Diabetes mellitus is not a single disorder but a heterogeneous group of disorders. All forms are characterized by hyperglycemia and disturbances of carbohydrate, fat, and protein metabolism which are associated with absolute or relative deficiencies of insulin action and/or insulin secretion. The World Health Organization (WHO) developed a now widely accepted classification of the disorder, largely based on clinical characteristics (see Table 1, WHO, 1985).
About 40% of diabetes sufferers require oral agents for satisfactory blood glucose control, and some 40% need insulin injections. This hormone was isolated by Frederic Banting and Charles Best in 1921 in Canada. It revolutionized the treatment of diabetes and prevention of its complications, transforming Type 1 diabetes from a fatal disease to one in which long-term survival became achievable.
Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels that result from defects in insulin secretion, or its action, or both. Diabetes mellitus, commonly referred to as diabetes (as it will be in this article) was first identified as a disease associated with "sweet urine," and excessive muscle loss in the ancient world. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine, hence the term sweet urine.
Ketoacidosis, a condition due to starvation or uncontrolled diabetes, is common in Type I diabetes. Ketones are acid compounds that form in the blood when the body breaks down fats and proteins. Symptoms include abdominal pain, vomiting, rapid breathing, extreme lethargy, and drowsiness. Patients with ketoacidosis will also have a sweet breath odor. Left untreated, this condition can lead to coma and death.
Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known ones above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.[23]
Type 1 diabetes mellitus is predominantly a disease of the young, usually developing before 20 years of age. Overall, type I DM makes up approximately 15% of all cases of diabetes. It develops in approximately 1 in 600 children and is one of the most common chronic diseases in children. The incidence is relatively low for children under the age of 5, increases between 5 and 15, and then tapers off.

Type 2 diabetes usually has a slower onset and can often go undiagnosed. But many people do have symptoms like extreme thirst and frequent urination. Other signs include sores that won't heal, frequent infections (including vaginal infections in some women), and changes in vision. Some patients actually go to the doctor with symptoms resulting from the complications of diabetes, like tingling in the feet (neuropathy) or vision loss (retinopathy), without knowing they have the disease. This is why screening people at risk for diabetes is so important. The best way to avoid complications is to get blood glucose under control before

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 of diabetes with 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.[110]


Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system.[10] However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also required.[13]
Is it your fault for getting type 2 diabetes? No – type 2 diabetes is not a personal failing. It develops through a combination of factors that are still being uncovered and better understood. Lifestyle (food, exercise, stress, sleep) certainly plays a major role, but genetics play a significant role as well. Type 2 diabetes is often described in the media as a result of being overweight, but the relationship is not that simple. Many overweight individuals never get type 2, and some people with type 2 were never overweight, (although obesity is probably an underlying cause of insulin resistance). To make matters worse, when someone gains weight (for whatever reason), the body makes it extremely difficult to lose the new weight and keep it off. If it were just a matter of choice or a bit of willpower, we would probably all be skinny. At its core, type 2 involves two physiological issues: resistance to the insulin made by the person’s beta cells and too little insulin production relative to the amount one needs.
Although there are dozens of known type 1 genes, about half of the risk attributable to heredity comes from a handful that coordinate a part of the immune system called HLA, which helps the body recognize nefarious foreign invaders, such as viruses, bacteria, and parasites. Type 1 diabetes is an autoimmune disease, in which the body's own immune system destroys the cells in the pancreas that produce insulin, so perhaps it is no surprise that immunity genes are involved. Other autoimmune diseases share the HLA gene link, which may be why people with type 1 are more likely to develop additional auto­immune disorders.
Diabetes mellitus is not a single disorder but a heterogeneous group of disorders. All forms are characterized by hyperglycemia and disturbances of carbohydrate, fat, and protein metabolism which are associated with absolute or relative deficiencies of insulin action and/or insulin secretion. The World Health Organization (WHO) developed a now widely accepted classification of the disorder, largely based on clinical characteristics (see Table 1, WHO, 1985).
Management. There is no cure for diabetes; the goal of treatment is to maintain blood glucose and lipid levels within normal limits and to prevent complications. In general, good control is achieved when the following occur: fasting plasma glucose is within a specific range (set by health care providers and the individual), glycosylated hemoglobin tests show that blood sugar levels have stayed within normal limits from one testing period to the next, the patient's weight is normal, blood lipids remain within normal limits, and the patient has a sense of health and well-being.
Diabetes: The differences between types 1 and 2 There are fundamental differences between diabetes type 1 and type 2, including when they might occur, their causes, and how they affect someone's life. Find out here what distinguishes the different forms of the disease, the various symptoms, treatment methods, and how blood tests are interpreted. Read now
FIGURE 19-1 ■. This figure shows the hyperbolic relationship of insulin resistance and beta cell function. On the y-axis is beta cell function as reflected in the first-phase insulin response during intravenous (IV) glucose infusion; on the x-axis is insulin sensitivity and its mirror image resistance. In a subject with normal glucose tolerance (NGT) and beta-cell reserve, an increase in insulin resistance results in increased insulin release and normal glucose tolerance. In an individual for whom the capacity to increase insulin release is compromised, increasing insulin resistance with partial or no beta-cell compensation results in progression from normal glucose tolerance, to impaired glucose tolerance (IGT), and finally to diabetes (T2D). Differences between these categories are small at high insulin sensitivity, which may be maintained by weight reduction, exercise, and certain drugs. At a critical degree of insulin resistance, due to obesity or other listed factors, only a further small increment in resistance requires a large increase in insulin output. Those that can increase insulin secretion to this extent retain normal glucose tolerance; those who cannot achieve this degree of insulin secretion (e.g., due to a mild defect in genes regulating insulin synthesis, insulin secretion, insulin action, or an ongoing immune destruction of beta cells) now unmask varying degrees of carbohydrate intolerance. The product of insulin sensitivity (the reciprocal of insulin resistance) and acute insulin response (a measurement beta-cell function) has been called the “disposition index.” This index remains constant in an individual with normal beta cell compensation in response to changes in insulin resistance. IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2D, type 2 diabetes.
How does high blood sugar (hyperglycemia) feel? To maintain the right amount of blood sugar, the body needs insulin, a hormone that delivers this sugar to the cells. When insulin is lacking, blood sugar builds up. We describe symptoms of high blood sugar, including fatigue, weight loss, and frequent urination. Learn who is at risk and when to see a doctor here. Read now
Diabetes develops when the body can't make any or enough insulin, and/or when it can't properly use the insulin it makes. For some people with diabetes, the body becomes resistant to insulin. In these cases, insulin is still produced, but the body does not respond to the effects of insulin as it should. This is called insulin resistance. Whether from not enough insulin or the inability to use insulin properly, the result is high levels of glucose in the blood, or hyperglycemia.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
Can type 2 diabetes be prevented? It is possible to reduce the risk of developing type 2 diabetes, although the underlying risk of type 2 diabetes depends strongly on genetic factors. But there was less type 2 diabetes around some years ago when people had a more active life and didn’t eat a modern Western diet. So it is fair to say that risk of getting type 2 diabetes is based on a genetic predisposition that is aggravated by lifestyle. Type 2 diabetes is associated with obesity, as well as a variety of environmental factors. To lower the risk of developing type 2 diabetes (as well as other diseases), it is highly recommended to exercise often, eat healthily, and maintain a healthy weight. 
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).
It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.
Type 1 diabetes mellitus has wide geographic variation in incidence and prevalence. [30] Annual incidence varies from 0.61 cases per 100,000 population in China to 41.4 cases per 100,000 population in Finland. Substantial variations are observed between nearby countries with differing lifestyles, such as Estonia and Finland, and between genetically similar populations, such as those in Iceland and Norway.

If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more "off limits" to people with diabetes than they are to people without diabetes. The key to sweets is to have a very small portion and save them for special occasions so you focus your meal on more healthful foods.
Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco.[2] Control of blood pressure and maintaining proper foot care are important for people with the disease.[2] Type 1 DM must be managed with insulin injections.[2] Type 2 DM may be treated with medications with or without insulin.[9] Insulin and some oral medications can cause low blood sugar.[13] Weight loss surgery in those with obesity is sometimes an effective measure in those with type 2 DM.[14] Gestational diabetes usually resolves after the birth of the baby.[15]
It’s not uncommon for patients to suddenly feel unsteady and immediately need to reach for carbs, says Marjorie Cypress, a nurse practitioner at an endocrinology clinic in Albuquerque, New Mexico, and 2014 president of health care and education for the American Diabetes Association. “When you have high blood sugar, your body has a problem regulating its glucose,” she explains. “If you’ve eaten something high in carbohydrates, your body shoots out a little too much insulin, and your glucose drops quickly. This makes you feel shaky, and you tend to crave carbs or sugar. This can lead to a vicious cycle.” These are the best foods for someone on a diabetic diet.

Sugar doesn't cause diabetes. But there is one way that sugar can influence whether a person gets type 2 diabetes. Consuming too much sugar (or sugary foods and drinks) can make people put on weight. Gaining too much weight leads to type 2 diabetes in some people. Of course, eating too much sugar isn't the only cause of weight gain. Weight gain from eating too much of any food can make a person's chance of getting diabetes greater.


When you have diabetes, your body becomes less efficient at breaking food down into sugar, so you have more sugar sitting in your bloodstream, says Dobbins. “Your body gets rid of it by flushing it out in the urine.” So going to the bathroom a lot could be one of the diabetes symptoms you’re missing. Most patients aren’t necessarily aware of how often they use the bathroom, says Dr. Cypess. “When we ask about it, we often hear, ‘Oh yeah, I guess I’m going more often than I used to,’” he says. But one red flag is whether the need to urinate keeps you up at night. Once or twice might be normal, but if it’s affecting your ability to sleep, that could be a diabetes symptom to pay attention to. Make sure you know these diabetes myths that could sabotage your health.
There are two main kinds of diabetes: type 1 diabetes and type 2 diabetes. More than 90% of all people with diabetes have type 2. Overall, more than 3 million Canadians have diabetes, and the number is rapidly rising. Over a third of people with type 2 diabetes are unaware they have the disease and are not receiving the required treatment because, for many people, early symptoms are not noticeable without testing.
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. Home telehealth support can be an effective management technique.[100]
When the blood glucose level rises above 160 to 180 mg/dL, glucose spills into the urine. When the level of glucose in the urine rises even higher, the kidneys excrete additional water to dilute the large amount of glucose. Because the kidneys produce excessive urine, people with diabetes urinate large volumes frequently (polyuria). The excessive urination creates abnormal thirst (polydipsia). Because excessive calories are lost in the urine, people may lose weight. To compensate, people often feel excessively hungry.
Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with type 1 associated with youth and type 2 with being overweight.[108] The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus, which is also associated with frequent urination.[108] Effective treatment was not developed until the early part of the 20th century, when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922.[108] This was followed by the development of the long-acting insulin NPH in the 1940s.[108]
Scientists have done studies of twins to help estimate how important genes are in determining one's risk of developing diabetes. Identical twins have identical genes and thus the same genetic risk for a disease. Research has found that if one identical twin has type 1 diabetes, the chance that the other twin will get the disease is roughly 40 or 50 percent. For type 2 diabetes, that risk goes up to about 80 or 90 percent. This might suggest that genes play a bigger role in type 2 than in type 1, but that isn't necessarily so. Type 2 is far more common in the general population than type 1, which means that regardless of genetics both twins are more likely to develop type 2 diabetes.
Home blood sugar (glucose) testing is an important part of controlling blood sugar. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Blood glucose levels are usually tested before and after meals, and at bedtime. The blood sugar level is typically determined by pricking a fingertip with a lancing device and applying the blood to a glucose meter, which reads the value. There are many meters on the market, for example, Accu-Check Advantage, One Touch Ultra, Sure Step and Freestyle. Each meter has its own advantages and disadvantages (some use less blood, some have a larger digital readout, some take a shorter time to give you results, etc.). The test results are then used to help patients make adjustments in medications, diets, and physical activities.

The elderly diabetic person is at increased risk of atrial fibrillation (odds ratio: 1.4 for men and 1.6 for women)232 and at twofold increased risk of thromboembolism from atrial fibrillation.233,234 We can find no subgroup analysis of the major atrial fibrillation trials to examine the benefits of warfarin specifically in older diabetic subjects. It appears that the adverse event rate in diabetic people drops from 8.6 events per 100 patients per year to 2.8 events with warfarin use.234 It is important to check for retinal new vessels when diabetic subjects are placed on warfarin, although the Early Treatment Diabetic Retinopathy Study235 showed no excess vitreous or preretinal hemorrhages in subjects given aspirin for vascular prophylaxis.

Clinical Manifestations. Diabetes mellitus can present a wide variety of symptoms, from none at all to profound ketosis and coma. If the disease manifests itself late in life, patients may not know they have it until it is discovered during a routine examination, or when the symptoms of chronic vascular disease, insidious renal failure, or impaired vision cause them to seek medical help. 

The glucose level at which symptoms develop varies greatly from individual to individual (and from time to time in the same individual), depending in part on the duration of diabetes, the frequency of hypoglycemic episodes, the rate of fall of glycemia, and overall control. (Glucose is also the sole energy source for erythrocytes and the kidney medulla.)
It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.

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