Diabetes mellitus 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,[101] where more than 80% of diabetic deaths occur.[105] The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030.[106] 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).[101][106] The global prevalence of diabetes might increase by 55% between 2013 and 2035.[101]
gestational diabetes diabetes mellitus with onset or first recognition during pregnancy, usually during the second or third trimester. In some cases mild, undetected glucose intolerance was present before pregnancy. It often disappears after the end of the pregnancy, but many women with this condition develop permanent diabetes mellitus in later life. Although the disordered carbohydrate metabolism is usually mild, prompt detection and treatment are necessary to avoid fetal and neonatal morbidity and mortality.
So what determines where fat is stored, and thus a person's propensity for insulin resistance and type 2 diabetes? Well, just having more fat in the body increases the risk that some of it will get misplaced. But exercise may also have a role in fat placement. Exercise is known to reduce insulin resistance; one way it may do this is by burning fat out of the muscle. Because of this, getting enough exercise may stave off type 2 in some cases. Genes may also help orchestrate the distribution of fat in the body, which illustrates how lifestyle and genetics interact.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly.
Diabetes mellitus (DM) is a strong predictor of cardiovascular morbidity and mortality and is associated with both micro- and macrovascular complications.1 Cardiovascular disease (CVD) causes up to 70% of all deaths in people with DM. The epidemic of DM will thus be followed by a burden of diabetes-related vascular diseases. The number of DM patients increases with aging of the population, in part because of the increasing prevalence of obesity and sedentary lifestyle. Although the mortality from coronary artery disease (CAD) in patients without DM has declined since the 1990s, the mortality in men with type 2 diabetes (T2DM) has not changed significantly.2 Moreover, DM is an independent risk factor for heart failure. Heart failure is closely related to diabetic cardiomyopathy: changes in the structure and function of the myocardium are not directly linked to CAD or hypertension. Diabetic cardiomyopathy is clinically characterized by an initial increase in left ventricular stiffness and subclinical diastolic dysfunction, gradually compromising left ventricular systolic function with loss of contractile function and progress into overt congestive heart failure. DM accounts for a significant percentage of patients with a diagnosis of heart failure in epidemiologic studies such as the Framingham Study and the UK Prospective Diabetes Study (UKPDS).2 A 1% increase in glycated hemoglobin (HbA1c) correlates to an increment of 8% in heart failure.3 The prevalence of heart failure in elderly diabetic patients is up to 30%.3

Regarding age, data shows that for each decade after 40 years of age regardless of weight there is an increase in incidence of diabetes. The prevalence of diabetes in persons 65 years of age and older is around 25%. Type 2 diabetes is also more common in certain ethnic groups. Compared with a 7% prevalence in non-Hispanic Caucasians, the prevalence in Asian Americans is estimated to be 8.0%, in Hispanics 13%, in blacks around 12.3%, and in certain Native American communities 20% to 50%. Finally, diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy (gestational diabetes).
The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.[23] Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue.[13] Many people, however, have no symptoms during the first few years and are diagnosed on routine testing.[13] A small number of people with type 2 diabetes mellitus can develop a hyperosmolar hyperglycemic state (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure).[13]

In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.
Diabetes mellitus is a diagnostic term for a group of disorders characterized by abnormal glucose homeostasis resulting in elevated blood sugar. It is among the most common of chronic disorders, affecting up to 5–10% of the adult population of the Western world. The prevalence of diabetes is increasing dramatically; it has been estimated that the worldwide prevalence will increase by more than 50% between the years 2000 and 2030 (Wild et al., 2004). It is clearly established that diabetes mellitus is not a single disease, but a genetically heterogeneous group of disorders that share glucose intolerance in common. The concept of genetic heterogeneity (i.e. that different genetic and/or environmental etiologic factors can result in similar phenotypes) has significantly altered the genetic analysis of this common disorder.
The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) and high blood sugar (such as, polyuria and polydipsia). When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and urine ketone levels are evaluated. Chronic management of DM is also based on periodic measurement of glycosylated hemoglobin levels (HbA1c). Elevated levels of HbA1c suggest poor long-term glucose control. The effects of diabetes on other body systems (such as cerebrovascular, coronary artery, and peripheral vascular) should be regularly assessed. Patients should be evaluated regularly for retinal disease and visual impairment and peripheral and autonomic nervous system abnormalities, e.g., loss of sensation in the feet. The patient is observed for signs and symptoms of diabetic neuropathy, e.g., numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy. The combination of peripheral neuropathy and peripheral arterial disease results in changes in the skin and microvasculature that lead to ulcer formation on the feet and lower legs with poor healing. Approx. 45,000 lower-extremity diabetic amputations are performed in the U.S. each year. Many amputees have a second amputation within five years. Most of these amputations are preventable with regular foot care and examinations. Diabetic patients and their providers should look for changes in sensation to touch and vibration, the integrity of pulses, capillary refill, and the skin. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, and bed linens or walking barefoot. The patient with ulcerated or insensitive feet is referred to a podiatrist for continuing foot care and is warned that decreased sensation can mask injuries.
Type 2 diabetes: Type 2 diabetes affects the way the body uses insulin. While the body still makes insulin, unlike in type I, the cells in the body do not respond to it as effectively as they once did. This is the most common type of diabetes, according to the National Institute of Diabetes and Digestive and Kidney Diseases, and it has strong links with obesity.
As part of proper diabetes management, it is important to be aware of the symptoms of abnormal blood glucose levels and know how to properly monitor your blood glucose levels using a home glucose meter. You should remember to always keep glucose tablets or candies containing sugar with you at all times to manage low blood glucose levels (hypoglycemia). Symptoms of low blood glucose include:
Pay attention if you find yourself feeling drowsy or lethargic; pain or numbness in your extremities; vision changes; fruity or sweet-smelling breath which is one of the symptoms of high ketones; and experiencing nausea or vomiting—as these are additional signs that something is not right. If there’s any question, see your doctor immediately to ensure that your blood sugar levels are safe and rule out diabetes.

Research has shown that there are some ways of preventing type 2 diabetes, or at least delaying its onset. Lifestyle changes such as becoming more active (or staying active, if you already engage in regular physical activity) and making sure your weight stays in a healthy range are two ways to help ward off type 2 diabetes, but talk to your doctor about what else you can do to prevent or manage the disease.
Type 1 diabetes occurs when the immune system attacks and destroys the insulin-producing cells in the pancreas (the beta cells). As a result, the body is left without enough insulin to function normally (i.e. it becomes insulin deficient). This is called an autoimmune reaction, because the body attacks itself and produces antibodies to its own insulin-producing cells, thereby destroying them.
The amount of glucose in the bloodstream is tightly regulated by insulin and other hormones. Insulin is always being released in small amounts by the pancreas. When the amount of glucose in the blood rises to a certain level, the pancreas will release more insulin to push more glucose into the cells. This causes the glucose levels in the blood (blood glucose levels) to drop.
Family or personal history. Your risk increases if you have prediabetes — a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes. You're also at greater risk if you had gestational diabetes during a previous pregnancy, if you delivered a very large baby or if you had an unexplained stillbirth.
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