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.
Culturally appropriate education may help people with type 2 diabetes control their blood sugar levels, for up to 24 months. If changes in lifestyle in those with mild diabetes has not resulted in improved blood sugars within six weeks, medications should then be considered. There is not enough evidence to determine if lifestyle interventions affect mortality in those who already have DM2.
A healthy lifestyle can prevent almost all cases of type 2 diabetes. A large research study called the Diabetes Prevention Program, found that patients who made intensive changes including diet and exercise, reduced their risk of developing diabetes by 58%. Patients who were over 60 years old seemed to experience extra benefit; they reduced their risk by 71%. In comparison, patients who were given the drug metformin for prevention only reduced their risk by 31%.
Is it your fault for getting type 2 diabetes? No – type 2 diabetes is not a personal failing. It develops through a combination of factors that are still being uncovered and better understood. Lifestyle (food, exercise, stress, sleep) certainly plays a major role, but genetics play a significant role as well. Type 2 diabetes is often described in the media as a result of being overweight, but the relationship is not that simple. Many overweight individuals never get type 2, and some people with type 2 were never overweight, (although obesity is probably an underlying cause of insulin resistance). To make matters worse, when someone gains weight (for whatever reason), the body makes it extremely difficult to lose the new weight and keep it off. If it were just a matter of choice or a bit of willpower, we would probably all be skinny. At its core, type 2 involves two physiological issues: resistance to the insulin made by the person’s beta cells and too little insulin production relative to the amount one needs.
Type 2 diabetes, the most common type of diabetes, is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes mainly from the food you eat. Insulin, a hormone made by the pancreas, helps glucose get into your cells to be used for energy. In type 2 diabetes, your body doesn’t make enough insulin or doesn’t use insulin well. Too much glucose then stays in your blood, and not enough reaches your cells.
According to the Mayo Clinic, your risk of developing type 2 diabetes increases as you age. Your risk goes up after age 45 in particular. However, the incidence of type 2 diabetes is increasing dramatically among children, adolescents, and younger adults. Likely factors include reduced exercise, decreased muscle mass, and weight gain as you age. Type 1 diabetes is usually diagnosed by the age of 30.
People with these risk factors should be screened for diabetes at least once every three years. Diabetes risk can be estimated using online risk calculators. Doctors may measure fasting blood glucose levels and hemoglobin A1C level, or do an oral glucose tolerance test. If the test results are on the border between normal and abnormal, doctors do the screening tests more often, at least once a year.
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The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that diabetics visit an eye doctor once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
The problem with sweetened drinks is that, due to their liquid form, they’re among the fastest simple carbs to be digested in the body, causing blood sugar levels to spike even more than a simple carb in solid-food form would. Research supports this idea: A review published in November 2010 in the journal Diabetes Care suggested adding only one serving of a sweetened beverage to your diet may increase your risk for type 2 diabetes by 15 percent.
Oral glucose tolerance test (OGTT): With this test you will be required to fast for at least 8 hours and then are given a drink with 75 g of carbohydrate. Your blood glucose is checked at fasting and then 2 hours after drinking the solution. If your blood glucose is 11.1 mmol/L or higher, your doctor may diagnose diabetes. If your blood glucose 2 hours after drinking the solution is between 7.8 to 11.1 mmol/L, your doctor may diagnose prediabetes. This is the preferred method to test for gestational diabetes.
Diabetes has been recorded throughout history, since Egyptian times. It was given the name diabetes by the ancient Greek physician Aratus of Cappadocia. The full term, however, was not coined until 1675 in Britain by Thomas Willis, who rediscovered that the blood and urine of people with diabetes were sweet. This phenomenon had previously been discovered by ancient Indians.
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.
Insulin is vital to patients with type 1 diabetes - they cannot live without a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death may result.
When you have diabetes, it’s important to avoid eating many packaged, processed snacks such as cookies, chips, cake, granola bars, and the like, in lieu of fresh, whole foods, like fiber-rich fruits, veggies, and whole grains. (27) Eating foods high in fiber can help keep blood sugar levels steady and fill you up, potentially promoting weight loss and improving insulin sensitivity. (28)
Though it may be transient, untreated GDM can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
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.
All children with type 1 diabetes mellitus require insulin therapy. Most require 2 or more injections of insulin daily, with doses adjusted on the basis of self-monitoring of blood glucose levels. Insulin replacement is accomplished by giving a basal insulin and a preprandial (premeal) insulin. The basal insulin is either long-acting (glargine or detemir) or intermediate-acting (NPH). The preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-acting (regular).
Hypoglycemia. Hypoglycemia or “insulin shock” is a common concern in DM management. It typically develops when a diabetic patient takes his or her normal dose of insulin without eating normally. As a result, the administered insulin can push the blood sugar to potentially dangerously low levels. Initially the patient may experience, sweating, nervousness, hunger and weakness. If the hypoglycemic patient is not promptly given sugar (sugar, cola, cake icing), he or she may lose consciousness and even lapse into coma. Questions and Answers about Diabetes and Your Mouth Q: If I have diabetes, will I develop the oral complications that were mentioned? A: It depends. There is a two-way relationship between your oral health and how well your blood sugar is controlled (glycemic control). Poor control of your blood sugar increases your risk of developing the multitude of complications associated with diabetes, including oral complications. Conversely, poor oral health interferes with proper glucose stabilization. Indeed, recent research has shown that diabetic patients who improve their oral health experience a modest improvement in their blood sugar levels. In essence, “Healthy mouths mean healthy bodies.” Q: What are the complications of diabetes therapy that can impact my oral health? A: One of the most worrisome urgent complications associated with diabetes management is the previously described hypoglycemia or insulin shock. In addition, many of the medications prescribed to treat diabetes and its complications, such as hypertension and heart disease, may induce adverse side effects affecting the mouth. Common side effects include dry mouth, taste aberrations, and mouth sores. Q: I have type-2 diabetes. Are my dental problems different than those experienced by people with type-1 diabetes? A: No. All patients with diabetes are at increased risk for the development of dental disease. What is different is that type-2 disease tends to progress more slowly than type-1 disease. Thus, most type-2 diabetes patients are diagnosed later in life, a time in which they are likely to already have existing dental problems. Remember, there is no dental disease unique to diabetes. Uncontrolled or poorly controlled diabetes simply compromises your body’s ability to control the existing disease.
Excessive hunger goes hand-in-hand with fatigue and cell starvation. Because the cells are resistant to the body's insulin, glucose remains in the blood. The cells are then unable to gain access to glucose, which can trigger hunger hormones that tell the brain that you are hungry. Excessive eating can complicate things further by causing blood sugars to increase.
Diabetic peripheral neuropathy is a condition where nerve endings, particularly in the legs and feet, become less sensitive. Diabetic foot ulcers are a particular problem since the patient does not feel the pain of a blister, callous, or other minor injury. Poor blood circulation in the legs and feet contribute to delayed wound healing. The inability to sense pain along with the complications of delayed wound healing can result in minor injuries, blisters, or callouses becoming infected and difficult to treat. In cases of severe infection, the infected tissue begins to break down and rot away. The most serious consequence of this condition is the need for amputation of toes, feet, or legs due to severe infection.
Sources of complex carbohydrates include whole-wheat bread and brown rice, legumes like black beans, and quinoa. These foods contain fiber, vitamins, and minerals that are appropriate for any eating plan, regardless of whether you have prediabetes, have diabetes, or are perfectly healthy. In fact, experts know including complex carbs in your daily diet can help you maintain a healthy weight, among other health benefits.
Q. My 7yr has Diabetes. She been Diabetic for about 5 weeks and we can't get numbers at a good spot. she aether way to low (30- 60 scary when she gets like this) and to high (300 - 400) We been looking at what she eating calling the physician. he been play with here shots but nothing working. Its when she at school is were the nuber are mostly going up an down. we been trying to work with the school but she the only one in the hole school that has Diabetes. what to do ?
Adult and pediatric endocrinologists, specialists in treating hormone imbalances and disorders of the endocrine system, are experts in helping patients with diabetes manage their disease. People with the disease also may be cared for by a number of primary care providers including family or internal medicine practitioners, naturopathic doctors, or nurse practitioners. When complications arise, these patients often consult other specialists, including neurologists, gastroenterologists, ophthalmologists, acupuncturists, surgeons, and cardiologists. Nutritionists, integrative and functional medicine doctors, and physical activity experts such as personal trainers are also important members of a diabetes treatment team. It is important to interview a new health care professional about their experience, expertise, and credentials to make sure they are well qualified to help you.
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.
Inhalable insulin has been developed. The original products were withdrawn due to side effects. Afrezza, under development by the pharmaceuticals company MannKind Corporation, was approved by the United States Food and Drug Administration (FDA) for general sale in June 2014. An advantage to inhaled insulin is that it may be more convenient and easy to use.
A study by Mayer-Davis et al indicated that between 2002 and 2012, the incidence of type 1 and type 2 diabetes mellitus saw a significant rise among youths in the United States. According to the report, after the figures were adjusted for age, sex, and race or ethnic group, the incidence of type 1 (in patients aged 0-19 years) and type 2 diabetes mellitus (in patients aged 10-19 years) during this period underwent a relative annual increase of 1.8% and 4.8%, respectively. The greatest increases occurred among minority youths. 
central diabetes insipidus a metabolic disorder due to injury of the neurohypophyseal system, which results in a deficient quantity of antidiuretic hormone (ADH or vasopressin) being released or produced, resulting in failure of tubular reabsorption of water in the kidney. As a consequence, there is the passage of a large amount of urine having a low specific gravity, and great thirst; it is often attended by voracious appetite, loss of strength, and emaciation. Diabetes insipidus may be acquired through infection, neoplasm, trauma, or radiation injuries to the posterior lobe of the pituitary gland or it may be inherited or idiopathic.
Insulin is a hormone made by your pancreas that acts like a key to let blood sugar into the cells in your body for use as energy. If you have type 2 diabetes, cells don’t respond normally to insulin; this is called insulin resistance. Your pancreas makes more insulin to try to get cells to respond. Eventually your pancreas can’t keep up, and your blood sugar rises, setting the stage for prediabetes and type 2 diabetes. High blood sugar is damaging to the body and can cause other serious health problems, such as heart disease, vision loss, and kidney disease.
Of course, you’re exhausted every now and then. But ongoing fatigue is an important symptom to pay attention to; it might mean the food you’re eating for energy isn’t being broken down and used by cells as it’s supposed to. “You’re not getting the fuel your body needs,” says Dobbins. “You’re going to be tired and feel sluggish.” But in many cases of type 2 diabetes, your sugar levels can be elevated for awhile, so these diabetes symptoms could come on slowly.
To explain what hemoglobin A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these hemoglobin proteins in these cells, it is known as glycosylated hemoglobin or hemoglobin A1c (HBA1c). Measurement of HBA1c gives us an idea of how much sugar is present in the bloodstream for the preceding three months. In most labs, the normal range is 4%-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%). The benefits of measuring A1c is that is gives a more reasonable and stable view of what's happening over the course of time (three months), and the value does not vary as much as finger stick blood sugar measurements. There is a direct correlation between A1c levels and average blood sugar levels as follows.
Low blood sugar (hypoglycemia). If your blood sugar level drops below your target range, it's known as low blood sugar (hypoglycemia). Your blood sugar level can drop for many reasons, including skipping a meal, inadvertently taking more medication than usual or getting more physical activity than normal. Low blood sugar is most likely if you take glucose-lowering medications that promote the secretion of insulin or if you're taking insulin.
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were found in children.
Healthy lifestyle choices can help you prevent type 2 diabetes. Even if you have diabetes in your family, diet and exercise can help you prevent the disease. If you've already received a diagnosis of diabetes, you can use healthy lifestyle choices to help prevent complications. And if you have prediabetes, lifestyle changes can slow or halt the progression from prediabetes to diabetes.
Diabetes: The differences between types 1 and 2 There are fundamental differences between diabetes type 1 and type 2, including when they might occur, their causes, and how they affect someone's life. Find out here what distinguishes the different forms of the disease, the various symptoms, treatment methods, and how blood tests are interpreted. Read now
The ketogenic, or keto, diet calls for dramatically increasing your fat intake and consuming a moderate amount of protein and a very low amount of carbs, with the aim of kicking your body into a natural metabolic state called ketosis, in which it relies on burning fat rather than carbs for energy. Ketosis is different from diabetic ketoacidosis, a health emergency that occurs when insulin levels are low in conjunction with high levels of ketones. (37) Ketones are by-products of metabolism that are released in the blood when carb intake is low.
When you have type 2 diabetes, your cells don't get enough glucose, which may cause you to lose weight. Also, if you are urinating more frequently because of uncontrolled diabetes, you may lose more calories and water, resulting in weight loss, says Daniel Einhorn, MD, medical director of the Scripps Whittier Diabetes Institute and clinical professor of medicine at the University of California in San Diego.