Skin care: High blood glucose and poor circulation can lead to skin problems such as slow healing after an injury or frequent infections. Make sure to wash every day with a mild soap and warm water, protect your skin by using sunscreen, take good care of any cuts or scrapes with proper cleansing and bandaging, and see your doctor when cuts heal slowly or if an infection develops.
The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in patients with diabetes.
It is especially important that persons with diabetes who are taking insulin not skip meals; they must also be sure to eat the prescribed amounts at the prescribed times during the day. Since the insulin-dependent diabetic needs to match food consumption to the available insulin, it is advantageous to increase the number of daily feedings by adding snacks between meals and at bedtime.
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.
The information contained in this monograph is for educational purposes only. This information is not a substitute for professional medical advice, diagnosis, or treatment. If you have or suspect you may have a health concern, consult your professional health care provider. Reliance on any information provided in this monograph is solely at your own risk.
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.
They may need to take medications in order to keep glucose levels within a healthy range. Medications for type 2 diabetes are usually taken by mouth in the form of tablets and should always be taken around meal times and as prescribed by the doctor. However, if blood glucose is not controlled by oral medications, a doctor may recommend insulin injections.
Low testosterone (low-T) can be caused by conditions such as type 2 diabetes, obesity, liver or kidney disease, hormonal disorders, certain infections, and hypogonadism. Signs and symptoms that a person may have low-T include insomnia, increased body fat, weight gain, reduced muscle, infertility, decreased sex drive, depression, and worsening of congestive heart failure or sleep apnea.
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.
Management. There is no cure for diabetes; the goal of treatment is to maintain blood glucose and lipid levels within normal limits and to prevent complications. In general, good control is achieved when the following occur: fasting plasma glucose is within a specific range (set by health care providers and the individual), glycosylated hemoglobin tests show that blood sugar levels have stayed within normal limits from one testing period to the next, the patient's weight is normal, blood lipids remain within normal limits, and the patient has a sense of health and well-being.
In the sunshine, molecules in the skin are converted to vitamin D. But people stay indoors more these days, which could lead to vitamin D deficiency. Research shows that if mice are deprived of vitamin D, they are more likely to become diabetic. In people, observational studies have also found a correlation between D deficiency and type 1. "If you don't have enough D, then [your immune system] doesn't function like it should," says Chantal Mathieu, MD, PhD, a professor of experimental medicine and endocrinology at Katholieke Universiteit Leuven in Belgium. "Vitamin D is not the cause of type 1 diabetes. [But] if you already have a risk, you don't want to have vitamin D deficiency on board because that's going to be one of the little pushes that pushes you in the wrong direction."
Diabetes is one of the first diseases described with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The first described cases are believed to be of type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or honey urine noting that the urine would attract ants. The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius Of Memphis. The disease was rare during the time of the Roman empire with Galen commenting that he had only seen two cases during his career.
A person of Asian origin aged 35 yr or more with two or more of the above risk factors, should undergo a screening test for diabetes. An oral glucose tolerance test (OGTT) is commonly used as the screening test10. Fasting and 2 h post glucose tests can identify impaired fasting glucose (IFG) (fasting glucose >110 - <125 mg/dl), impaired glucose tolerance (IGT) (2 h glucose >140-<200 mg/dl) and presence of diabetes (fasting > 126 and 2 h glucose >200 mg/dl). If a random blood glucose value is > 150 mg/dl, further confirmation by an OGTT is warranted. Recently, glycosylated haemoglobin (HbA1c) has been recommended as the test for diagnosis of diabetes (>6.5%). Presence of pre-diabetes is indicated by HbA1c values between 5.7 - 6.4 per cent11.
Studies show that good control of blood sugar levels decreases the risk of complications from diabetes. Patients with better control of blood sugar have reduced rates of diabetic eye disease, kidney disease, and nerve disease. It is important for patients to measure their measuring blood glucose levels. Hemoglobin A1c can also be measured with a blood test and gives information about average blood glucose over the past 3 months.
Although urine can also be tested for the presence of glucose, checking urine is not a good way to monitor treatment or adjust therapy. Urine testing can be misleading because the amount of glucose in the urine may not reflect the current level of glucose in the blood. Blood glucose levels can get very low or reasonably high without any change in the glucose levels in the urine.
Excessive thirst typically goes hand-in-hand with increased urination. As your body pulls water out of the tissues to dilute your blood and to rid your body of sugar through the urine, the urge to drink increases. Many people describe this thirst as an unquenchable one. To stay hydrated, you drink excessive amounts of liquids. And if those liquids contain simple sugars (soda, sweet iced tea, lemonade, or juice, for example) your sugars will skyrocket even higher.
Insulin is a hormone produced by the beta cells within the pancreas in response to the intake of food. The role of insulin is to lower blood sugar (glucose) levels by allowing cells in the muscle, liver and fat to take up sugar from the bloodstream that has been absorbed from food, and store it away as energy. In type 1 diabetes (previously called insulin-dependent diabetes mellitus), the insulin-producing cells are destroyed and the body is not able to produce insulin naturally. This means that sugar is not stored away but is constantly released from energy stores giving rise to high sugar levels in the blood. This in turn causes dehydration and thirst (because the high glucose ‘spills over’ into the urine and pulls water out of the body at the same time). To exacerbate the problem, because the body is not making insulin it ‘thinks’ that it is starving so does everything it can to release even more stores of energy into the bloodstream. So, if left untreated, patients become increasingly unwell, lose weight, and develop a condition called diabetic ketoacidosis, which is due to the excessive release of acidic energy stores and causes severe changes to how energy is used and stored in the body.
There is no single gene that “causes” type 1 diabetes. Instead, there are a large number of inherited factors that may increase an individual’s likelihood of developing diabetes. This is known as multifactorial inheritance. The genes implicated in the development of type 1 diabetes mellitus control the human leukocyte antigen (HLA) system. This system is involved in the complex process of identifying cells which are a normal part of the body, and distinguishing them from foreign cells, such as those of bacteria or viruses. In an autoimmune disease such as diabetes mellitus, this system makes a mistake in identifying the normal ‘self’ cells as ‘foreign’, and attacks the body.
When the blood glucose level rises above 160 to 180 mg/dL, glucose spills into the urine. When the level of glucose in the urine rises even higher, the kidneys excrete additional water to dilute the large amount of glucose. Because the kidneys produce excessive urine, people with diabetes urinate large volumes frequently (polyuria). The excessive urination creates abnormal thirst (polydipsia). Because excessive calories are lost in the urine, people may lose weight. To compensate, people often feel excessively hungry.
a chronic metabolic disorder in which the use of carbohydrate is impaired and that of lipid and protein is 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.
Diabetes mellitus is a chronic disease for which there is treatment but no known cure. Treatment is aimed at keeping blood glucose levels as close to normal as possible. This is achieved with a combination of diet, exercise and insulin or oral medication. People with type 1 diabetes need to be hospitalized right after they are diagnosed to get their glucose levels down to an acceptable level.
Patients with type 1 DM, unless they have had a pancreatic transplant, require insulin to live; intensive therapy with insulin to limit hyperglycemia (“tight control”) is more effective than conventional therapy in preventing the progression of serious microvascular complications such as kidney and retinal diseases. Intensive therapy consists of three or more doses of insulin injected or administered by infusion pump daily, with frequent self-monitoring of blood glucose levels as well as frequent changes in therapy as a result of contacts with health care professionals. Some negative aspects of intensive therapy include a three times more frequent occurrence of severe hypoglycemia, weight gain, and an adverse effect on serum lipid levels, i.e., a rise in total cholesterol, LDL cholesterol, and triglycerides and a fall in HDL cholesterol. Participation in an intensive therapy program requires a motivated patient, but it can dramatically reduce eye, nerve, and renal complications compared to conventional therapy. See: insulin pump for illus.
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.
^ Jump up to: a b c Simpson, Terry C.; Weldon, Jo C.; Worthington, Helen V.; Needleman, Ian; Wild, Sarah H.; Moles, David R.; Stevenson, Brian; Furness, Susan; Iheozor-Ejiofor, Zipporah (2015-11-06). "Treatment of periodontal disease for glycaemic control in people with diabetes mellitus". Cochrane Database of Systematic Reviews (11): CD004714. doi:10.1002/14651858.CD004714.pub3. ISSN 1469-493X. PMID 26545069.
Medications used to treat diabetes do so by lowering blood sugar levels. There is broad consensus that when people with diabetes maintain tight glucose control (also called "tight glycemic control") -- keeping the glucose levels in their blood within normal ranges - that they experience fewer complications like kidney problems and eye problems. There is however debate as to whether this is cost effective for people later in life.
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.
The United Kingdom Prospective Diabetes Study (UKPDS) was a clinical study conducted by Z that was published in The Lancet in 1998. Around 3,800 people with type 2 diabetes were followed for an average of ten years, and were treated with tight glucose control or the standard of care, and again the treatment arm had far better outcomes. This confirmed the importance of tight glucose control, as well as blood pressure control, for people with this condition.
What does the research say about proactive type 2 diabetes management? Research shows that proactive management can pay off in fewer complications down the road. In the landmark UKPDS study, 5,102 patients newly diagnosed with type 2 diabetes were followed for an average of 10 years to determine whether intensive use of blood glucose-lowering drugs would result in health benefits. Tighter average glucose control (an A1c of 7.0% vs. an A1c of 7.9%) reduced the rate of complications in the eyes, kidneys, and nervous system, by 25%. For every percentage point decrease in A1c (e.g., from 9% to 8%), there was a 25% reduction in diabetes-related deaths, and an 18% reduction in combined fatal and nonfatal heart attacks.
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
nephrogenic diabetes insipidus a rare form caused by failure of the renal tubules to reabsorb water; there is excessive production of antidiuretic hormone but the tubules fail to respond to it. Characteristics include polyuria, extreme thirst, growth retardation, and developmental delay. The condition does not respond to exogenous vasopressin. It may be inherited as an X-linked trait or be acquired as a result of drug therapy or systemic disease.
Unlike people with type 1 diabetes, people with type 2 diabetes produce insulin; however, the insulin their pancreas secretes is either not enough or the body is unable to recognize the insulin and use it properly (insulin resistance). When there isn't enough insulin or the insulin is not used as it should be, glucose (sugar) can't get into the body's cells and builds up in the bloodstream instead. When glucose builds up in the blood instead of going into cells, it causes damage in multiple areas of the body. Also, since cells aren't getting the glucose they need, they can't function properly.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose. people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).
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Diabetes is a metabolic disorder that occurs when your blood sugar (glucose), is too high (hyperglycemia). Glucose is what the body uses for energy, and the pancreas produces a hormone called insulin that helps convert the glucose from the food you eat into energy. When the body does not produce enough insulin - or does not produce any at all - the glucose does not reach your cells to be used for energy. This results in diabetes.