Other studies have focused, not on sugar overall but specifically on sodas and other sugar-sweetened beverages. Many have found no significant relationship, apart from sugar’s extra calories that lead to weight gain. For example, the Women’s Health Study,8 the Atherosclerosis Risk in Communities Study,9 the Black Women’s Health Study,10 and the Multi-Ethnic Study of Atherosclerosis found no significant associations between sugar consumption and diabetes risk after adjustment for measures of body weight. Some studies have had mixed results, exonerating sucrose, but indicting glucose and fructose.12,13 And some studies have shown associations between sugar-sweetened beverages and diabetes that persist after adjustment for body weight.14,15
As with many conditions, treatment of type 2 diabetes begins with lifestyle changes, particularly in your diet and exercise. If you have type 2 diabetes, speak to your doctor and diabetes educator about an appropriate diet. You may be referred to a dietitian. It is also a good idea to speak with your doctor before beginning an exercise program that is more vigourous than walking to determine how much and what kind of exercise is appropriate.
Originally described in approximately 30% of patients with type 1 diabetes mellitus, limited joint mobility occurs in 50% of patients older than age 10 years who have had diabetes for longer than 5 years. The condition restricts joint extension, making it difficult to press the hands flat against each other. The skin of patients with severe joint involvement has a thickened and waxy appearance.
Blood sugar should be regularly monitored so that any problems can be detected and treated early. Treatment involves lifestyle changes such as eating a healthy and balanced diet and regular physical exercise. If lifestyle changes alone are not enough to regulate the blood glucose level, anti-diabetic medication in the form of tablets or injections may be prescribed. In some cases, people who have had type 2 diabetes for many years are eventually prescribed insulin injections.
People with type 1 diabetes sometimes receive transplantation of an entire pancreas or of only the insulin-producing cells from a donor pancreas. This procedure may allow people with type 1 diabetes mellitus to maintain normal glucose levels. However, because immunosuppressant drugs must be given to prevent the body from rejecting the transplanted cells, pancreas transplantation is usually done only in people who have serious complications due to diabetes or who are receiving another transplanted organ (such as a kidney) and will require immunosuppressant drugs anyway.
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.
Insulin, a hormone released from the pancreas (an organ behind the stomach that also produces digestive enzymes), controls the amount of glucose in the blood. Glucose in the bloodstream stimulates the pancreas to produce insulin. Insulin helps glucose to move from the blood into the cells. Once inside the cells, glucose is converted to energy, which is used immediately, or the glucose is stored as fat or glycogen until it is needed.
People with type 2 diabetes have insulin resistance, which means the body cannot use insulin properly to help glucose get into the cells. In people with type 2 diabetes, insulin doesn’t work well in muscle, fat, and other tissues, so your pancreas (the organ that makes insulin) starts to put out a lot more of it to try and compensate. "This results in high insulin levels in the body,” says Fernando Ovalle, MD, director of the multidisciplinary diabetes clinic at the University of Alabama in Birmingham. This insulin level sends signals to the brain that your body is hungry.
More common in adults, type 2 diabetes increasingly affects children as childhood obesity increases. There's no cure for type 2 diabetes, but you may be able to manage the condition by eating well, exercising and maintaining a healthy weight. If diet and exercise aren't enough to manage your blood sugar well, you also may need diabetes medications or insulin therapy.
The food that people eat provides the body with glucose, which is used by the cells as a source of energy. If insulin isn't available or doesn't work correctly to move glucose from the blood into cells, glucose will stay in the blood. High blood glucose levels are toxic, and cells that don't get glucose are lacking the fuel they need to function properly.
Rates of diabetes in 1985 were estimated at 30 million, increasing to 135 million in 1995 and 217 million in 2005. This increase is believed to be primarily due to the global population aging, a decrease in exercise, and increasing rates of obesity. The five countries with the greatest number of people with diabetes as of 2000 are India having 31.7 million, China 20.8 million, the United States 17.7 million, Indonesia 8.4 million, and Japan 6.8 million. It is recognized as a global epidemic by the World Health Organization.
Test Your Blood Sugar: Blood sugar testing is an important part of helping to manage your diabetes. Whether you choose to do selective blood sugar testing or test your blood sugar at the same times daily, blood sugar testing gives you another piece of information and can help you change your diet and adjust your fitness routine or medicines. Keeping your blood sugars at target will help to reduce diabetes complications.
Low glycemic index foods also may be helpful. The glycemic index is a measure of how quickly a food causes a rise in your blood sugar. Foods with a high glycemic index raise your blood sugar quickly. Low glycemic index foods may help you achieve a more stable blood sugar. Foods with a low glycemic index typically are foods that are higher in fiber.
Over recent decades, and particularly in the past five years, researchers have found dozens of genes with links to diabetes. The count stands at about 50 genes for type 1 and 38 for type 2. The numbers have risen quickly in recent years because of advances in the gene-sequencing technology used to conduct genome-wide association studies. This technique involves taking the genetic compositions of a group of people with a disease and comparing them en masse to the genomes of people who don't have the disease.
What is type 2 diabetes and prediabetes? Behind type 2 diabetes is a disease where the body’s cells have trouble responding to insulin – this is called insulin resistance. Insulin is a hormone needed to store the energy found in food into the body’s cells. In prediabetes, insulin resistance starts growing and the beta cells in the pancreas that release insulin will try to make even more insulin to make up for the body’s insensitivity. This can go on for a long time without any symptoms. Over time, though, the beta cells in the pancreas will fatigue and will no longer be able to produce enough insulin – this is called “beta burnout.” Once there is not enough insulin, blood sugars will start to rise above normal. Prediabetes causes people to have higher-than-normal blood sugars (and an increased risk for heart disease and stroke). Left unnoticed or untreated, blood sugars continue to worsen and many people progress to type 2 diabetes. After a while, so many of the beta cells have been damaged that diabetes becomes an irreversible condition.
Diabetes insipidus is considered very rare in less 20,000 cases diagnosed per year. Diabetes mellitus is more common, with type 2 diabetes being more common than type 1. There are more than 3 million cases of type 2 diabetes. Unlike diabetes mellitus, diabetes insipidus is not treated by controlling insulin levels. Depending on your symptoms, your doctor may prescribe a low-salt diet, hormone therapy, or have you increase your water intake.
What his theory boils down to is that type 2 diabetes is caused not by extra fat alone, but by fat stored in the wrong places. "Virtually all the individuals [with insulin resistance] have fat accumulation in liver and muscle," Shulman says, where it may disrupt normal biological processes, leading to insulin resistance. "If you can understand this, you can ideally come up with new ways to prevent insulin resistance and type 2 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.
About 40% of diabetes sufferers require oral agents for satisfactory blood glucose control, and some 40% need insulin injections. This hormone was isolated by Frederic Banting and Charles Best in 1921 in Canada. It revolutionized the treatment of diabetes and prevention of its complications, transforming Type 1 diabetes from a fatal disease to one in which long-term survival became achievable.
Jump up ^ Qaseem, Amir; Wilt, Timothy J.; Kansagara, Devan; Horwitch, Carrie; Barry, Michael J.; Forciea, Mary Ann (6 March 2018). "Hemoglobin A Targets for Glycemic Control With Pharmacologic Therapy for Nonpregnant Adults With Type 2 Diabetes Mellitus: A Guidance Statement Update From the American College of Physicians". Annals of Internal Medicine. doi:10.7326/M17-0939.
Sequelae. The long-term consequences of diabetes mellitus can involve both large and small blood vessels throughout the body. That in large vessels is usually seen in the coronary arteries, cerebral arteries, and arteries of the lower extremities and can eventually lead to myocardial infarction, stroke, or gangrene of the feet and legs. atherosclerosis is far more likely to occur in persons of any age who have diabetes than it is in other people. This predisposition is not clearly understood. Some believe that diabetics inherit the tendency to develop severe atherosclerosis as well as an aberration in glucose metabolism, and that the two are not necessarily related. There is strong evidence to substantiate the claim that optimal control will mitigate the effects of diabetes on the microvasculature, particularly in the young and middle-aged who are at greatest risk for developing complications involving the arterioles. Pathologic changes in the small blood vessels serving the kidney lead to nephrosclerosis, pyelonephritis, and other disorders that eventually result in renal failure. Many of the deaths of persons with type 1 diabetes are caused by renal failure.
Type 1 diabetes occurs because the insulin-producing cells of the pancreas (beta cells) are damaged. In type 1 diabetes, the pancreas makes little or no insulin, so sugar cannot get into the body's cells for use as energy. People with type 1 diabetes must use insulin injections to control their blood glucose. Type 1 is the most common form of diabetes in people who are under age 30, but it can occur at any age. Ten percent of people with diabetes are diagnosed with type 1.
DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance
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.
The World Health Organization recommends testing those groups at high risk and in 2014 the USPSTF is considering a similar recommendation. High-risk groups in the United States include: those over 45 years old; those with a first degree relative with diabetes; some ethnic groups, including Hispanics, African-Americans, and Native-Americans; a history of gestational diabetes; polycystic ovary syndrome; excess weight; and conditions associated with metabolic syndrome. The American Diabetes Association recommends screening those who have a BMI over 25 (in people of Asian descent screening is recommended for a BMI over 23).
Does having type 2 diabetes affect life expectancy? While continued improvements in therapies and care for type 2 diabetes may be helping patients live longer, the unfortunate reality is that type 2 diabetes has been shown to decrease life expectancy by up to ten years, according to Diabetes UK. There is still much to be done to ensure that all patients have access to appropriate healthcare and treatments to live a happier and healthier life with type 2 diabetes.
The elderly diabetic person is at increased risk of atrial fibrillation (odds ratio: 1.4 for men and 1.6 for women)232 and at twofold increased risk of thromboembolism from atrial fibrillation.233,234 We can find no subgroup analysis of the major atrial fibrillation trials to examine the benefits of warfarin specifically in older diabetic subjects. It appears that the adverse event rate in diabetic people drops from 8.6 events per 100 patients per year to 2.8 events with warfarin use.234 It is important to check for retinal new vessels when diabetic subjects are placed on warfarin, although the Early Treatment Diabetic Retinopathy Study235 showed no excess vitreous or preretinal hemorrhages in subjects given aspirin for vascular prophylaxis.
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).
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.
Endocrinology A chronic condition which affects ±10% of the general population, characterized by ↑ serum glucose and a relative or absolute ↓ in pancreatic insulin production, or ↓ tissue responsiveness to insulin; if not properly controlled, the excess glucose damages blood vessels of the eyes, kidneys, nerves, heart Types Insulin dependent–type I and non-insulin dependent–type II diabetes Symptoms type 1 DM is associated with ↑ urine output, thirst, fatigue, and weight loss (despite an ↑ appetite), N&V; type 2 DM is associated with, in addition, non-healing ulcers, oral and bladder infections, blurred vision, paresthesias in the hands and feet, and itching Cardiovascular MI, stoke Eyes Retinal damage, blindness Legs/feet Nonhealing ulcers, cuts leading to gangrene and amputation Kidneys HTN, renal failure Neurology Paresthesias, neuropathy Diagnosis Serum glucose above cut-off points after meals or when fasting; once therapy is begun, serum levels of glycosylated Hb are measured periodically to assess adequacy of glucose control Management Therapy reflects type of DM; metformin and triglitazone have equal and additive effects on glycemic control Prognosis A function of stringency of glucose control and presence of complications. See ABCD Trial, Brittle diabetes, Bronze diabetes, Chemical diabetes, Gestational diabetes, Insulin-dependent diabetes, Metformin, MODY diabetes, Nephrogenic diabetes insipidus, Non-insulin-dependent diabetes mellitus, Pseudodiabetes, Secondary diabetes, Starvation diabetes, Troglitazone.
Manage mild hypoglycemia by giving rapidly absorbed oral carbohydrate or glucose; for a comatose patient, administer an intramuscular injection of the hormone glucagon, which stimulates the release of liver glycogen and releases glucose into the circulation. Where appropriate, an alternative therapy is intravenous glucose (preferably no more than a 10% glucose solution). All treatments for hypoglycemia provide recovery in approximately 10 minutes. (See Treatment.)
Watch for thirst or a very dry mouth, frequent urination, vomiting, shortness of breath, fatigue and fruity-smelling breath. You can check your urine for excess ketones with an over-the-counter ketones test kit. If you have excess ketones in your urine, consult your doctor right away or seek emergency care. This condition is more common in people with type 1 diabetes but can sometimes occur in people with type 2 diabetes.
Type 2 diabetes is a preventable disease that affects more than 9 percent of the U.S. population, or about 29 million people. According to the Centers for Disease Control and Prevention, more than a quarter — some 8 million people — remain undiagnosed. With complications including nerve damage, kidney damage, poor blood circulation, and even death, it’s important for us all to know the early signs of type 2 diabetes.