A condition characterized by discolored patches in the skin folds of the armpits, neck, or groin, ranging from tan to dark brown. Acanthosis nigricans is associated with hyperinsulinemia (a higher-than-normal level of insulin in the blood), which results from obesity-related insulin resistance.  In rare cases, the condition is associated with cancer, usually of the gastrointestinal tract. Acanthosis nigricans is often an important early marker of Type 2 diabetes or evidence that a person has a high risk of developing the condition. About 90% of children who develop Type 2 diabetes have acanthosis nigricans. Any overweight person with this symptom should be tested for insulin in the blood and impaired glucose tolerance, or prediabetes. The appearance of acanthosis nigricans can usually be improved through increased physical activity and weight loss, healthy lifestyle changes that can often delay the development of Type 2 diabetes or, if diabetes is already diagnosed, help control blood glucose levels. Topical agents such as lactic acid or antifungal drugs can sometimes be used to improve a person’s cosmetic appearance.

A class of medicine usually used to treat high blood pressure. Angiotensin-converting enzyme (ACE) inhibitors also appear to protect people with diabetes from diabetic nephropathy (kidney disease).

People with diabetes are especially prone to hypertension (defined as a blood pressure level of 140/90 mm Hg or greater). Some 20% to 60% of individuals with diabetes have high blood pressure. Hypertension increases their risk not only of heart disease and stroke, but also of peripheral vascular disease, diabetic rentinopathy, diabetic nephropathy, and possibly diabetic neuropathy. The American Diabetes Association (ADA) currently recommends a target blood pressure level of under 130/80 mm Hg in people with diabetes.

The ADA recommends a number of different measures for lowering blood pressure, including weight loss, sodium restriction, and exercise. When these measures aren’t enough, the addition of one or more medicines is warranted. There are several different classes of blood pressure drugs, including angiotensin-receptor blockers (ARBs), diuretics, beta blockers, and ACE inhibitors. Overall, drug therapy has been shown to substantially decrease the risk of cardiovascular disease, diabetic retinopathy, and diabetic nephropathy.

ACE inhibitors may have a special advantage in terms of slowing the progression of diabetic nephropathy. Research findings show that ACE inhibitors can slow the progression of kidney disease to a greater degree than other antihypertensive drugs that lower blood pressure by a similar amount and that they may be able to protect the kidneys even in people with diabetes whose blood pressure levels are in the normal range. This suggests that ACE inhibitors protect the kidneys by mechanisms other than just blood pressure control.

Currently, the ADA recommends ACE inhibitors for people with high blood pressure and microalbuminuria or clinical albuminuria (clinical markers of kidney disease). The ADA also recommends that ACE inhibitors be considered for people over 55 with or without high blood pressure but with another cardiovascular risk factor (such as a history of cardiovascular disease, abnormal blood lipid levels, microalbuminuria, or smoking).

ACE inhibitors include quinapril (Accupril), perindopril (Aceon), ramipril (Altace), captopril (Capoten), benazepril (Lotensin), trandolapril (Mavik), fosinopril (Monopril), lisinopril (Prinivil, Zestril), moexipril (Univasc), and enalapril (Vasotec). Pregnant women should not take ACE inhibitors.

One of a group of simple proteins widely distributed in animals and plants. Albumin is found in such substances as blood, milk, and egg whites. In humans it has special relevance to people with diabetes because its presence in urine is a marker of diabetic kidney disease.

The job of the kidneys is to filter protein by-products and water from the bloodstream and to maintain the proper balance of sodium and potassium in the blood. Albumin in the blood has many functions, including the maintenance of a proper balance of fluids between the blood and other tissues. In an early stage of diabetic kidney disease, the kidneys begin removing too much albumin from the blood, and very small amounts of albumin begin to show up in the urine, a condition known as microalbuminuria. Normally, a person has less than 25 milligrams of albumin in their urine each day. A person with microalbuminuria has 30 to 300 milligrams. Microalbuminuria in not uncommon in people who have had diabetes for five years or more.

There is a specific laboratory test to check for microalbuminuria. (The usual urine dipstick tests for protein are not sensitive enough for this purpose.) If the test is positive, measures can be taken—including lowering blood pressure and tightening blood glucose control—to slow or prevent the development of more serious stages of the disease

A class of diabetes drugs sometimes called “starch blockers” that blocks the action of enzymes that normally begin to break down certain carbohydrates in the upper part of the small intestine.

Different classes of diabetes medicines work in different ways to control high blood glucose. Biguanides such as metformin (brand name Glucophage) decrease the production of glucose in the liver. Sulfonylureas (Amaryl, DiaBeta, Glucotrol, Micronase) and meglitinides (Prandin, Starlix) stimulate the pancreas to release more insulin. Thiazolidinediones (Actos, Avandia) increase the sensitivity of fat and muscle cells to insulin.

Taken with the first bite of a meal, alpha-glucosidase inhibitors are especially well-suited to treat postprandial hyperglycemia (a sharp rise in blood sugar after meals), a common and serious problem faced by many people with Type 2 diabetes. Because the drugs prevent the immediate breakdown of starches into monosaccharides, or simple sugars, which would be absorbed into the bloodstream quickly, more of the carbohydrate consumed at a meal gets absorbed further “downstream” in the gastrointestinal tract, toward the end of the small intestine or the colon. Slowing the absorption of carbohydrate gives the betacells in the pancreas more time to secrete adequate insulin to cover the meal.

Because of their novel mechanism of action, these drugs can also be combined effectively with other classes of diabetes drugs. However, while alpha-glucosidase inhibitors themselves do not cause low blood glucose, when they are used in combination with another diabetes medicines, hypoglycemia can occur. In addition, because these drugs slow the absorption of certain carbohydrates (including orange juice and white sugar), these sources will not work immediately to treat an episode of hypoglycemia. Pure glucose, in the form of gel or tablets, is the best treatment for hypoglycemia in this case.

One of the biggest drawbacks to the alpha-glucosidase inhibitors is their side effects. Because they affect carbohydrate absorption in the small intestine, they can cause bloating, nausea, diarrhea, and flatulence. Usually, these side effects can be minimized by starting therapy with a small dose and slowly working up to the most effective dose. These side effects also tend to diminish over time.

The first alpha-glucosidase inhibitor to become available in the United States was acarbose (Precose), which was approved by the U.S. Food and Drug Administration in 1995. A second alpha-glucosidase inhibitor, miglitol (Glyset) became available in 1999. They may be used by people with either Type 1 or Type 2 diabetes.

Blood glucose self-monitoring using a blood sample from somewhere other than the fingertips, namely the palm, upper arm, forearm, abdomen, calf, or thigh.

The fingertips have traditionally been used for blood glucose self-monitoring because they’re rife with capillaries, and it is relatively easy to obtain a large enough drop of blood for accurate readings. However, the fingertips are also full of nerve endings and are very sensitive to pain. Many people would welcome a break from fingersticks, especially people who use their fingers a great deal, such as musicians or people who spend a lot of time at a computer keyboard.

Alternate-site testing is possible only with certain newer blood glucose meters that require a smaller drop of blood to produce accurate blood glucose readings and have been approved by the U.S. Food and Drug Administration for this purpose. Among the alternate-site meters currently available are the Accu-Chek Active and Compact (marketed by Roche Diagnostics); the Ascencia Breeze, Contour, DEX2, Elite, and Elite XL (Bayer); the FreeStyle Freedom and FreeStyle Flash (Abbott); and the InDuo, One-Touch Ultra, One-Touch Ultra 2, and OneTouch UltraSmart (LifeScan). Each meter’s user manual specifies what parts of the body can be used to obtain the blood sample.

In the past few years, a number of studies have been performed to compare the accuracy of alternate-site testing results with results from fingertip blood glucose monitoring. The studies have generally shown that during "routine" blood glucose monitoring, such as before meals (when fasting) or two hours or more after meals or exercise, the results from alternate sites correspond well with results from fingertip monitoring. However, because glucose utilization in the fingertips is faster than in the arms or other sites, when blood glucose level is falling rapidly (for example, immediately after exercise) or rising rapidly (during the first hour after a meal, say), alternate-site readings lag behind fingertip readings. This could result in delayed detection of hypoglycemia or sharp changes in blood glucose level. Therefore, alternate-site testing should not be performed directly after a meal or exercise or when you think your blood glucose level is low or falling. It is also recommended that you confirm alternate-site low readings with a fingerstick check before treating hypoglycemia. While these limitations may make alternate-site meters less convenient and attractive to some, many people find that periodic alternate-site testing provides a welcome relief from the pain of fingersticks.

The basic structural units, or building blocks, of protein. The body uses protein to build up and repair tissue. Protein is found in muscles, organs, bones, and skin and in many of the body's hormones, or chemical messengers. There are about 20 amino acids in the human body, and they can combine in different ways to form a vast array of proteins with very different properties. For example, the insulin molecule is composed of a chain of 51 amino acids. Interestingly, human insulin varies from pig insulin by only a single amino acid along this chain.

Plants and bacteria can manufacture all the amino acids they need, but there are about nine that the human body needs but cannot make. These are called essential amino acids, because they must be obtained from food. Sources of dietary protein, including meat, poultry, fish, eggs, cheese, milk, grains, legumes, and nuts, can provide the essential amino acids.

A decrease in the number of red blood cells or in the amount of hemoglobin (an oxygen-carrying protein) in these cells that may cause such symptoms as weakness, fatigue, dizziness, shortness of breath, headache, or insomnia. Anemia, in turn, may contribute to cardiovascular disease by forcing the heart to work harder to deliver sufficient oxygen to the brain and other organs.

There are several distinct types of anemia, which can be caused by vitamin or iron deficiencies, blood loss, a genetic abnormality in the shape of the cells, or some chronic diseases. Decreased production of red blood cells is a common complication of some kidney diseases, including diabetic nephropathy.

The red blood cells, which carry oxygen to tissues and organs throughout the body, are produced in the bone marrow. Healthy kidneys produce a hormone called erythropoietin (EPO), which stimulates the bone marrow to produce red blood cells when the blood oxygen concentration is low. However, diseased kidneys often don’t make enough EPO, causing a decline in red blood cell production.

Anemia may begin to develop in the early stages of kidney disease, when the individual still has 20% to 50% of his normal kidney function; it gets progressively worse as kidney function diminishes. Nearly everyone with end-stage kidney disease has anemia. In people receiving hemodialysis for kidney failure (a therapy in which the person’s blood is slowly pumped out of the body, through a special machine that filters out wastes and extra fluid, and back into the body), the treatment itself can sometimes contribute to the problem, through blood loss.

Doctors use a laboratory test called a complete blood count (CBC) to check for anemia. The CBC counts the number of red and white blood cells and the amount of hemoglobin (Hgb) in the blood, and it also determines the hematocrit (Hct), the percentage of whole blood that consists of red blood cells. When evaluating anemia, doctors will also test for iron deficiency and blood loss in the stool to rule out these potential causes of anemia.

In people with kidney disease, anemia can usually be treated with a genetically engineered form of EPO, which is usually injected under the skin two or three times a week. Often, they may need both EPO and iron supplements to raise their hematocrit level. Iron is sometimes given by pill, but intravenous iron supplementation appears to work better in people with kidney failure. Iron can also be injected directly into the tube that carries blood back to the body during hemodialysis.

Pain or tightness in the chest, a symptom of coronary heart disease (CHD). People with diabetes are at increased risk for CHD, a condition in which the heart muscle does not get a sufficient supply of blood, oxygen, and nutrients to meet its needs because of partial or complete blockage of the coronary blood vessels. This is usually due to atheroslerosis, the buildup of plaque (fatty deposits) on artery walls in the coronary vessels that feed the heart. There are a number of risk factors for CHD, including high blood pressure, diabetes, a family history of CHD, smoking, high cholesterol levels, high triglyceride levels, obesity, and inactivity.

Angina can vary considerably from person to person. It usually takes the form of chest pain that comes on gradually over a period of 30 seconds to several minutes. In some cases it may become more severe; in others it may remain mild and go away. The pain may also affect the left arm, shoulder, armpit, neck, or jaw. It may be brought on by exercise or emotional stress, but it may also occur at rest. Sometimes angina may produce symptoms of nausea and upper abdominal discomfort, when it can be mistaken for heartburn.

Two different types of drugs are commonly used to treat angina. Coronary vasodilators (such as nitroglycerin) cause the vessels of the heart to relax and widen, allowing for improved blood flow. Blood-pressure-lowering drugs can decrease the heart's workload and need for oxygen.

Another method for restoring blood flow to the heart is percutaneous transluminal coronary angioplasty (PTCA), also known as balloon angioplasty. In this method, a special balloon at the end of a catheter is threaded up to the site of arterial blockage, inflated to compress the plaque, and then withdrawn. This procedure enlarges the inner diameter of the blood vessel to allow for greater blood flow. In many cases, a stent (a small metal device in the shape of a spring or mesh cylinder) is placed in the vessel to keep it open. There is evidence that angioplasty may not be an optimal choice in people with diabetes, because their coronary vessels tend to abruptly close again following angioplasty.

Another technique is coronary artery bypass grafting (CABG), in which a blood vessel from another part of the body (usually the leg or inside the chest wall) is used to form a detour around the blocked part of the coronary artery. Studies have shown that in people with diabetes, CABG is much more effective than balloon angioplasty over the long term.

There are a number of preventive measures you and your doctor can take to lower your risk of developing angina and CHD:

Proteins made by white blood cells in response to bacteria, viruses, and other substances. Antibodies and white blood cells are both components of the body's immune system, which protects it from infections and diseases. Specific antibodies are designed to attack specific foreign proteins, or antigens.

Diabetes researchers now recognize that Type 1 diabetes is an autoimmune disease, in which the immune system mistakenly launches an attack on the beta cells of the pancreas. In the mid-1970's, researchers in London first detected antibodies to pancreatic islet cells in people with newly diagnosed diabetes. These antibodies react to islet cell cytoplasm, the intracellular substance outside the nucleus of the cell, and thus came to be called islet cell cytoplasmic antibodies, or ICAs. Since that time, scientists have found a number of other antibodies in people who already have diabetes or who will develop diabetes in the near future, including ICA512 and antibodies to glutamic acid decarboxylase and to insulin.

Clinical researchers can now use tests for these antibodies to fairly accurately predict who will develop diabetes within a given period of time. More and more, using combinations of these antibody tests, researchers are gradually improving their ability to reliably predict the onset of diabetes. Better prediction, in turn, has allowed scientists to test a variety of approaches to prevention—approaches that previously had only been tried in animals. So far, the most notable effort has been the Diabetes Prevention Trial-Type 1 (DPT-1), which tested whether insulin given in low-dose injections or orally can prevent or delay the onset of diabetes in people at "intermediate" or "high" risk for developing it. The researchers recruited close relatives of people with Type 1 diabetes and then tested them for ICAs to predict their risk of developing diabetes. At the end of the trial, the researchers concluded that neither oral insulin nor injected insulin prevented or delayed diabetes.

Drugs used to treat clinical depression, a medical condition characterized by long-standing feelings of sadness, apathy, and hopelessness. People with diabetes are especially prone to depression: By some estimates, 15% to 30% of people with diabetes may suffer from depression at any given time. Depression may worsen diabetes control by making people less active and less vigilant about their diabetes care.

Many people feel “down” or “blue” some of the time, but sadness that lasts two weeks or more or interferes with a person’s ability to carry out daily tasks or to enjoy formerly enjoyed activities are signs of depression, in which the brain is not functioning properly. Other signs of depression include having insomnia or sleeping too much, loss of appetite and weight loss (or eating too much and gaining weight), and lack of energy. Since depression can be debilitating and carries the risk of suicide, it should be considered a serious condition. If you experience symptoms of depression, be sure to consult your health-care team.

In certain cases, antidepressants may be warranted, and health-care professionals now have a number of different types of antidepressants to choose from. One of the first types of antidepressants, which became available in the late 1950’s, are the tricyclic antidepressants, which include imipramine (brand name Tofranil), amitriptyline (Elavil, Endep), nortriptyline (Pamelor), and desipramine (Norpramin). These drugs are as effective as the newer antidepressants but have more unpleasant side effects, which include dry mouth, constipation, bladder problems, sexual dysfunction, blurred vision, and drowsiness.

Another older type of antidepressant, monoamine oxidase inhibitors (MAOIs) such as tranylcypromine (Parnate), can benefit people with depression who aren’t adequately helped by other antidepressants. The side effects of MAOIs include restlessness, insomnia, weakness, drowsiness, dry mouth, nausea, diarrhea, and constipation. Certain foods, beverages, and medicines may interact in dangerous ways with MAOIs, so people must be carefully instructed in their use.

If it seems as if more and more people are taking antidepressants, this may reflect the fact that many of the newer antidepressants have fewer or less pronounced side effects than the older ones. Selective serotonin reuptake inhibitors (SSRIs), which include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), and citalopram (Celexa), work primarily on a neurotransmitter, or chemical nerve messenger, called serotonin. SSRIs work as well as the older antidepressants but have fewer side effects. Other new (non-SSRI) antidepressants include venlafaxine (Effexor), nefazodone (Serzone), and bupropion (Wellbutrin). Side effects of these newer drugs include sexual problems, headache, nausea, nervousness, and insomnia.

It generally takes six to eight weeks for antidepressants to start to work. The effectiveness and side effects vary from one drug to another and from one person to another, so part of the health-care professional’s job is to tailor the choice of antidepressant to the individual.

If the antidepressant you’re taking seems ineffective after eight weeks or has unpleasant side effects, your health-care provider may change your dose or start you on a different antidepressant. Never discontinue an antidepressant without consulting your health-care team: In most cases, the dose must be tapered down gradually and carefully to avoid withdrawal symptoms.

Drugs that reduce the formation or inhibit the action of chemicals that promote the activation and aggregation of platelets, blood components important for the clotting of blood. Although clotting is an important step in wound healing, inappropriate clotting can be harmful. The most familiar and most used antiplatelet drug is aspirin. Other members of this family of drugs include abciximab (brand name Reopro), clopidogrel (Plavix), dipyridamole (Persantine), eptifibatide (Integrilin), ticlopidine (Ticlid), and tirofiban (Aggrastat). They are used to treat and prevent cardiovascular disease; to treat angina (chest pain), some strokes, and transient ischemic attacks (ministrokes); to prevent clot formation in people with atrial fibrillation (irregular heartbeat); and to prevent blood vessels and grafts from closing up after angioplasty and heart bypass surgery.

As platelets circulate through the bloodstream, they’re constantly sensing and measuring the levels of certain signaling molecules. Normally, the balance of chemical signals keeps platelets in an inert state. When the level of chemicals calling for activation outweighs the level of chemicals promoting their free circulation—such as occurs near the site of a break in a blood vessel—platelet activation occurs. Once activated, platelets change their outer membranes, clump together at the site of the injury, and release chemicals that promote further platelet aggregation. People with diabetes tend to have hyperactive platelets that are more likely to form clots.

Users of antiplatelet drugs are at increased risk for bleeding problems such as hemorrhagic stroke and gastrointestinal bleeding and are also at risk for neutropenia (having an abnormally small number of a type of an infection-fighting white blood cell). Some of these medicines can cause significant sodium retention, so if you take one, your doctor may have you work with a dietitian to reduce or even eliminate sodium from your diet.

In addition to taking part in wound healing, platelets also have a role in the progression of atherosclerosis, a disease of artery narrowing. In atherosclerosis, fat, cholesterol, platelets, and calcium are deposited on the walls of blood vessels whose linings have been damaged. (Blood vessel damage is caused by factors such as high blood pressure, diabetes, and smoking.) These deposits, or plaques, gradually narrow the blood vessel and reduce the flow of blood through it. Depending on the location of a plaque, reduced blood and oxygen flow can cause symptoms such as angina or claudication (pain in the legs that starts when walking but eases with rest). If part of a plaque ruptures and breaks free, it can travel through the circulatory system and block off a blood vessel, causing problems such as stroke or a heart attack.

Studies have shown, though, that aspirin can be used as a preventive measure that reduces the incidence of strokes by 20% and heart attacks by about 30%. These reductions are not insignificant when you consider that cardiovascular diseases are the leading cause of death for people with diabetes and that people with diabetes are at higher risk for cardiovascular diseases.

The American Diabetes Association (ADA) recommends aspirin therapy (the use of a daily aspirin as preventive medicine) for adults with diabetes who have increased risks for cardiovascular diseases. That group includes people over 40, smokers, people with high blood pressure, people with a family history of cardiovascular disease, people who have high cholesterol levels, and people who have protein in the urine (albuminuria). Aspirin therapy is not recommended for people under 21 because its use increases the risk of Reye syndrome

Because higher doses of aspirin may increase the risk of side effects without an increase in cardiovascular benefits, the ADA and the American Heart Association recommend that people with cardiovascular risk factors use low doses (75–160 mg) of aspirin. Despite its name, enteric-coated aspirin does not appear to help reduce the risk of gastrointestinal bleeding. People who are aspirin-intolerant may gain similar cardiovascular benefits from using clopidogrel instead of aspirin.

A disease in which arteries become dangerously narrowed by lipid deposits. People with diabetes are at increased risk for atherosclerosis.

Atherosclerosis begins when the endothelium, the inner lining of the arteries that has direct contact with the bloodstream, becomes damaged. Over time, fats, cholesterol, fibrin (the principal component of blood clots), platelets, and calcium are deposited in the arterial walls. These materials form plaque, deposits that build up and narrow or block the arteries.

Narrowing of the arteries can cause a number of problems. When atherosclerosis affects the coronary arteries, it can cause coronary heart disease, which in turn can cause angina or a heart attack. Angina pectoris, a type of chest pain, occurs when the heart cannot get enough blood and, hence, oxygen for a given amount of work. Chest pain can be a sign that someone is at risk for a heart attack. A heart attack, or myocardial infarction, occurs when blood flow to the heart muscle abruptly slows or stops. A blockage in the arteries that supply blood to the brain can result in a stroke.

Atherosclerosis can also affect blood vessels in the rest of the body, a condition called peripheral vascular disease. Peripheral vascular disease is common in people with diabetes, and it can place them at risk for developing gangrene of the feet. One symptom of peripheral vascular disease is intermittent claudication, the "on-again-off-again" leg pain that occurs while walking but not at rest. The pain results when not enough blood and oxygen reach the exercising muscles.

The risk factors for atherosclerosis include a sedentary lifestyle, advanced age (it is more common after age 50), a family history of heart disease, high levels of stress, and smoking. Other health conditions that raise one's risk of developing atherosclerosis include high levels of low-density lipoprotein (LDL) cholesterol (the "bad" cholesterol) and low levels of high-density lipoprotein (HDL) cholesterol (the "good" cholesterol), high blood pressure, obesity, and diabetes. In fact, heart attack and stroke are about twice as likely to occur in people with diabetes.

Sometimes, drugs are prescribed to delay the progression or alleviate the symptoms of atherosclerosis. In some cases, surgery may be required to improve blood flow. Prevention—including stopping smoking, treating high blood pressure, maintaining a low-fat, high-fiber diet and a healthy body weight, staying physically active, and keeping blood sugar in good control—is always the best medicine.

A condition in which the body's immune system identifies the body's own tissues as "foreign" rather than self. The purpose of the body's immune system is to fight off infections, such as those caused by viruses and bacteria. Some degree of autoimmunity exists in everybody and usually does no harm. It may be useful, in fact, for destroying cancer cells and recognizing and removing old blood cells and damaged tissues. Yet in a small percentage of people the immune system wages an all-out war on certain proteins and tissues in the body, causing autoimmune diseases. Scientists have isolated more than 80 specific autoimmune diseases, including such common or well-known diseases as rheumatoid arthritis, Graves disease, Hashimoto thyroiditis, multiple sclerosis, systemic lupus erythematosus, Addison disease, and Type 1 diabetes.

Rheumatoid arthritis is a disease in which the immune system launches an attack on collagen (a fibrous protein) in the joints. White blood cells pour into the synovial membrane that lines these joints, causing pain, redness, and swelling.

In Graves disease, the immune system produces antibodies against certain proteins on the surface of the cells of the thyroid gland, a gland that regulates many processes throughout the body. These antibodies stimulate the thyroid gland to produce too much of its hormones, producing such symptoms as nervousness, heart palpitations, weight loss, sweating, and intolerance to heat.

Hashimoto thyroiditis is a disorder in which the immune system gradually destroys the thyroid gland, causing it to secrete less and less of its hormones. This destruction causes a slowing down of various body functions, producing fatigue, lethargy, poor concentration, thinning hair, depression, constipation, feeling cold, tingling in the extremities, and weight gain.

Multiple sclerosis results when the immune system destroys segments of myelin, the substance that sheathes and insulates nerve pathways in the brain and spinal cord and is necessary for efficient conduction of nerve impulses. Destruction of myelin can affect the body in many ways, causing a wide variety of symptoms, such as numbness, muscle weakness, unsteady movement, slurred speech, and blurry vision.

In systemic lupus erythematosus, the immune system forms antibodies against the nuclei of cells, DNA, RNA, and other material, causing inflammation of the connective tissue in one or more parts of the body. It may damage the skin, joints, and internal organs.

Addison disease occurs when the immune system gradually destroys the adrenal cortex, the outer layer of the adrenal glands that produce corticosteroid hormones. As a result, production of hormone decreases, causing loss of appetite, weight loss, weakness, and anemia.

Type 1 diabetes develops when the immune system recognizes and attacks proteins on the surface of the beta cells, the cells of the pancreas that secrete insulin. White blood cells flood into the pancreatic islets (cell clusters that include the beta cells) and cause an inflammation known as insulitis. Once enough beta cells have been destroyed, the symptoms of diabetes begin to appear.

While everyone has some autoimmunity, not everyone develops autoimmune diseases. Scientists believe that certain people are genetically susceptible to developing autoimmune diseases, but that environmental factors play a role in causing or "triggering" these diseases. They have identified a number of potential triggers for autoimmune diseases, including certain drugs, environmental pollutants, and viruses.

Researchers have identified two basic types of autoimmune disease: organ-specific and non-organ-specific. Organ-specific autoimmune diseases are those that attack specific types of tissues in specific organs, such as the thyroid gland, the adrenal glands, and the pancreas. Type 1 diabetes is one example of an organ-specific autoimmune disease. Non-organ-specific autoimmune diseases target more general types of tissues, such as connective tissue. The best known of the non-organ-specific autoimmune diseases are rheumatoid arthritis and systemic lupus erythematosus.

These two distinct clusters of autoimmune diseases tend to run together within individuals and within families. For example, some 15% to 20% of people with Type 1 diabetes have at least the early manifestations of autoimmune thyroid disease (Graves disease or Hashimoto thyroiditis). Their first-degree relatives (parents, siblings, and children) are at increased risk of developing these disorders as well. People with Type 1 diabetes also have a slightly elevated risk for developing Addison disease.

An estimated 40% of families in which one member has Type 1 diabetes has another member with at least the early indications of autoimmune disease.

The rate at which an insulin pump infuses small, “background” doses of short-acting insulin. Over a 24-hour period, the basal flow of insulin accounts for about 50% of a person’s total daily insulin requirement. However, this may vary depending on overall caloric intake or activity level.

Many people use an insulin pump because it closely mimics what a healthy pancreas does: It provides a steady flow of insulin all the time to help the body utilize the glucose that is always in the bloodstream, providing energy for thinking, breathing, and other automatic functions. In addition, a pump allows users to give themselves larger insulin doses (“boluses”) at mealtimes to cover the amount of carbohydrate ingested. This combination of basal and bolus doses helps keep blood glucose levels close to normal at all times, which in the long run can help prevent diabetic complications. (For people who inject insulin, the intermediate- or long-acting insulin serves as the basal insulin, and short- or rapid-acting insulin injections are used to cover meals. The long-acting insulin analog glargine [brand name Lantus] provides “peakless” basal coverage for up to 24 hours.)

Pump users can program the pump to deliver higher or lower basal doses at certain times of day to meet the body’s changing insulin needs. For example, the nighttime release of counterregulatory hormones (such as growth hormone, epinephrine, and cortisol) can cause a rise in blood sugar in the morning called the dawn phenomenon. For this reason, pump users often need to program a higher basal rate in the morning. Usually, only 2–4 different rates are needed during a 24-hour period. One 24-hour sequence of basal rates is called a basal flow pattern, or basal profile.

Pump users may also need to program different basal profiles for specific days. For example, someone who is a sedentary desk jockey during the work week but is active on weekends may need to program two different basal rate profiles—one for weekdays and another for weekends, when the extra activity helps him burn glucose better during the day. People who work different shifts may need to program different basal profiles depending on which shift they’re working on a given day. Some women may need a different basal profile for the days before menstruation, when blood glucose levels often run higher than usual.

In addition, pump users can set temporary basal rates, which they activate during exercise, for example; after the set period of time, the pump automatically returns to the original basal profile.

When first starting insulin pump therapy, your health-care provider will help you determine your initial basal rate and fine-tune your basal profiles through frequent blood glucose self-monitoring. Frequent low blood glucose could indicate that the basal rate on the pump is too high; frequent highs could mean that the basal rate should be increased.