Viral infections may be the most important environmental factor in the development of type 1 diabetes mellitus,  probably by initiating or modifying an autoimmune process. Instances have been reported of a direct toxic effect of infection in congenital rubella. One survey suggests enteroviral infection during pregnancy carries an increased risk of type 1 diabetes mellitus in the offspring. Paradoxically, type 1 diabetes mellitus incidence is higher in areas where the overall burden of infectious disease is lower.
People with type 1 diabetes and certain people with type 2 diabetes may use carbohydrate counting or the carbohydrate exchange system to match their insulin dose to the carbohydrate content of their meal. "Counting" the amount of carbohydrate in a meal is used to calculate the amount of insulin the person takes before eating. However, the carbohydrate-to-insulin ratio (the amount of insulin taken for each gram of carbohydrate in the meal) varies for each person, and people with diabetes need to work closely with a dietician who has experience in working with people with diabetes to master the technique. Some experts have advised use of the glycemic index (a measure of the impact of an ingested carbohydrate-containing food on the blood glucose level) to delineate between rapid and slowly metabolized carbohydrates, although there is little evidence to support this approach.
WELL-CONTROLLED DIABETES MELLITUS: Daily blood sugar abstracted from the records of a patient whose DM is well controlled (hemoglobin A1c=6.4). The average capillary blood glucose level is 104 mg/dL, and the standard deviation is 19. Sixty-five percent of the readings are between 90 and 140 mg/dL; the lowest blood sugar is 67 mg/dL (on April 15) and the highest is about 190 (on March 21).
Management of type 2 diabetes focuses on lifestyle interventions, lowering other cardiovascular risk factors, and maintaining blood glucose levels in the normal range. Self-monitoring of blood glucose for people with newly diagnosed type 2 diabetes may be used in combination with education, however the benefit of self monitoring in those not using multi-dose insulin is questionable. In those who do not want to measure blood levels, measuring urine levels may be done. Managing other cardiovascular risk factors, such as hypertension, high cholesterol, and microalbuminuria, improves a person's life expectancy. Decreasing the systolic blood pressure to less than 140 mmHg is associated with a lower risk of death and better outcomes. Intensive blood pressure management (less than 130/80 mmHg) as opposed to standard blood pressure management (less than 140-160 mmHg systolic to 85–100 mmHg diastolic) results in a slight decrease in stroke risk but no effect on overall risk of death.
The United Kingdom Prospective Diabetes Study (UKPDS) was a clinical study conducted by Z that was published in The Lancet in 1998. Around 3,800 people with type 2 diabetes were followed for an average of ten years, and were treated with tight glucose control or the standard of care, and again the treatment arm had far better outcomes. This confirmed the importance of tight glucose control, as well as blood pressure control, for people with this condition.
Persons with diabetes are prone to infection, delayed healing, and vascular disease. The ease with which poorly controlled diabetic persons develop an infection is thought to be due in part to decreased chemotaxis of leukocytes, abnormal phagocyte function, and diminished blood supply because of atherosclerotic changes in the blood vessels. An impaired blood supply means a deficit in the protective defensive cells transported in the blood. Excessive glucose allows organisms to grow out of control.
Having diabetes requires life-long treatment and follow-up by health professionals. Diabetes can be linked to damage of the eyes, kidneys and feet. It is also associated with increased risk of strokes, heart attacks and poor blood circulation to the legs. Medical care aims to minimise these risks by controlling diabetes, blood pressure and cholesterol and screening for possible complications caused by the diabetes.
Certain genetic markers have been shown to increase the risk of developing Type 1 diabetes. Type 2 diabetes is strongly familial, but it is only recently that some genes have been consistently associated with increased risk for Type 2 diabetes in certain populations. Both types of diabetes are complex diseases caused by mutations in more than one gene, as well as by environmental factors.
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.
Risk factors for type 2 diabetes include obesity, high cholesterol, high blood pressure, and physical inactivity. The risk of developing type 2 diabetes also increases as people grow older. People who are over 40 and overweight are more likely to develop type 2 diabetes, although the incidence of this type of diabetes in adolescents is growing. Diabetes is more common among Native Americans, African Americans, Hispanic Americans and Asian Americans/Pacific Islanders. Also, people who develop diabetes while pregnant (a condition called gestational diabetes) are more likely to develop type 2 diabetes later in life.
Say that two people have the same genetic mutation. One of them eats well, watches their cholesterol, and stays physically fit, and the other is overweight (BMI greater than 25) and inactive. The person who is overweight and inactive is much more likely to develop type 2 diabetes because certain lifestyle choices greatly influence how well your body uses insulin.
Women seem to be at a greater risk as do certain ethnic groups, such as South Asians, Pacific Islanders, Latinos, and Native Americans. This may be due to enhanced sensitivity to a Western lifestyle in certain ethnic groups. Traditionally considered a disease of adults, type 2 diabetes is increasingly diagnosed in children in parallel with rising obesity rates. Type 2 diabetes is now diagnosed as frequently as type 1 diabetes in teenagers in the United States.
Yes. In fact, being sick can actually make the body need more diabetes medicine. If you take insulin, you might have to adjust your dose when you're sick, but you still need to take insulin. People with type 2 diabetes may need to adjust their diabetes medicines when they are sick. Talk to your diabetes health care team to be sure you know what to do.
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. Insulin plays a critical role in balancing 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.
Type 2 diabetes is different. A person with type 2 diabetes still produces insulin but the body doesn't respond to it normally. Glucose is less able to enter the cells and do its job of supplying energy (a problem called insulin resistance). This raises the blood sugar level, so the pancreas works hard to make even more insulin. Eventually, this strain can make the pancreas unable to produce enough insulin to keep blood sugar levels normal.
People with type 1 diabetes sometimes receive transplantation of an entire pancreas or of only the insulin-producing cells from a donor pancreas. This procedure may allow people with type 1 diabetes mellitus to maintain normal glucose levels. However, because immunosuppressant drugs must be given to prevent the body from rejecting the transplanted cells, pancreas transplantation is usually done only in people who have serious complications due to diabetes or who are receiving another transplanted organ (such as a kidney) and will require immunosuppressant drugs anyway.
At present, the American Diabetes Association does not recommend general screening of the population for type 1 diabetes, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age; however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Of all the people with diabetes, only approximately 10% have type 1 diabetes and the remaining 90% have type 2 diabetes.
Insulin-dependent diabetes mellitus is believed to result from autoimmune, environmental, and/or genetic factors. Whatever the cause, the end result is destruction of insulin-producing pancreatic beta cells, a dramatic decrease in the secretion of insulin, and hyperglycemia. Non-insulin-dependent diabetes mellitus is presumably heterogeneous in origin. It is associated with older age, obesity, a family history of diabetes, and ethnicity (genetic components). The vast majority of those with non-insulin-dependent diabetes are overweight Kahn (2003). This form of the disorder has a much slower rate of progression than insulin-dependent diabetes. Over time the ability to respond to insulin decreases, resulting in increased levels of blood glucose. The pancreatic secretion of insulin increases in an attempt to compensate for the elevated levels of glucose. If the condition is untreated, the pancreatic production of insulin decreases and may even cease.
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.
Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue. In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood. The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.
Autonomic changes involving cardiovascular control (eg, heart rate, postural responses) have been described in as many as 40% of children with diabetes. Cardiovascular control changes become more likely with increasing duration and worsening control.  In a study by 253 patients with type 1 diabetes (mean age at baseline 14.4 y), Cho et al reported that the prevalence of cardiac autonomic dysfunction increases in association with higher body mass index and central adiposity. 
Type 2 diabetes (T2D) is more common than type 1 diabetes with about 90 to 95 percent of people with diabetes having T2D. According to the Centers for Disease Control and Prevention’s report, 30.3 million Americans, or 9.4% of the US population have diabetes.1 More alarming, an estimated 84 million more American adults have prediabetes, which if not treated, will advance to diabetes within five years.1
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.
Diabetes is a condition in which the body cannot properly store and use fuel for energy. The body's main fuel is a form of sugar called glucose, which comes from food (after it has been broken down). Glucose enters the blood and is used by cells for energy. To use glucose, the body needs a hormone called insulin that's made by the pancreas. Insulin is important because it allows glucose to leave the blood and enter the body's cells.
Retinopathy: If blood sugar levels are too high, they can damage the eyes and cause vision loss and blindness. Retinopathy causes the development and leaking of new blood vessels behind the eye. Other effects of diabetes, such as high blood pressure and high cholesterol, can make this worse. According to the CDC, early treatment can prevent or reduce the risk of blindness in an estimated 90 percent of people with diabetes.
A chronic metabolic disorder marked by hyperglycemia. DM results either from failure of the pancreas to produce insulin (type 1 DM) or from insulin resistance, with inadequate insulin secretion to sustain normal metabolism (type 2 DM). Either type of DM may damage blood vessels, nerves, kidneys, the retina, and the developing fetus and the placenta during pregnancy. Type 1 or insulin-dependent DM has a prevalence of just 0.3 to 0.4%. Type 2 DM (formerly called adult-onset DM) has a prevalence in the general population of 6.6%. In some populations (such as older persons, Native Americans, African Americans, Pacific Islanders, Mexican Americans), it is present in nearly 20% of adults. Type 2 DM primarily affects obese middle-aged people with sedentary lifestyles, whereas type 1 DM usually occurs in children, most of whom are active and thin, although extremely obese children are now being diagnosed with type 2 diabetes as well. See: table; dawn phenomenon; insulin; insulin pump; insulin resistance; diabetic polyneuropathy; Somogyi phenomenon
Dr. Erica Oberg, ND, MPH, received a BA in anthropology from the University of Colorado, her doctorate of naturopathic medicine (ND) from Bastyr University, and a masters of public health (MPH) in health services research from the University of Washington. She completed her residency at the Bastyr Center for Natural Health in ambulatory primary care and fellowship training at the Health Promotion Research Center at the University of Washington.
a broadly applied term used to denote a complex group of syndromes that have in common a disturbance in the oxidation and utilization of glucose, which is secondary to a malfunction of the beta cells of the pancreas, whose function is the production and release of insulin. Because insulin is involved in the metabolism of carbohydrates, proteins and fats, diabetes is not limited to a disturbance of glucose homeostasis alone.
a complex disorder of carbohydrate, fat, and protein metabolism that is primarily a result of a deficiency or complete lack of insulin secretion by the beta cells of the pancreas or resistance to insulin. The disease is often familial but may be acquired, as in Cushing's syndrome, as a result of the administration of excessive glucocorticoid. The various forms of diabetes have been organized into categories developed by the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus of the American Diabetes Association. Type 1 diabetes mellitus in this classification scheme includes patients with diabetes caused by an autoimmune process, dependent on insulin to prevent ketosis. This group was previously called type I, insulin-dependent diabetes mellitus, juvenile-onset diabetes, brittle diabetes, or ketosis-prone diabetes. Patients with type 2 diabetes mellitus are those previously designated as having type II, non-insulin-dependent diabetes mellitus, maturity-onset diabetes, adult-onset diabetes, ketosis-resistant diabetes, or stable diabetes. Those with gestational diabetes mellitus are women in whom glucose intolerance develops during pregnancy. Other types of diabetes are associated with a pancreatic disease, hormonal changes, adverse effects of drugs, or genetic or other anomalies. A fourth subclass, the impaired glucose tolerance group, also called prediabetes, includes persons whose blood glucose levels are abnormal although not sufficiently above the normal range to be diagnosed as having diabetes. Approximately 95% of the 18 million diabetes patients in the United States are classified as type 2, and more than 70% of those patients are obese. About 1.3 million new cases of diabetes mellitus are diagnosed in the United States each year. Contributing factors to the development of diabetes are heredity; obesity; sedentary life-style; high-fat, low-fiber diets; hypertension; and aging. See also impaired glucose tolerance, potential abnormality of glucose tolerance, previous abnormality of glucose tolerance.
Diabetes mellitus, or as it's more commonly known diabetes, is a disease characterized by an excess of blood glucose, or blood sugar, which builds up in the bloodstream when your body isn't able to adequately process the sugar in food. High blood sugar is an abnormal state for the body and creates specific symptoms and possible long-term health problems if blood sugar is not managed well.
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).
When there is excess glucose present in the blood, as with type 2 diabetes, the kidneys react by flushing it out of the blood and into the urine. This results in more urine production and the need to urinate more frequently, as well as an increased risk of urinary tract infections (UTIs) in men and women. People with type 2 diabetes are twice as likely to get a UTI as people without the disease, and the risk is higher in women than in men.