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.
Another diabetes-related sexual dysfunction symptom in men is reduced amounts of ejaculation, or retrograde ejaculation. Retrograde ejaculation is a condition in which the semen goes into the bladder, rather than out of the body through the urethra. Diabetes and damage to the blood vessels causes nerve damage to the muscles that control the bladder and urethra, which results in this problem.
A proper diet and exercise are the foundations of diabetic care, with a greater amount of exercise yielding better results. Exercise improves blood sugar control, decreases body fat content and decreases blood lipid levels, and these effects are evident even without weight loss. Aerobic exercise leads to a decrease in HbA1c and improved insulin sensitivity. Resistance training is also useful and the combination of both types of exercise may be most effective.
Brittle diabetics are a subgroup of Type I where patients have frequent and rapid swings of blood sugar levels between hyperglycemia (a condition where there is too much glucose or sugar in the blood) and hypoglycemia (a condition where there are abnormally low levels of glucose or sugar in the blood). These patients may require several injections of different types of insulin during the day to keep the blood sugar level within a fairly normal range.
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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.
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.
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.
Over time, a prolonged exposure to high blood sugar can damage the nerves throughout the body — a condition called diabetic neuropathy. Some people may not have any symptoms of the damage, while others may notice numbness, tingling, or pain in the extremities. “At the beginning, [diabetic neuropathy] usually starts in the feet and then it progresses upward,” says Dr. Ovalle. Although most common in people who have had type 2 diabetes for 25 years or more, it can occur in people who have prediabetes as well. In some studies, almost 50 percent of unexplained peripheral neuropathy [in the extremities], whether painful or otherwise, turns out to be caused by prediabetes or diabetes, says Dr. Einhorn.