Periodontal Disease. Periodontal disease is a commonly observed dental problem for patients with diabetes. It is similar to the periodontal disease encountered among nondiabetic patients. However, as a consequence of the impaired immunity and healing associated with diabetes, it may be more severe and progress more rapidly (see Right). The potential for these changes points to the need for periodic professional evaluation and treatment.
Clear evidence suggests a genetic component in type 1 diabetes mellitus. Monozygotic twins have a 60% lifetime concordance for developing type 1 diabetes mellitus, although only 30% do so within 10 years after the first twin is diagnosed. In contrast, dizygotic twins have only an 8% risk of concordance, which is similar to the risk among other siblings.
Examples of simple or refined carbohydrates, on the other hand, exist in various forms — from the sucrose in the table sugar you use to bake cookies, to the various kinds of added sugar in packaged snacks, fruit drinks, soda, and cereal. Simple carbohydrates are natural components of many fresh foods, too, such as the lactose in milk and the fructose in fruits, and therefore, a healthy, well-balanced diet will always contain these types of sugars.
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
The body will attempt to dilute the high level of glucose in the blood, a condition called hyperglycemia, by drawing water out of the cells and into the bloodstream in an effort to dilute the sugar and excrete it in the urine. It is not unusual for people with undiagnosed diabetes to be constantly thirsty, drink large quantities of water, and urinate frequently as their bodies try to get rid of the extra glucose. This creates high levels of glucose in the urine.
Can you “exercise your way” out of this problem? Sometimes you can; however, the key is exercising properly. For younger patients, it is best to exercise briefly and intensely. Within the first 20 minutes of intense exercise, your body burns its sugar stores, which are hanging out in liver and muscle again. After that, you start burning fat. Although this sounds good; and to some extent it is, if you spend hours running or exercising excessively, you train your body to burn fat efficiently, which subsequently lead to also training your body to store fat efficiently.
Type I diabetes, sometimes called juvenile diabetes, begins most commonly in childhood or adolescence. In this form of diabetes, the body produces little or no insulin. It is characterized by a sudden onset and occurs more frequently in populations descended from Northern European countries (Finland, Scotland, Scandinavia) than in those from Southern European countries, the Middle East, or Asia. In the United States, approximately three people in 1,000 develop Type I diabetes. This form also is called insulin-dependent diabetes because people who develop this type need to have daily injections of insulin.
A chronic metabolic disorder marked by hyperglycemia. DM results either from failure of the pancreas to produce insulin (type 1 DM) or from insulin resistance, with inadequate insulin secretion to sustain normal metabolism (type 2 DM). Either type of DM may damage blood vessels, nerves, kidneys, the retina, and the developing fetus and the placenta during pregnancy. Type 1 or insulin-dependent DM has a prevalence of just 0.3 to 0.4%. Type 2 DM (formerly called adult-onset DM) has a prevalence in the general population of 6.6%. In some populations (such as older persons, Native Americans, African Americans, Pacific Islanders, Mexican Americans), it is present in nearly 20% of adults. Type 2 DM primarily affects obese middle-aged people with sedentary lifestyles, whereas type 1 DM usually occurs in children, most of whom are active and thin, although extremely obese children are now being diagnosed with type 2 diabetes as well. See: table; dawn phenomenon; insulin; insulin pump; insulin resistance; diabetic polyneuropathy; Somogyi phenomenon
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.[53]
Diet. In general, the diabetic diet is geared toward providing adequate nutrition with sufficient calories to maintain normal body weight; the intake of food is adjusted so that blood sugar and serum cholesterol levels are kept within acceptable limits. Overweight diabetic patients should limit caloric intake until target weight is achieved. In persons with type 2 diabetes this usually results in marked improvement and may eliminate the need for drugs such as oral hypoglycemic agents.
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
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Because both yeast and bacteria multiply more quickly when blood sugar levels are elevated, women with diabetes are overall at a higher risk of feminine health issues, such as bacterial infections, yeast infections, and vaginal thrush, especially when blood sugar isn't well controlled. And a lack of awareness about having prediabetes or diabetes can make managing blood sugar impossible.
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