Exercise is very important if you have this health condition. Exercise makes cells more insulin sensitive, pulling glucose out of the blood. This brings down blood sugar, and more importantly, gives you better energy because the glucose is being transferred to the cells. Any type of exercise will do this, but extra benefit is gained when the activity helps build muscle, such as weight training or using resistance bands. The benefits of exercise on blood sugar last about 48-72 hours, so it is important for you to be physically active almost every day.
Type 2 diabetes can be prevented with lifestyle changes. People who are overweight and lose as little as 7 percent of their body weight and who increase physical activity (for example, walking 30 minutes per day) can decrease their risk of diabetes mellitus by more than 50%. Metformin and acarbose, drugs that are used to treat diabetes, may reduce the risk of diabetes in people with impaired glucose regulation.
Type 2 diabetes usually has a slower onset and can often go undiagnosed. But many people do have symptoms like extreme thirst and frequent urination. Other signs include sores that won't heal, frequent infections (including vaginal infections in some women), and changes in vision. Some patients actually go to the doctor with symptoms resulting from the complications of diabetes, like tingling in the feet (neuropathy) or vision loss (retinopathy), without knowing they have the disease. This is why screening people at risk for diabetes is so important. The best way to avoid complications is to get blood glucose under control before
Most pediatric patients with diabetes have type 1 diabetes mellitus (T1DM) and a lifetime dependence on exogenous insulin. Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Insulin is produced by the beta cells of the islets of Langerhans located in the pancreas, and the absence, destruction, or other loss of these cells results in type 1 diabetes (insulin-dependent diabetes mellitus [IDDM]). A possible mechanism for the development of type 1 diabetes is shown in the image below. (See Etiology.)
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.
Jump up ^ Ahlqvist, Emma; Storm, Petter; Käräjämäki, Annemari; Martinell, Mats; Dorkhan, Mozhgan; Carlsson, Annelie; Vikman, Petter; Prasad, Rashmi B; Aly, Dina Mansour (2018). "Novel subgroups of adult-onset diabetes and their association with outcomes: a data-driven cluster analysis of six variables". The Lancet Diabetes & Endocrinology. 0 (5): 361–369. doi:10.1016/S2213-8587(18)30051-2. ISSN 2213-8587. PMID 29503172.
Jump up ^ Seida, Jennifer C.; Mitri, Joanna; Colmers, Isabelle N.; Majumdar, Sumit R.; Davidson, Mayer B.; Edwards, Alun L.; Hanley, David A.; Pittas, Anastassios G.; Tjosvold, Lisa; Johnson, Jeffrey A. (Oct 2014). "Effect of Vitamin D3 Supplementation on Improving Glucose Homeostasis and Preventing Diabetes: A Systematic Review and Meta-Analysis". The Journal of Clinical Endocrinology & Metabolism. 99 (10): 3551–60. doi:10.1210/jc.2014-2136. PMC 4483466. PMID 25062463.
DKA usually follows increasing hyperglycemia and symptoms of osmotic diuresis. Users of insulin pumps, by virtue of absent reservoirs of subcutaneous insulin, may present with ketosis and more normal blood glucose levels. They are more likely to present with nausea, vomiting, and abdominal pain, symptoms similar to food poisoning. DKA may manifest as respiratory distress.
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.
Although many of the symptoms of type 1 and type 2 diabetes are similar, they present in very different ways. Many people with type 2 diabetes won’t have symptoms for many years. Then often the symptoms of type 2 diabetes develop slowly over the course of time. Some people with type 2 diabetes have no symptoms at all and don’t discover their condition until complications develop.
Get Educated: The American Diabetes Association advises that all persons with diabetes receive diabetes self-management education (DSME) at diagnosis and thereafter. A certified diabetes educator or other qualified health professional can give you the tools you need to understand and take care of your diabetes. In addition, these individuals are trained to create a customized plan that works for you. Diabetes self-management education is a patient-centered approach that enables patients to get involved in their care.
Though not routinely used any longer, the oral glucose tolerance test (OGTT) is a gold standard for making the diagnosis of type 2 diabetes. It is still commonly used for diagnosing gestational diabetes and in conditions of pre-diabetes, such as polycystic ovary syndrome. With an oral glucose tolerance test, the person fasts overnight (at least eight but not more than 16 hours). Then first, the fasting plasma glucose is tested. After this test, the person receives an oral dose (75 grams) of glucose. There are several methods employed by obstetricians to do this test, but the one described here is standard. Usually, the glucose is in a sweet-tasting liquid that the person drinks. Blood samples are taken at specific intervals to measure the blood glucose.
People with glucose levels between normal and diabetic have impaired glucose tolerance (IGT) or insulin resistance. People with impaired glucose tolerance do not have diabetes, but are at high risk for progressing to diabetes. Each year, 1% to 5% of people whose test results show impaired glucose tolerance actually eventually develop diabetes. Weight loss and exercise may help people with impaired glucose tolerance return their glucose levels to normal. In addition, some physicians advocate the use of medications, such as metformin (Glucophage), to help prevent/delay the onset of overt diabetes.
Triglycerides are a common form of fat that we digest. Triglycerides are the main ingredient in animal fats and vegetable oils. Elevated levels of triglycerides are a risk factor for heart disease, heart attack, stroke, fatty liver disease, and pancreatitis. Elevated levels of triglycerides are also associated with diseases like diabetes, kidney disease, and medications (for example, diuretics, birth control pills, and beta blockers). Dietary changes, and medication if necessary can help lower triglyceride blood levels.
Type 2 diabetes usually begins with insulin resistance, a condition in which muscle, liver, and fat cells do not use insulin well. As a result, your body needs more insulin to help glucose enter cells. At first, the pancreas makes more insulin to keep up with the added demand. Over time, the pancreas can’t make enough insulin, and blood glucose levels rise.
These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication).
1. Monitoring of blood glucose status. In the past, urine testing was an integral part of the management of diabetes, but it has largely been replaced in recent years by self monitoring of blood glucose. Reasons for this are that blood testing is more accurate, glucose in the urine shows up only after the blood sugar level is high, and individual renal thresholds vary greatly and can change when certain medications are taken. As a person grows older and the kidney is less able to eliminate sugar in the urine, the renal threshold rises and less sugar is spilled into the urine. The position statement of the American Diabetes Association on Tests of Glycemia in Diabetes notes that urine testing still plays a role in monitoring in type 1 and gestational diabetes, and in pregnancy with pre-existing diabetes, as a way to test for ketones. All people with diabetes should test for ketones during times of acute illness or stress and when blood glucose levels are consistently elevated.
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.
The beta cells may be another place where gene-environment interactions come into play, as suggested by the previously mentioned studies that link beta cell genes with type 2. "Only a fraction of people with insulin resistance go on to develop type 2 diabetes," says Shulman. If beta cells can produce enough insulin to overcome insulin resistance, a factor that may be genetically predetermined, then a person can stay free of diabetes. But if the beta cells don't have good genes propping them up, then diabetes is the more likely outcome in a person with substantial insulin resistance.
Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.
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.
Some patients with type 2 DM can control their disease with a calorically restricted diet (for instance 1600 to 1800 cal/day), regular aerobic exercise, and weight loss. Most patients, however, require the addition of some form of oral hypoglycemic drug or insulin. Oral agents to control DM include sulfonylurea drugs (such as glipizide), which increase pancreatic secretion of insulin; biguanides or thiazolidinediones (such as metformin or pioglitazone), which increase cellular sensitivity to insulin; or a-glucosidase inhibitors (such as acarbose), which decrease the absorption of carbohydrates from the gastrointestinal tract. Both types of diabetics also may be prescribed pramlintide (Symlin), a synthetic analog of human amylin, a hormone manufactured in the pancreatic beta cells. It enhances postprandial glucose control by slowing gastric emptying, decreasing postprandial glucagon concentrations, and regulating appetite and food intake; thus pramlintide is helpful for patients who do not achieve optimal glucose control with insulin and/or oral antidiabetic agents. When combinations of these agents fail to normalize blood glucose levels, insulin injections are added. Tight glucose control can reduce the patient’s risk of many of the complications of the disease. See: illustration
You have a higher risk of type 2 diabetes if you are older, have obesity, have a family history of diabetes, or do not exercise. Having prediabetes also increases your risk. Prediabetes means that your blood sugar is higher than normal but not high enough to be called diabetes. If you are at risk for type 2 diabetes, you may be able to delay or prevent developing it by making some lifestyle changes.
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.
Because people with type 2 diabetes produce some insulin, ketoacidosis does not usually develop even when type 2 diabetes is untreated for a long time. Rarely, the blood glucose levels become extremely high (even exceeding 1,000 mg/dL). Such high levels often happen as the result of some superimposed stress, such as an infection or drug use. When the blood glucose levels get very high, people may develop severe dehydration, which may lead to mental confusion, drowsiness, and seizures, a condition called hyperosmolar hyperglycemic state. Currently, many people with type 2 diabetes are diagnosed by routine blood glucose testing before they develop such severely high blood glucose levels.
; DM multiaetiology metabolic disease due to reduced/absent production of pancreatic insulin, and/or insulin resistance by peripheral tissue insulin receptors; characterized by reduced carbohydrate metabolism and increased fat and protein metabolism, leading to hyperglycaemia, increasing glycosuria, water and electrolyte imbalance, ketoacidosis, coma and death if left untreated; chronic long-term complications of DM include nephropathy, retinopathy, neuropathy and generalized degenerative changes in large and small arteries; treatment (with insulin/oral hypoglycaemic agents/diet) aims to stabilize blood glucose levels to the normal range (difficult to achieve fully; patients may tend to hyperglycaemia or hypoglycaemia due to mismanagement of glycaemic control); Tables D4-D7
Studies in type 1 patients have shown that in intensively treated patients, diabetic eye disease decreased by 76%, kidney disease decreased by 54%, and nerve disease decreased by 60%. More recently the EDIC trial has shown that type 1 diabetes is also associated with increased heart disease, similar to type 2 diabetes. However, the price for aggressive blood sugar control is a two to three fold increase in the incidence of abnormally low blood sugar levels (caused by the diabetes medications). For this reason, tight control of diabetes to achieve glucose levels between 70 to120 mg/dl is not recommended for children under 13 years of age, patients with severe recurrent hypoglycemia, patients unaware of their hypoglycemia, and patients with far advanced diabetes complications. To achieve optimal glucose control without an undue risk of abnormally lowering blood sugar levels, patients with type 1 diabetes must monitor their blood glucose at least four times a day and administer insulin at least three times per day. In patients with type 2 diabetes, aggressive blood sugar control has similar beneficial effects on the eyes, kidneys, nerves and blood vessels.
Constant advances are being made in development of new oral medications for persons with diabetes. In 2003, a drug called Metaglip combining glipizide and metformin was approved in a dingle tablet. Along with diet and exercise, the drug was used as initial therapy for Type 2 diabetes. Another drug approved by the U.S. Food and Drug Administration (FDA) combines metformin and rosiglitazone (Avandia), a medication that increases muscle cells' sensitivity to insulin. It is marketed under the name Avandamet. So many new drugs are under development that it is best to stay in touch with a physician for the latest information; physicians can find the best drug, diet and exercise program to fit an individual patient's need.
Diabetes has been coined the “silent killer” because the symptoms are so easy to miss. Over 24 million people in America have diabetes, so this is no tiny issue. Kids years ago hardly ever knew another child with diabetes, but such is no longer the case. Approximately 1.25 million children in the United States living with diabetes, which is very telling for state of health in America in 2016 when children are having to endure a medical lifestyle at such a young age.
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.
In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood.
Alternatively, if you hit it really hard for 20 minutes or so, you may never enter the fat burning phase of exercise. Consequently, your body becomes more efficient at storing sugar (in the form of glycogen) in your liver and muscles, where it is needed, as glycogen is the muscles’ primary fuel source. If your body is efficient at storing and using of glycogen, it means that it is not storing fat.
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.
Low blood sugar (hypoglycemia), is common in people with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases. Moderately low blood sugar may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Insulin is a hormone that — in people without diabetes — ferries glucose, or blood sugar, to cells for energy or to be stored for later use. In people with diabetes, cells are resistant to insulin; as a result of this insulin resistance, sugar accumulates in the blood. While eating sugar by itself does not cause insulin resistance, Grieger says, foods with sugar and fat can contribute to weight gain, thereby reducing insulin sensitivity in the body.
Can diabetes be prevented? Why are so many people suffering from it now over decades past? While there will never be anyway to possibly avoid genetic diabetes, there have been cases where dietary changes could perhaps have been made to delay or prevent the ailment from further developing. Doctors report that obesity plays a role, as well as activity levels, and even overall mental health often can be common threads of pre-diabetic patients.
The American Diabetes Association sponsored an international panel in 1995 to review the literature and recommend updates of the classification of diabetes mellitus. The definitions and descriptions that follow are drawn from the Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. The report was first approved in 1997 and modified in 1999. Although other terms are found in older literature and remain in use, their use in current clinical practice is inappropriate. Epidemiologic and research studies are facilitated by use of a common language.
Insulin Therapy. Exogenous insulin is given to patients with diabetes mellitus as a supplement to the insufficient amount of endogenous insulin that they produce. In some cases, this must make up for an absolute lack of insulin from the pancreas. Exogenous insulin is available in various types. It must be given by injection, usually subcutaneously, and because it is a potent drug, the dosage must be measured meticulously. Commonly, regular insulin, which is a fast-acting insulin with a short span of action, is mixed with one of the longer-acting insulins and both types are administered in one injection.
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.
People who are obese -- more than 20% over their ideal body weight for their height -- are at particularly high risk of developing type 2 diabetes and its related medical problems. Obese people have insulin resistance. With insulin resistance, the pancreas has to work overly hard to produce more insulin. But even then, there is not enough insulin to keep sugars normal.
Insulin — the hormone that allows your body to regulate sugar in the blood — is made in your pancreas. Essentially, insulin resistance is a state in which the body’s cells do not use insulin efficiently. As a result, it takes more insulin than normal to transport blood sugar (glucose) into cells, to be used immediately for fuel or stored for later use. A drop in efficiency in getting glucose to cells creates a problem for cell function; glucose is normally the body’s quickest and most readily available source of energy.
Glucagon is a hormone that causes the release of glucose from the liver (for example, it promotes gluconeogenesis). Glucagon can be lifesaving and every patient with diabetes who has a history of hypoglycemia (particularly those on insulin) should have a glucagon kit. Families and friends of those with diabetes need to be taught how to administer glucagon, since obviously the patients will not be able to do it themselves in an emergency situation. Another lifesaving device that should be mentioned is very simple; a medic-alert bracelet should be worn by all patients with diabetes.
There is an overall lack of public awareness of the signs and symptoms of type 1 diabetes. Making yourself aware of the signs and symptoms of type 1 diabetes is a great way to be proactive about your health and the health of your family members. If you notice any of these signs or symptoms, it’s possible that you have (or your child has) type 1 diabetes. A doctor can make that diagnosis by checking blood glucose levels.
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.