Damage to small blood vessels can affect the eyes, kidneys, and nerves. Damage to eyes, specifically the retina, is called diabetic retinopathy and is the leading cause of blindness. Damage to the kidneys, called diabetic nephropathy, can lead to kidney failure and the need for dialysis. Damage to the nerves that supply the legs and arms and gastrointestinal tract is called diabetic neuropathy. Some people with diabetes who develop peripheral neuropathy (damage to the nerves in the legs) and have poor blood flow to the legs may eventually need an amputation.
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.
The blood vessels and blood are the highways that transport sugar from where it is either taken in (the stomach) or manufactured (in the liver) to the cells where it is used (muscles) or where it is stored (fat). Sugar cannot go into the cells by itself. The pancreas releases insulin into the blood, which serves as the helper, or the "key," that lets sugar into the cells for use as energy.
Some people with type 2 diabetes are treated with insulin. Insulin is either injected with a syringe several times per day, or delivered via an insulin pump. The goal of insulin therapy is to mimic the way the pancreas would produce and distribute its own insulin, if it were able to manufacture it. Taking insulin does not mean you have done a bad job of trying to control your blood glucose—instead it simply means that your body doesn’t produce or use enough of it on its own to cover the foods you eat.
What medication is available for diabetes? Diabetes causes blood sugar levels to rise. The body may stop producing insulin, the hormone that regulates blood sugar, and this results in type 1 diabetes. In people with type 2 diabetes, insulin is not working effectively. Learn about the range of treatments for each type and recent medical developments here. Read now
Patients who suffer from diabetes have a lifelong struggle to attain and maintain blood glucose levels as close to the normal range as possible. With appropriate blood sugar control, the risk of both microvascular (small blood vessel) and neuropathic (nerve) complications is decreased markedly. Additionally, if hypertension (high blood pressure) and hyperlipidemia (high cholesterol) are treated promptly and aggressively, the risk of cardiovascular complications should decrease as well.
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Diabetes mellitus is a condition in which the pancreas no longer produces enough insulin or cells stop responding to the insulin that is produced, so that glucose in the blood cannot be absorbed into the cells of the body. Symptoms include frequent urination, lethargy, excessive thirst, and hunger. The treatment includes changes in diet, oral medications, and in some cases, daily injections of insulin.
Screening for undiagnosed T2DM is recommended at the first prenatal visit in women with above risk factors, using standard diagnostic method criteria. Screening for gestational diabetes (GDM) at 24-28 wk of gestation is recommended in women who do not have previous history of diabetes, as GDM remains asymptomatic11. A history of GDM carries a high risk for developing diabetes.
Hyperglycemia (ie, random blood glucose concentration of more than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with type 1 diabetes mellitus wastes away and eventually dies due to DKA. The effects of insulin deficiency are shown in the image below.
No single environmental trigger has been identified as causing diabetes mellitus, however both infectious agents and dietary factors are thought to be important. Various viruses have been implicated in the development of type I DM. They may act by initiating or modifying the autoimmune process. In particular, the rubella virus and coxsackie viruses have been closely studied. In particular, congenital rubella infection has shown direct relationships with the development of type 1 diabetes mellitus. This is presumably due to the virus (or antibodies against it) damaging the beta cells of the pancreas. Some research has looked at dietary factors that may be associated with type 1 diabetes. In particular, cow’s milk proteins (such as bovine serum albumin) which may have some similarities to pancreatic islet cell markers may be able to trigger the autoimmune process. Other chemicals including nitrosamines have been identified as causes of diabetes mellitus in animal models, but not in humans.
According to the National Institutes of Health, the reported rate of gestational diabetes is between 2% to 10% of pregnancies. Gestational diabetes usually resolves itself after pregnancy. Having gestational diabetes does, however, put mothers at risk for developing type 2 diabetes later in life. Up to 10% of women with gestational diabetes develop type 2 diabetes. It can occur anywhere from a few weeks after delivery to months or years later.
Patients with type 2 diabetes can still make insulin, but not enough to control their glucose levels. Type 2 diabetes is therefore initially treated with a combination of lifestyle changes (diet and exercise) which reduce the need for insulin and therefore lower glucose levels. If this is insufficient to achieve good glucose control, a range of tablets are available. These include metformin and pioglitazone, which, like diet and exercise, reduce insulin requirements; sulphonylureas (e.g. gliclazide), which stimulate insulin secretion; DPP4 inhibitors (e.g sitagliptin) and GLP-1 agonists (e.g. liraglutide), which stimulate insulin production and reduce appetite; and SGLT2 inhibitors (e.g. dapagliflozin), which lower blood sugar levels by causing sugar to pass out of the body in the urine. In many patients, particularly after several years of treatment, insulin production is so low or so insufficient compared with the patient's needs that patients with type 2 diabetes have to be treated with insulin injections, either alone or in combination with tablets.
Type 1 diabetes in pediatric patients has been linked to changes in cognition and brain structure, with a study by Siller et al finding lower volume in the left temporal-parietal-occipital cortex in young patients with type 1 diabetes than in controls. The study also indicated that in pediatric patients, higher severity of type 1 diabetes presentation correlates with greater structural differences in the brain at about 3 months following diagnosis. The investigators found that among study patients with type 1 diabetes, an association existed between the presence of diabetic ketoacidosis at presentation and reduced radial, axial, and mean diffusivity in the major white matter tracts on magnetic resonance imaging (MRI). In those with higher glycated hemoglobin (HbA1c) levels, hippocampal, thalamic, and cerebellar white matter volumes were lower, as was right posterior parietal cortical thickness, while right occipital cortical thickness was greater. Patients in the study were aged 7-17 years. 
Knowledge is power. A certified diabetes educator can provide you with diabetes self-management education. They specialize in diabetes and can help you learn about complicated or easier things. For example, they can help you set up your glucose meter, teach you about how your medicines work, or help you put together a meal plan. You can meet with them one on one or in group setting.
Weight fluctuations also fall under the umbrella of possible diabetes signs and symptoms. When you lose sugar through frequent urination, you also lose calories. At the same time, diabetes may keep the sugar from your food from reaching your cells — leading to constant hunger. The combined effect is potentially rapid weight loss, especially if you have type 1 diabetes.
Because type 2 diabetes is linked to high levels of sugar in the blood, it may seem logical to assume that eating too much sugar is the cause of the disease. But of course, it’s not that simple. “This has been around for years, this idea that eating too much sugar causes diabetes — but the truth is, type 2 diabetes is a multifactorial disease with many different types of causes,” says Lynn Grieger, RDN, CDE, a nutrition coach in Prescott, Arizona, and a medical reviewer for Everyday Health. “Type 2 diabetes is really complex.”
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.
When you have diabetes, excess sugar (glucose) builds up in your blood. Your kidneys are forced to work overtime to filter and absorb the excess sugar. If your kidneys can't keep up, the excess sugar is excreted into your urine, dragging along fluids from your tissues. This triggers more frequent urination, which may leave you dehydrated. As you drink more fluids to quench your thirst, you'll urinate even more.
Progression toward type 2 diabetes may even be self-perpetuating. Once a person begins to become insulin resistant, for whatever reason, things may snowball from there. The increased levels of circulating insulin required to compensate for resistance encourage the body to pack on pounds. That extra weight will in turn make the body more insulin resistant. Furthermore, the heavier a person is, the more difficult it can be to exercise, continuing the slide toward diabetes.
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.
Clear evidence suggests a genetic component in type 1 diabetes mellitus. Monozygotic twins have a 60% lifetime concordance for developing type 1 diabetes mellitus, although only 30% do so within 10 years after the first twin is diagnosed. In contrast, dizygotic twins have only an 8% risk of concordance, which is similar to the risk among other siblings.
Rosiglitazone, a thiazolidinedione, has not been found to improve long-term outcomes even though it improves blood sugar levels. Additionally it is associated with increased rates of heart disease and death. Angiotensin-converting enzyme inhibitors (ACEIs) prevent kidney disease and improve outcomes in those with diabetes. The similar medications angiotensin receptor blockers (ARBs) do not. A 2016 review recommended treating to a systolic blood pressure of 140 to 150 mmHg.
There is evidence that certain emotions can promote type 2 diabetes. A recent study found that depression seems to predispose people to diabetes. Other research has tied emotional stress to diabetes, though the link hasn't been proved. Researchers speculate that the emotional connection may have to do with the hormone cortisol, which floods the body during periods of stress. Cortisol sends glucose to the blood, where it can fuel a fight-or-flight response, but overuse of this system may lead to dysfunction.
Diabetes mellitus is a chronic disease caused by inherited and/or acquired deficiency in production of insulin by the pancreas, or by the ineffectiveness of the insulin produced. Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
Diabetes is a serious and costly disease which is becoming increasingly common, especially in developing countries and disadvantaged minorities. However, there are ways of preventing it and/or controlling its progress. Public and professional awareness of the risk factors for, and symptoms of diabetes are an important step towards its prevention and control.
And go easy on yourself: Sometimes you can be doing everything perfectly and your blood sugars start to creep up. Because diabetes is a progressive disease, your body slowly stops making insulin over time. If you've had diabetes for a very long time, try not to be discouraged if your doctor has to increase your medication or discusses insulin with you. Continue to do what you can to improve your health.
Persons with diabetes who take insulin must be careful about indulging in unplanned exercise. Strenuous physical activity can rapidly lower their blood sugar and precipitate a hypoglycemic reaction. For a person whose blood glucose level is over 250 mg/dl, the advice would be not to exercise at all. At this range, the levels of insulin are too low and the body would have difficulty transporting glucose into exercising muscles. The result of exercise would be a rise in blood glucose levels.
In type 2 diabetes (adult onset diabetes), the pancreas makes insulin, but it either doesn't produce enough, or the insulin does not work properly. Nine out of 10 people with diabetes have type 2. This type occurs most often in people who are over 40 years old but can occur even in childhood if there are risk factors present. Type 2 diabetes may sometimes be controlled with a combination of diet, weight management and exercise. However, treatment also may include oral glucose-lowering medications (taken by mouth) or insulin injections (shots).
Type 1 DM is caused by autoimmune destruction of the insulin-secreting beta cells of the pancreas. The loss of these cells results in nearly complete insulin deficiency; without exogenous insulin, type 1 DM is rapidly fatal. Type 2 DM results partly from a decreased sensitivity of muscle cells to insulin-mediated glucose uptake and partly from a relative decrease in pancreatic insulin secretion.
People with Type 1 diabetes are usually totally dependent on insulin injections for survival. Such people require daily administration of insulin. The majority of people suffering from diabetes have the Type 2 form. Although they do not depend on insulin for survival, about one third of sufferers needs insulin for reducing their blood glucose levels.
Type 2 diabetes is a progressive, chronic disease related to your body's challenges with regulating blood sugar. It is often associated with generalized inflammation. Your pancreas produces the hormone insulin to convert sugar (glucose) to energy that you either use immediately or store. With type 2 diabetes, you are unable to use that insulin efficiently. Although your body produces the hormone, either there isn't enough of it to keep up with the amount of glucose in your system, or the insulin being produced isn't being used as well as it should be, both of which result in high blood sugar levels.
A metabolic disease in which carbohydrate use is reduced and that of lipid and protein enhanced; it is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma; long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
How does type 2 diabetes progress over time? Type 2 diabetes is a progressive disease, meaning that the body’s ability to regulate blood sugar gets worse over time, despite careful management. Over time, the body’s cells become increasingly less responsive to insulin (increased insulin resistance) and beta cells in the pancreas produce less and less insulin (called beta-cell burnout). In fact, when people are diagnosed with type 2 diabetes, they usually have already lost up to 50% or more of their beta cell function. As type 2 diabetes progresses, people typically need to add one or more different types of medications. The good news is that there are many more choices available for treatments, and a number of these medications don’t cause as much hypoglycemia, hunger and/or weight gain (e.g., metformin, pioglitazone, DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, and better insulin). Diligent management early on can help preserve remaining beta cell function and sometimes slow progression of the disease, although the need to use more and different types of medications does not mean that you have failed.
Jump up ^ McBrien, K; Rabi, DM; Campbell, N; Barnieh, L; Clement, F; Hemmelgarn, BR; Tonelli, M; Leiter, LA; Klarenbach, SW; Manns, BJ (6 August 2012). "Intensive and Standard Blood Pressure Targets in Patients With Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis". Archives of Internal Medicine. 172 (17): 1–8. doi:10.1001/archinternmed.2012.3147. PMID 22868819.
Type 1 Diabetes: About 5 to 10 percent of those with diabetes have type 1 diabetes. It's an autoimmune disease, meaning the body's own immune system mistakenly attacks and destroys the insulin-producing cells in the pancreas. Patients with type 1 diabetes have very little or no insulin, and must take insulin everyday. Although the condition can appear at any age, typically it's diagnosed in children and young adults, which is why it was previously called juvenile diabetes.
Diabetes mellitus (DM) comprises a group of disorders characterized by hyperglycemia. It is the sixth leading cause of death in the United States and results in $132 billion in total direct and indirect costs. Although the incidence of Type 1 diabetes has doubled over the past 30 years, the increase in Type 2 diabetes has been even more dramatic. An estimated 20–40% of cases in large pediatric diabetes centers are now Type 2, and the rates are expected to rise along with the epidemic of childhood and adolescent obesity (Chapter 11).
Fatigue and muscle weakness occur because the glucose needed for energy simply is not metabolized properly. Weight loss in type 1 diabetes patients occurs partly because of the loss of body fluid and partly because in the absence of sufficient insulin the body begins to metabolize its own proteins and stored fat. The oxidation of fats is incomplete, however, and the fatty acids are converted into ketone bodies. When the kidney is no longer able to handle the excess ketones the patient develops ketosis. The overwhelming presence of the strong organic acids in the blood lowers the pH and leads to severe and potentially fatal ketoacidosis.
The most common complication of treating high blood glucose levels is low blood glucose levels (hypoglycemia). The risk is greatest for older people who are frail, who are sick enough to require frequent hospital admissions, or who are taking several drugs. Of all available drugs to treat diabetes, long-acting sulfonylurea drugs are most likely to cause low blood glucose levels in older people. When they take these drugs, they are also more likely to have serious symptoms, such as fainting and falling, and to have difficulty thinking or using parts of the body due to low blood glucose levels.
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Regular ophthalmological examinations are recommended for early detection of diabetic retinopathy. The patient is educated about diabetes, its possible complications and their management, and the importance of adherence to the prescribed therapy. The patient is taught the importance of maintaining normal blood pressure levels (120/80 mm Hg or lower). Control of even mild-to-moderate hypertension results in fewer diabetic complications, esp. nephropathy, cerebrovascular disease, and cardiovascular disease. Limiting alcohol intake to approximately one drink daily and avoiding tobacco are also important for self-management. Emotional support and a realistic assessment of the patient's condition are offered; this assessment should stress that, with proper treatment, the patient can have a near-normal lifestyle and life expectancy. Long-term goals for a patient with diabetes should include achieving and maintaining optimal metabolic outcomes to prevent complications; modifying diet and lifestyle to prevent and treat obesity, dyslipidemia, cardiovascular disease, hypertension, and nephropathy; improving physical activity; and allowing for the patient’s nutritional and psychosocial needs and preferences. Assistance is offered to help the patient develop positive coping strategies. It is estimated that 23 million Americans will be diabetic by the year 2030. The increasing prevalence of obesity coincides with the increasing incidence of diabetes; approx. 45% of those diagnosed receive optimal care according to established guidelines. According to the CDC, the NIH, and the ADA, about 40% of Americans between ages 40 and 74 have prediabetes, putting them at increased risk for type 2 diabetes and cardiovascular disease. Lifestyle changes with a focus on decreasing obesity can prevent or delay the onset of diabetes in 58% of this population. The patient and family should be referred to local and national support and information groups and may require psychological counseling.
A study by Chan et al indicated that in pediatric patients with type 1 diabetes, the presence of hypoglycemia is a sign of decreased insulin sensitivity, while hyperglycemia in these patients, especially overnight, signals improved sensitivity to insulin. In contrast, the investigators found evidence that in pediatric patients with type 2 diabetes, markers of metabolic syndrome and hyperglycemia are associated with reduced insulin sensitivity. Patients in the study were between ages 12 and 19 years. 
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.
A growing number of people in the U.S. and throughout the world are overweight and more prone to develop Type 2 diabetes, particularly if they have the genetics for it. "Type 2 diabetes can be caused by genetic inheritance, but by far the obesity epidemic has created massive increases in the occurrence of Type 2 diabetes. This is due to the major insulin resistance that is created by obesity," Gage says.
What you need to know about borderline diabetes Borderline diabetes, known as prediabetes, is a condition where blood sugar levels are higher than normal but not yet high enough to be type 2 diabetes. This MNT Knowledge Center article explains the signs to look out for, how to monitor the disease, and ways to prevent it becoming full diabetes. Read now