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.
It will surely be tough eating salads and vegetables when everyone else at your dinner table is eating pizza. Decide that this diagnosis can benefit the health of the entire family. Educate your family about the benefits of eating a healthy diet. Take your children grocery shopping with you. Practice the plate method: Aim to make half your plate non-starchy vegetables; a quarter lean protein; and a quarter whole grains or starchy vegetables, like sweet potatoes. Make exercise part of your daily routine and include your family. Go for walks after dinner. Head to the pool on the weekends, or enroll in an exercise class. If you don't have children, aim to find others with diabetes or friends that can act as your workout partners.
Diabetes is one of the first diseases described[21] with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine."[110] The first described cases are believed to be of type 1 diabetes.[110] Indian physicians around the same time identified the disease and classified it as madhumeha or honey urine noting that the urine would attract ants.[110] The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius Of Memphis.[110] The disease was rare during the time of the Roman empire with Galen commenting that he had only seen two cases during his career.[110]
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
Information on mortality rates for type 1 diabetes mellitus is difficult to ascertain without complete national registers of childhood diabetes, although age-specific mortality is probably double that of the general population. [35, 36] Children aged 1-4 years are particularly at risk and may die due to DKA at the time of diagnosis. Adolescents are also a high-risk group. Most deaths result from delayed diagnosis or neglected treatment and subsequent cerebral edema during treatment for DKA, although untreated hypoglycemia also causes some deaths. Unexplained death during sleep may also occur and appears more likely to affect young males. [37]
The tuberculosis skin test is based on the fact that infection with M. tuberculosis produces a delayed-type hypersensitivity skin reaction to certain components of the bacterium. The standard recommended tuberculin test is administered by injecting 0.1mL of 5 TU (tuberculin units) PPD into the top layers of skin of the forearm. "Reading" the skin test means detecting a raised, thickened local area of skin reaction, referred to as induration. The area of induration (palpable, raised, hardened area) around the site of injection is the reaction to tuberculin.
Type 1 DM is caused by autoimmune destruction of the insulin-secreting beta cells of the pancreas. The loss of these cells results in nearly complete insulin deficiency; without exogenous insulin, type 1 DM is rapidly fatal. Type 2 DM results partly from a decreased sensitivity of muscle cells to insulin-mediated glucose uptake and partly from a relative decrease in pancreatic insulin secretion.
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.
Type 2 diabetes typically starts with insulin resistance. That is, the cells of the body resist insulin’s efforts to escort glucose into the cells. What causes insulin resistance? It appears to be caused by an accumulation of microscopic fat particles within muscle and liver cells.4 This fat comes mainly from the diet—chicken fat, beef fat, cheese fat, fish fat, and even vegetable fat. To try to overcome insulin resistance, the pancreas produces extra insulin. When the pancreas can no longer keep up, blood sugar rises. The combination of insulin resistance and pancreatic cell failure leads to type 2 diabetes.
“I don’t think that anybody has put their finger on what the true cause of diabetes is, or that we’re going to find a single cause,” Grieger says. So if you’ve been diagnosed with prediabetes or have other risk factors for the disease, avoiding any one food group entirely — even sugar — won’t completely offset your risk. Rather, it’s important to prioritize proper nutrition, exercise regularly, and maintain a healthy weight — all steps the American Diabetes Association recommends for preventing type 2 diabetes.
There are other factors that also fall into the category of environmental (as opposed to genetic) causes of diabetes. Certain injuries to the pancreas, from physical trauma or from drugs, can harm beta cells, leading to diabetes. Studies have also found that people who live in polluted areas are prone to type 2, perhaps because of inflammation. And an alternate theory of insulin resistance places the blame on damage caused by inflammation. Age also factors into type 2; beta cells can wear out over time and become less capable of producing enough insulin to overcome insulin resistance, which is why older people are at greater risk of type 2.
In ‘type 2 diabetes’ (previously called non-insulin-dependent diabetes mellitus), which accounts for 90% of all diabetes, the beta cells do not stop making insulin completely, but the insulin produced does not work properly so it struggles to store the sugar found in the blood. As a consequence, the pancreas has to produce more insulin to compensate for this reduction in insulin function. This is called insulin resistance and is commonly linked to obesity. This type of diabetes is seen more commonly over the age of 40 years but can occur at any age.  

Jump up ^ Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, Seshasai SR, McMurray JJ, Freeman DJ, Jukema JW, Macfarlane PW, Packard CJ, Stott DJ, Westendorp RG, Shepherd J, Davis BR, Pressel SL, Marchioli R, Marfisi RM, Maggioni AP, Tavazzi L, Tognoni G, Kjekshus J, Pedersen TR, Cook TJ, Gotto AM, Clearfield MB, Downs JR, Nakamura H, Ohashi Y, Mizuno K, Ray KK, Ford I (February 2010). "Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials". Lancet. 375 (9716): 735–42. doi:10.1016/S0140-6736(09)61965-6. PMID 20167359.
Type 2 diabetes is mainly caused by insulin resistance. This means no matter how much or how little insulin is made, the body can't use it as well as it should. As a result, glucose can't be moved from the blood into cells. Over time, the excess sugar in the blood gradually poisons the pancreas causing it to make less insulin and making it even more difficult to keep blood glucose under control.
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Most people with diabetes should keep a record of their blood glucose levels and report them to their doctor or nurse for advice in adjusting the dose of insulin or the oral antihyperglycemic drug. Many people can learn to adjust the insulin dose on their own as necessary. Some people who have mild or early type 2 diabetes that is well-controlled with one or two drugs may be able to monitor their fingerstick glucose levels relatively infrequently.
With gestational diabetes, risks to the unborn baby are even greater than risks to the mother. Risks to the baby include abnormal weight gain before birth, breathing problems at birth, and higher obesity and diabetes risk later in life. Risks to the mother include needing a cesarean section due to an overly large baby, as well as damage to heart, kidney, nerves, and eye.
Jump up ^ McBrien, K; Rabi, DM; Campbell, N; Barnieh, L; Clement, F; Hemmelgarn, BR; Tonelli, M; Leiter, LA; Klarenbach, SW; Manns, BJ (6 August 2012). "Intensive and Standard Blood Pressure Targets in Patients With Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis". Archives of Internal Medicine. 172 (17): 1–8. doi:10.1001/archinternmed.2012.3147. PMID 22868819.
Diabetes mellitus results mainly from a deficiency or diminished effectiveness of insulin that is normally produced by the beta cells of the pancreas. It is characterised by high blood sugar, altered sugar and glucose metabolism and this affects blood vessels and causes several organ damage. Causes of diabetes can be classified according to the types of diabetes.
It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.
A final note about type 1: Some people have a "honeymoon" period, a brief remission of symptoms while the pancreas is still secreting some insulin. The honeymoon phase typically occurs after insulin treatment has been started. A honeymoon can last as little as a week or even up to a year. But the absence of symptoms doesn't mean the diabetes is gone. The pancreas will eventually be unable to secrete insulin, and, if untreated, the symptoms will return.
Taking the drugs used to treat diabetes, particularly insulin, may be difficult for some older people. For those with vision problems or other problems that make accurately filling a syringe difficult, a caregiver can prepare the syringes ahead of time and store them in the refrigerator. People whose insulin dose is stable may purchase pre-filled syringes. Prefilled insulin pen devices may be easier for people with physical limitations. Some of these devices have large numbers and easy-to-turn dials.
Classic symptoms of DM are polyuria, polydipsia, and weight loss. In addition, patients with hyperglycemia often have blurred vision, increased food consumption (polyphagia), and generalized weakness. When a patient with type 1 DM loses metabolic control (such as during infections or periods of noncompliance with therapy), symptoms of diabetic ketoacidosis occur. These may include nausea, vomiting, dizziness on arising, intoxication, delirium, coma, or death. Chronic complications of hyperglycemia include retinopathy and blindness, peripheral and autonomic neuropathies, glomerulosclerosis of the kidneys (with proteinuria, nephrotic syndrome, or end-stage renal failure), coronary and peripheral vascular disease, and reduced resistance to infections. Patients with DM often also sustain infected ulcerations of the feet, which may result in osteomyelitis and the need for amputation.
"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas.
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.
Hyperglycemia or high blood sugar is a serious health problem for diabetics. There are two types of hyperglycemia, 1) fasting, and 2)postprandial or after meal hyperglycemia. Hyperglycemia can also lead to ketoacidosis or hyperglycemic hyperosmolar nonketotic syndrome (HHNS). There are a variety of causes of hyperglycemia in people with diabetes. Symptoms of high blood sugar may include increased thirst, headaches, blurred vision, and frequent urination.Treatment can be achieved through lifestyle changes or medications changes. Carefully monitoring blood glucose levels is key to prevention.
In type 2 diabetes (formerly called non– insulin-dependent diabetes or adult-onset diabetes), the pancreas often continues to produce insulin, sometimes even at higher-than-normal levels, especially early in the disease. However, the body develops resistance to the effects of insulin, so there is not enough insulin to meet the body’s needs. As type 2 diabetes progresses, the insulin-producing ability of the pancreas decreases.
Hypoglycemia means abnormally low blood sugar (glucose). In patients with diabetes, the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications, to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. When low blood sugar levels occur because of too much insulin, it is called an insulin reaction. Sometimes, low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion.
Regarding age, data shows that for each decade after 40 years of age regardless of weight there is an increase in incidence of diabetes. The prevalence of diabetes in persons 65 years of age and older is around 25%. Type 2 diabetes is also more common in certain ethnic groups. Compared with a 7% prevalence in non-Hispanic Caucasians, the prevalence in Asian Americans is estimated to be 8.0%, in Hispanics 13%, in blacks around 12.3%, and in certain Native American communities 20% to 50%. Finally, diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy (gestational diabetes).
Type 2 diabetes, which is often diagnosed when a person has an A1C of at least 7 on two separate occasions, can lead to potentially serious issues, like neuropathy, or nerve damage; vision problems; an increased risk of heart disease; and other diabetes complications. A person’s A1C is the two- to three-month average of his or her blood sugar levels.
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