It is recommended that all people with type 2 diabetes get regular eye examination. There is weak evidence suggesting that treating gum disease by scaling and root planing may result in a small short-term improvement in blood sugar levels for people with diabetes. There is no evidence to suggest that this improvement in blood sugar levels is maintained longer than 4 months. There is also not enough evidence to determine if medications to treat gum disease are effective at lowering blood sugar levels.
With type 1, a disease that often seems to strike suddenly and unexpectedly, the effects of environment and lifestyle are far less clear. But several theories attempt to explain why cases of type 1 have increased so dramatically in recent decades, by around 5 percent per year since 1980. The three main suspects now are too little sun, too good hygiene, and too much cow's milk.
Many studies have shown that awareness about the diabetes and its complications is poor among the general population specially in the rural areas6,7. There is an urgent need to create awareness among the population regarding diabetes and about the serious consequences of this chronic disorder. Epidemiological data from India have shown the presence of a number of risk factors which can be easily identified by simple non-invasive risk scores8,9. The major risk factors are listed in Box 1.
Using insulin to get blood glucose levels to a healthy level is a good thing, not a bad one. For most people, type 2 diabetes is a progressive disease. When first diagnosed, many people with type 2 diabetes can keep their blood glucose at a healthy level with a combination of meal planning, physical activity, and taking oral medications. But over time, the body gradually produces less and less of its own insulin, and eventually oral medications may not be enough to keep blood glucose levels in a healthy range.
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.
In people with type 1 diabetes, the symptoms often begin abruptly and dramatically. A serious condition called diabetic ketoacidosis, a complication in which the body produces excess acid, may quickly develop. In addition to the usual diabetes symptoms of excessive thirst and urination, the initial symptoms of diabetic ketoacidosis also include nausea, vomiting, fatigue, and—particularly in children—abdominal pain. Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity (see Acidosis), and the breath smells fruity and like nail polish remover. Without treatment, diabetic ketoacidosis can progress to coma and death, sometimes very quickly.
What you need to know about borderline diabetes Borderline diabetes, known as prediabetes, is a condition where blood sugar levels are higher than normal but not yet high enough to be type 2 diabetes. This MNT Knowledge Center article explains the signs to look out for, how to monitor the disease, and ways to prevent it becoming full diabetes. Read now
There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes or "other specific types of diabetes"). These include maturity onset diabetes of the young (MODY), Donohue syndrome, and Rabson–Mendenhall syndrome, among others. Maturity onset diabetes of the young constitute 1–5% of all cases of diabetes in young people.
Sugar doesn't cause diabetes. But there is one way that sugar can influence whether a person gets type 2 diabetes. Consuming too much sugar (or sugary foods and drinks) can make people put on weight. Gaining too much weight leads to type 2 diabetes in some people. Of course, eating too much sugar isn't the only cause of weight gain. Weight gain from eating too much of any food can make a person's chance of getting diabetes greater.
No single environmental trigger has been identified as causing diabetes mellitus, however both infectious agents and dietary factors are thought to be important. Various viruses have been implicated in the development of type I DM. They may act by initiating or modifying the autoimmune process. In particular, the rubella virus and coxsackie viruses have been closely studied. In particular, congenital rubella infection has shown direct relationships with the development of type 1 diabetes mellitus. This is presumably due to the virus (or antibodies against it) damaging the beta cells of the pancreas. Some research has looked at dietary factors that may be associated with type 1 diabetes. In particular, cow’s milk proteins (such as bovine serum albumin) which may have some similarities to pancreatic islet cell markers may be able to trigger the autoimmune process. Other chemicals including nitrosamines have been identified as causes of diabetes mellitus in animal models, but not in humans.
Diabetes mellitus is not a single disorder but a heterogeneous group of disorders. All forms are characterized by hyperglycemia and disturbances of carbohydrate, fat, and protein metabolism which are associated with absolute or relative deficiencies of insulin action and/or insulin secretion. The World Health Organization (WHO) developed a now widely accepted classification of the disorder, largely based on clinical characteristics (see Table 1, WHO, 1985).
The Diabetes Control and Complications Trial (DCCT) was a clinical study conducted by the United States National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) that was published in the New England Journal of Medicine in 1993. Test subjects all had diabetes mellitus type 1 and were randomized to a tight glycemic arm and a control arm with the standard of care at the time; people were followed for an average of seven years, and people in the treatment had dramatically lower rates of diabetic complications. It was as a landmark study at the time, and significantly changed the management of all forms of diabetes.
Some people with type 2 diabetes are treated with insulin. Insulin is either injected with a syringe several times per day, or delivered via an insulin pump. The goal of insulin therapy is to mimic the way the pancreas would produce and distribute its own insulin, if it were able to manufacture it. Taking insulin does not mean you have done a bad job of trying to control your blood glucose—instead it simply means that your body doesn’t produce or use enough of it on its own to cover the foods you eat.
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.
High blood sugar levels (hyperglycemia) can lead to a condition called glucose toxicity. This leads to further damage to the pancreas, and the body is less able to produce insulin. Without insulin, glucose levels continue to rise to levels that can cause damage to organs such as the eyes, nerves, and kidneys. These problems are similar to the complications associated with type 1 diabetes.
Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia).
The good news is that behavior still seems to help shape whether someone with the genetic disposition actually develops type 2—and that changes in diet and exercise can sometimes be enough to ward off the disease. "People sometimes have the misconception that if we say something is genetic, then they can't do anything about preventing diabetes and its complications," says Hanis. But he notes that in a landmark study, lifestyle interventions prevented or delayed type 2 in nearly 60 percent of people at high risk. "If we focus on changing the environment, we can prevent diabetes," he says. "As we understand the genetics, we can prevent more of it."
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.
When there is excess glucose present in the blood, as with type 2 diabetes, the kidneys react by flushing it out of the blood and into the urine. This results in more urine production and the need to urinate more frequently, as well as an increased risk of urinary tract infections (UTIs) in men and women. People with type 2 diabetes are twice as likely to get a UTI as people without the disease, and the risk is higher in women than in men.