". Journal of Occupational and Environmental Medicine. 49 (6): 672–679. doi:10.1097/JOM.0b013e318065b83a. PMID   17563611. S2CID   21487348.
  165. Washington R.E.; Andrews R.M.; Mutter R.L. (November 2013). "Emergency Department Visits for Adults with Diabetes, 2010". HCUP Statistical Brief #167. Rockville MD: Agency for Healthcare Research and Quality. PMID   24455787. Archived from the original on 2013-12-03.
  166. "Type 1 vs. Type 2 Diabetes Differences: Which One Is Worse?". MedicineNet. Retrieved 2021-03-21.
  167. Parker K (2008). Living with diabetes . New York: Facts On File. p.  143. ISBN   978-1-4381-2108-6.
  168. Niaz K, Maqbool F, Khan F, Hassan FI, Momtaz S, Abdollahi M (April 2018). "Comparative occurrence of diabetes in canine, feline, and few wild animals and their association with pancreatic diseases and ketoacidosis with therapeutic approach". Veterinary World. 11 (4): 410–422. doi:10.14202/vetworld.2018.410-422. PMC   5960778 . PMID   29805204.
  169. Stahl SJ (2006-01-01). "Hyperglycemia in Reptiles". In Mader DR (ed.). Reptile Medicine and Surgery (Second ed.). Saint Louis: W.B. Saunders. pp. 822–830. doi:10.1016/b0-72-169327-x/50062-6. ISBN   978-0-7216-9327-9.
  170. Sweazea KL (8 July 2022). "Revisiting glucose regulation in birds - A negative model of diabetes complications". Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology. 262: 110778. doi:10.1016/j.cbpb.2022.110778. PMID   35817273. S2CID   250404382.
  171. 1 2 "Diabetes mellitus". Merck Veterinary Manual (9th ed.). 2005. Archived from the original on 2011-09-27. Retrieved 2011-10-23.
  172. Öhlund M. Feline diabetes mellitus Aspects on epidemiology and pathogenesis (PDF). Acta Universitatis agriculturae Sueciae. ISBN   978-91-7760-067-1.