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Michael Jay Katz has taught anatomy, physical diagnosis, and scientific writing in the medical school of Case Western Reserve University for more than twenty-five years. He has written sixteen books and eighty papers and essays. He is currently the anatomy and physiology consultant for Taber's Cyclopedic Medical Dictionary.
Copyright © 2007 Wild Iris Medical Education, Inc. All Rights Reserved.
Upon completion of this course, you will be able to:
Diabetes mellitus—or, simply, diabetes—is a chronic illness, in which the body is exposed to continual high levels of blood glucose, a condition known as hyperglycemia. Glucose is a simple sugar and an important source of energy, especially for the brain. Low levels of blood glucose (hypoglycemia) cause generalized weakness, and if the hypoglycemia is severe and lasts longer than 30 minutes or so, brain cells begin to die.
On the other hand, too much blood glucose is also a serious health problem. In the short term, very high blood glucose levels can lead to life-threatening dehydration and coma. Over the long term, hyperglycemia damages capillaries and larger blood vessels by thickening their walls and narrowing their inner diameters. This reduces the blood flow to many areas of the body and causes permanent tissue damage, notably to the retinas and the kidneys. Long-term high blood glucose levels also damage nerve endings.
Diabetes causes persistent hyperglycemia, and it is a major health problem. It is the sixth leading cause of death listed on U.S. death certificates, although it contributes to a great many more deaths. People with diabetes are 2 to 4 times more likely to die of heart disease or stroke. Diabetes is the leading cause of new cases of blindness in adults and is the leading cause of endstage renal disease. More than 60% of nontraumatic lower limb amputations are performed on people with diabetes.
Almost all forms of diabetes stem from problems in the body's production and use of insulin, the hormone that is responsible for keeping blood glucose levels in check. One cause of diabetes is the inability to produce enough insulin; for this problem, treatments range from oral medications that increase insulin secretion (i.e., secretagogues, such as tolbutamide) to injections of insulin itself.
Another cause of diabetes is the inability of body tissues to respond sufficiently to normal amounts of insulin, or insulin resistance; here, the treatments include exercise, weight loss, and, when needed, oral medications (insulin sensitizers, such as Metformin, Glyburide) that increase tissue responsiveness to insulin.
Of the various forms of diabetes, the two most common are:
About 90% of people with diabetes have the type 2 form. The typical patient with type 2 diabetes is an adult who has had the disease for many years before it worsened sufficiently to cause symptoms that brought it to a physician's attention.
People who do not have especially high levels of blood glucose, but who do have inefficient ("impaired") mechanisms for handling blood glucose have a condition called prediabetes. Prediabetes often evolves into type 2 diabetes, but concerted lifestyle changes—weight loss, regular physical exercise, and a controlled diet—can delay or even prevent prediabetes from becoming diabetes.
Currently, diabetes is incurable, and it takes daily work to prevent or delay further damage to the body. The most successful model for treating diabetes is a team effort. The patient is the daily healthcare manager, and a group of professionals—including physicians, nutritionists, and nurses—act as guides, advisors, monitors, and counselors.
Type 2 diabetes is one of the two main forms of diabetes mellitus, a disease that has been a problem during all of recorded human history. Diabetes is a Greek word that means "to pass through." Diabetes was the name given to diseases in which a person continually drinks great quantities of fluid, which then pass through the body and are excreted as great quantities of urine. Diabetes is thus characterized by polydipsia (prodigious drinking) and polyuria (prodigious urinating).
Even in early times, two different diabetes diseases were distinguished: diabetes insipidus and diabetes mellitus. Diabetes insipidus ("flavorless" diabetes) produces dilute, watery urine. This disease is now known to be caused most often by the insufficient secretion of ADH (anti-diuretic hormone) by the pituitary. In contrast, diabetes mellitus ("sweet" diabetes) produces urine that is thicker than normal, that tastes sweet, and that leaves crystals of sugar when the water in the urine is evaporated. Diabetes insipidus is rare and, even before the physiologic bases of the diseases were understood, when someone spoke simply of "diabetes," they were usually referring to diabetes mellitus.
Before the 20th century, diabetes mellitus was usually fatal. Most often, diabetes occurred in obese people older than 50 years of age. The disease came on gradually, with increasing thirst and correspondingly voluminous urination. The patient's mouth and skin were always dry, and the breath often had a sweetish odor.
The disease progressed inexorably, bringing with it a host of problems. Eyesight failed from cataracts and nerve problems. Muscles weakened, skin infections and pneumonias were common, and people developed gangrene of the lower limbs. Diabetes led to digestive troubles, kidney disease, and heart failure. Death was usually from what was then called "diabetic coma" (now called diabetic ketoacidosis), which came on suddenly and was always fatal within a few days.
In the less common cases in which children, teenagers, or young adults developed diabetes, the disease worsened much more rapidly. There were no good treatments for diabetes, although a low-carbohydrate diet slowed the progression of the disease in some obese people who developed the disease late in life.
By the early 1800s, pancreatic damage was recognized in autopsies of people who died of diabetes, and late in that century German scientists showed that removing the pancreas from a dog would cause diabetes in the animal. However, diabetes could be prevented in these dogs if a piece of pancreas was sewn under the dog's skin, and this suggested that the pancreas made a substance that prevented diabetes.
Attempts to extract this substance failed because the pancreas also makes a number of destructive enzymes, the presence of which in the extracts would destroy the key anti-diabetes substance. In the early 1920s, the Canadian surgeon Frederick Banting and his assistant Charles Best, a medical student, devised a way to rid the pancreas of most of its destructive enzymes. From the remaining pancreatic tissue they extracted a hormone that would decrease the amount of sugar in the bloodstream and in the urine of diabetic dogs. They named this anti-diabetes hormone insulin. Before the discovery and purification of insulin, diabetes was a fatal disease; after Banting and Best's work, diabetes became a chronic illness.
At the beginning of the 20th century, diabetes mellitus was considered one disease, although young people who developed the disease died much more quickly than people who first became ill in middle or old age. The new treatment with insulin, however, began to highlight a number of other differences. As early as the 1930s, clinicians found that people with diabetes could be divided into two classes according to the way they reacted to an injection of insulin.
People with insulin-sensitive diabetes (who tended to be young and prone to developing ketosis) easily disposed of an oral dose of glucose after receiving an injection of insulin. In contrast, people with insulin-insensitive diabetes (who were usually middle-aged and did not have ketotic episodes) did not significantly reduce their blood glucose levels after receiving the same amount of insulin.
Today, insulin-sensitive diabetes are usually categorized as type 1 diabetes. In type 1 diabetes, the pancreas produces little or no insulin because the beta cells in the islets of Langerhans of the pancreas are not functioning. Type 1 diabetes shows up most commonly in young people, although it can occur in any age group (Eisenbarth et al., 2003).
Insulin-insensitive diabetes, on the other hand, is generally categorized as type 2 diabetes. Type 2 diabetes usually shows up in older adults, although it can occur at any age. A distinguishing feature of type 2 diabetes is that, even when there is a normal amount of circulating insulin, body tissues do not take up glucose as readily as normal. This is called insulin resistance, a condition in which normal concentrations of insulin in the blood produce less than the normal effects in the body.
More than 90% of people with diabetes have the type 2 form, previously called insulin-insensitive diabetes, non-insulin-dependent diabetes, type II diabetes, or adult-onset diabetes. In type 2 diabetes, the pancreas produces enough insulin to prevent ketone formation but, because of insulin resistance, not enough to prevent hyperglycemia. Although there is a hereditary (i.e., genetic) predisposition for the disease, type 2 diabetes does not appear to have a single cause. Aging, a sedentary lifestyle, or excess intra-abdominal fat can activate or enhance a person's predisposition to develop type 2 diabetes.
Type 2 diabetes worsens more quickly if it is not treated. Both hyperglycemia and higher than normal circulating insulin levels (hyperinsulinemia) increases the existing insulin resistance. Hyperglycemia also injures the beta cells (the insulin-manufacturing cells) in the pancreas, and this makes it increasingly difficult for the pancreas to lower high levels of blood glucose. As these processes continue and interact with each other, the patient has more frequent and higher episodes of hyperglycemia, which, over time, damage the eyes, kidneys, nerves, and blood vessels (Masharani & German, 2004; Masharani, 2007).
Approximately 180 million people in the world have type 2 diabetes. Undiagnosed type 2 diabetes is thought to be common; it is estimated that half of the cases remain undiagnosed (Buse et al., 2003). In the United States, more than 6% of the population has diabetes, and 9 out of 10 of those have type 2 diabetes.
DIABETES IN THE U.S. POPULATION
People with diagnosed diabetes = 13.0 million
People with undiagnosed diabetes = 5.2 million
Total number of people with diabetes = 18.2 million (6.3% of the population)
Source: National Diabetes Fact Sheet, 2007.
Diabetes is more common in older people.
Total prevalence of diabetes by age group in the United States (National Diabetes Fact Sheet, 2007).
In the United States, diabetes is more common among non-whites.
Prevalence of diabetes by race/ethnicity in the United States (National Diabetes Fact Sheet, 2007).
Not only is diabetes common but it is also costly. In the United States, the life expectancy of people with diabetes is 10 years less than people without the disease, and people with diabetes are 3 times more likely to be hospitalized than people without the disease. Diabetes is the leading cause of blindness and of amputations not due to injury. Almost half the new cases of endstage renal disease are the result of diabetes. All told, more than 15% of American healthcare dollars are spent treating diabetes and its complications (DeWitt & Hirsch, 2003).
Diabetes is a disease that unbalances the metabolism of carbohydrates (sugars and molecules built of sugars). Normally, one of the central sources of metabolic energy is the simple sugar glucose, which is carried throughout the body in the bloodstream and which is stored mainly in the liver and muscles. Glucose is the source of quick energy, and we always need a certain minimum amount of glucose in the bloodstream. On the other hand, excess blood glucose can damage tissues. Insulin is the hormone that keeps blood glucose levels from getting too high, but diabetes disrupts the body's ability to use insulin effectively.
Carbohydrates come in all sizes. Large carbohydrates such as polysaccharides (e.g., starch) are chains of individual sugar molecules. The smallest carbohydrates are monosaccharides, individual sugar molecules. Glucose, which is a small water-soluble molecule, is a monosaccharide (Nussey & Whitehead, 2001).
Glucose is central to a number of chemical reactions in the cells, and it is the most important of the carbohydrates for most mammals. In addition to being used for energy, glucose molecules are the building blocks of certain structural molecules, glycoproteins and proteoglycans, and of the informational molecules, ribo- and deoxyribo-nucleic acids (Bender & Mayes, 2006).
Glucose is an essential molecule, but most tissues of the body can survive when there are low levels of blood glucose. The brain, however, is quite sensitive to low blood glucose, and it suffers irreversible damage if hypoglycemia lasts more than about half an hour (Ropper & Brown, 2005). The dependence of the brain on continuous supplies of glucose makes it crucial that the body maintain sufficient blood glucose levels at all times.
Much of the glucose in our bodies comes directly from the carbohydrates in our food. In a typical American diet, 60% of our carbohydrates is eaten in the form of starches, 30% in the form of sucrose, and 10% in the form of lactose. In the gastrointestinal tract, enzymes break these carbohydrates into monosaccharides (glucose, galactose, fructose), which are the only forms we can absorb. All carbohydrate absorption takes place in the small intestine.
Excess blood glucose is stored in the liver and in muscles as long chains (polysaccharides) called glycogens. After a meal, insulin in the bloodstream lowers the amount of circulating glucose by encouraging its storage in the form of glycogen molecules. Between meals, liver glycogen is broken down to maintain sufficient glucose in the bloodstream, and the production of glucose from glycogen is encouraged by another pancreatic enzyme, glucagon. In this way, two pancreatic hormones, insulin and glucagon, balance the amount of glucose in the bloodstream: insulin lowers the level of plasma glucose by encouraging liver cells to take up glucose and store it in the form of glycogen, while glucagon raises the level of plasma glucose by encouraging the liver to break down stored glycogen and release the resulting glucose molecules (Bender & Mayes, 2006).
The healthy fasting level of blood sugar is less than 126 mg of glucose per 100 ml of plasma (126 mg/dl). Higher levels cause tissue damage. Normally, the body uses the kidneys to reduce the excesses of most chemicals in the blood. Unfortunately, the kidneys only begin excreting glucose in the urine when the plasma concentration is above 180 mg/dl, and the kidneys only excrete significant amounts when the plasma glucose levels are above 275 mg/dl (Bonnardeaux & Bichet, 2004). Therefore, by themselves, the kidneys cannot keep blood sugar levels low enough to prevent diabetes.
Blood sugar levels are kept low by the liver and muscle cells, which can absorb large amounts of glucose from the circulation. Insulin is the main signal that tells the liver and the muscles when to remove glucose from the blood.
Insulin is a protein molecule made in beta cells that are clustered in islets within the pancreas. During the production of insulin, a piece of the precursor molecule is cut off. This extra piece is called C-peptide. C-peptide is an unnecessary protein, and it is released into the bloodstream along with insulin. By measuring the amount of C-peptide in the blood, it is possible to calculate how much insulin has been produced by the pancreas (Davis, 2005).
Glucose is the main stimulus for insulin secretion, but the pancreas also releases insulin in response to elevated blood levels of amino acids or when signaled by the parasympathetic (vagal) nervous system. The opposite response—slowing or stopping insulin secretion—is caused by signals from the sympathetic nervous system. The sympathetic nervous system (the fight-or-flight system) is activated in stressful situations when higher blood glucose levels would be useful, such as in hypoglycemia, exercise, hypothermia, and trauma.
After they have been secreted from the pancreas, insulin molecules remain outside cells, and they work by interacting with specific receptors on a cell's membrane. Once activated, the receptor molecules speed up glucose transport into the cell. The insulin receptors also set off a cascade of intracellular events that regulate oxidation of glucose and lipids, storage and release of glucose, transport and metabolism of amino acids, protein synthesis, cell growth, cell differentiation, and even cell death (Buse et al., 2003; Davis, 2005).
When a person has not eaten in many hours, the pancreas secretes about 2 units (40 x 10-3 mg) of insulin per hour. After a meal, the person's blood insulin level rises quickly, and in an hour it reaches a peak about 5 times the fasting level. During a typical 24-hour period, the pancreas secretes 18 to 32 units (0.7–1.3 mg).
Circulating insulin is taken up and deactivated by the liver, the kidney, and the muscles. On average, an insulin molecule stays in the bloodstream for less than 10 minutes (Buse et al., 2003; Davis, 2005).
Type 2 diabetes results from the interaction of at least two different disorders. One is insulin resistance, a disorder arising in most of the tissues that respond to insulin. Another disorder arises only in the pancreatic beta cells, which do not secrete insulin efficiently in people with type 2 diabetes. Some of the problems associated with type 2 diabetes, such as obesity and hypertension, worsen insulin resistance and beta cell dysfunction.
Insulin resistance is one of the two key disorders underlying type 2 diabetes. Insulin resistance is a molecular problem in which most tissues do not respond normally to insulin in the bloodstream, whether the insulin has been secreted by the pancreas or has been administered therapeutically.
INSULIN RESISTANCE
In a person with insulin resistance, a normal amount of circulating insulin produces:
All people with type 2 diabetes have insulin resistance. Insulin resistance exists in a person years before the diabetes is diagnosed, and the presence of insulin resistance in an asymptomatic person predicts the high probability of developing type 2 diabetes. Although diabetes is often thought of as a disease of the pancreas, insulin resistance is a problem in the cells throughout the body that respond to insulin. Usually, it is a problem in the molecular mechanisms by which cells recognize the insulin molecule and then produce the intracellular effects of this recognition.
There are many separate molecular sites that can be the source of insulin resistance. Insulin receptors (which are in the membranes of responding cells) are complex structures made of a number of separate subunits. The malfunctioning or mutation of any of these subunits can make them work inefficiently or make them insensitive to insulin, leading to insulin resistance. Insulin resistance can also be caused by the malfunctioning of any of the components of the intracellular cascade that connects the insulin receptors in the cell membrane to the glucose-processing machinery inside the cell (Buse et al., 2003).
As with many pathologic processes, insulin resistance develops most readily in people with a genetic predisposition for it. In predisposed people, certain genes produce poorly functioning insulin receptor subunits or other molecules in the intracellular chain leading from the receptor to the actual glucose utilization machinery.
Intra-abdominal fat is strongly associated with insulin resistance—more so than is extra-abdominal (subcutaneous) fat. Intra-abdominal fat is visceral fat, and an overabundance of visceral fat cells both causes and worsens insulin resistance. How does excess visceral fat cause insulin resistance?
The sympathetic nervous system signals fat cells to break down and release their stored fat. Insulin gives the opposite message; insulin tells fat cells to slow or stop the release of fat. Visceral fat cells are more responsive than other fat cells to the neural signals, but visceral fat cells are less responsive to insulin. In other words, visceral fat cells are easy to turn on and difficult to turn off. Thus, having too many visceral fat cells leads to too much free fatty acid in the bloodstream.
All the energy-balancing systems interact. When the level of free fatty acids in the bloodstream gets too high, the liver releases more glucose into the blood and less glucose is taken up by the liver and muscles, even when there is sufficient insulin available. At this point, therefore, the high level of free fatty acids has caused hyperglycemia.
Now the pancreas is activated. Hyperglycemia stimulates the pancreas to release more insulin. And in this way, the excess free fatty acids have indirectly triggered, at least temporarily, higher than normal levels of circulating insulin, i.e., hyperinsulinemia.
If it had been subcutaneous fat cells that were releasing the excess fatty acids, the newly released insulin would turn off the tap by slowing or stopping the fatty acid release. Visceral fat cells, however, are less sensitive to insulin signals, and the feedback circuit is not very effective when visceral fat cells are the culprits. When visceral fat is the source of excess free fatty acids, the natural balancing mechanisms do not work well, and the hyperinsulinemia persists. This persistent hyperinsulinemia is a direct cause of insulin resistance (Rasouli et al., 2007).
FROM EXCESS FATTY ACIDS TO INSULIN RESISTANCE
This sequence of events can be expressed as the formula:
Fatty acids → Hyperglycemia → Hyperinsulinemia → Insulin resistance
and can be triggered by anything that causes high blood levels of free fatty acids, glucose, or insulin. Conditions that lead to insulin resistance through this mechanism include high levels of glucocorticoids (eg, Cushing disease or long-term treatment with prednisone), nonalcoholic fatty liver disease, and treatment with protease inhibitors (e.g., for HIV) (Buse et al., 2003; Bechmann et al., 2005; Eckel et al., 2005).
Together, both genes and life experiences cause obesity. The tendency to be obese is heritable; thus genes are usually one cause of obesity. In rare cases, a single gene can cause obesity; in most cases, however, obese people have more than one contributory gene.
In addition to an inherited metabolic tendency to be overweight, eating patterns developed over time are key causes of excess weight gain. Aspects of a person's eating patterns are learned, but other parts are inborn and probably genetic. Normally, a number of proteins, hormones, and neural signals communicate with the hunger and satiety centers in the brain. These biochemical cues are triggered by fullness of the stomach, the presence of food in the small intestine, and the levels of fat and glucose in the blood. In many obese people, the food signals do not work properly, and these people's brains do not recognize when they have eaten a sufficient meal. This "satiety blindness" leads to overeating and weight gain.
The nongenetic contributions to a person's obesity can start in the womb. For example, a fetus who is undernourished in the first two trimesters of pregnancy will have a higher than normal chance of becoming an obese adult. In addition, psychological factors can contribute to obesity. Depression, especially when part of bipolar disorder, can lead to excess eating and weight gain. Emotional, physical, and sexual abuse can also lead to obesity. Finally, many medications can cause weight gain as a side effect.
DRUGS THAT CAN CAUSE WEIGHT GAIN
Because obesity puts a person at risk for type 2 diabetes, all the causes of obesity, from genes to life experiences to medications, can contribute to a person's tendency to develop type 2 diabetes (Bechmann et al., 2005).
In addition to insulin resistance, people with type 2 diabetes have another key disorder. The beta cells in their pancreases do not secrete insulin normally. Together, insulin resistance and poorly functioning beta cells lead to the continual hyperglycemia that characterizes type 2 diabetes.
Insulin resistance means that a higher than normal amount of insulin in the bloodstream is needed to keep the plasma glucose levels low (<126 mg/dl). To maintain healthy blood glucose levels, the pancreatic beta cells in a person with insulin resistance are forced to secrete more than the normal amount of insulin. Therefore, people with insulin resistance generally have hyperinsulinemia (excess insulin in the bloodstream).
People with type 2 diabetes have insulin resistance; therefore, they often have hyperinsulinemia. But even when they have hyperinsulinemia the blood insulin levels are not high enough to prevent hyperglycemia. In other words, even when secreting high levels of insulin, their pancreas does not keep up with the demand. Part of the problem is that people with type 2 diabetes have fewer beta cells than normal. In addition, the existing beta cells in type 2 diabetics do not secrete insulin as quickly and in as large amounts as normal.
Even before type 2 diabetes develops, beta cell problems can be detected in glucose tolerance tests, which give abnormal test results in prediabetic individuals. As with insulin resistance, beta cell dysfunction precedes the development of overt hyperglycemia by many years (Buse et al., 2003).
In another parallel with insulin resistance, treating type 2 diabetes can improve the functioning of the beta cells, but it cannot bring beta cell functioning up to normal. At present, both insulin resistance and beta cell dysfunction can be improved but not cured (Nussey & Whitehead, 2001).
Metabolic syndrome is the name for a particular group of health problems that are frequently found together. (It is also called dysmetabolic syndrome, insulin resistance syndrome, obesity dyslipidemia syndrome, or syndrome X.) Core problems of metabolic syndrome are obesity and insulin resistance; three additional problems are high blood pressure, high blood levels of triglycerides, and low blood levels of high-density lipoprotein cholesterol (HDLs). It is not clear whether metabolic syndrome causes type 2 diabetes, but it has been shown that having the syndrome quintuples a person's chances of developing type 2 diabetes (Eckel et al., 2005; Wassink et al., 2007).
DEFINITION OF METABOLIC SYNDROME
A diagnosis of metabolic syndrome is made if at least three of the following are present:
Source: Lorenzo et al., 2007.
The direct causes for type 2 diabetes include insulin resistance and abnormal insulin secretion by beta cells. The development of type 2 diabetes from these two underlying problems is hastened by the other disorders found in metabolic syndrome. Some aspects of all these predisposing problems are inherited, and in this way, the propensity for developing type 2 diabetes is inherited.
The specific genetic causes are not known in detail for most variants of type 2 diabetes, but most cases appear to be polygenic, that is, they involve more than one inherited problem (Buse et al., 2003; Davis, 2005).
Type 2 diabetes comes in many variants. A few uncommon variants result from single genetic mutations. These monogenic forms usually show up in young people, who then develop the disease no matter what their lifestyle. More than seventy variants of monogenic diabetes have been identified that are caused by different mutations of the insulin receptor—a problem that then leads to insulin resistance. Monogenic diabetes has also been caused by a mutation of the insulin molecule itself. Individual mutations in six different genes have been shown to cause alterations in the beta cells that can also lead to monogenic type 2 diabetes; these particular mutations cause a syndrome called maturity-onset diabetes of the young (MODY).
The most common variants of type 2 diabetes, however, are polygenic. Polygenic type 2 diabetes usually occurs in older people, and it develops from a complex mix of genetic predispositions and outside factors. Some of the involved genes have been identified, but most are not yet known.
The health problems of diabetes come directly from hyperglycemia, and the medical diagnosis of the disease is not based on its cause but rather on evidence of persistent high plasma glucose levels, regardless of the cause. Diabetes is diagnosed in the presence of any of these hyperglycemic conditions:
The lab work necessary to diagnose diabetes should be included in, or followed by, a complete examination of the patient. The goal of the initial workup is to survey the health of the patient from head to toe. For a person who has or is suspected of having diabetes, there are four specific objectives:
Here are some aspects of the standard medical history that are especially important in a person with type 2 diabetes.
Find out whether patients have increased urination (ask how many times a night they get up to go to the bathroom) or increased thirst. Are they frequently tired? Have they been feeling weak? Have they lost or gained weight? Are they unusually hungry? Do they have blurred vision? Do they have dry skin? Do people tell them their breath smells fruity?
Ask about signs and symptoms of peripheral vascular disease and neuropathies. Do their feet always seem cold? Do they turn white or blue? Do their feet feel numb, uncomfortable, or tingly? Do they have these problems in the hands? Are they sometimes surprised by sores on the feet that went unnoticed? Do they get pain or weakness in the legs when walking? Do they tumble?
If patients have already been diagnosed with diabetes, find out at what age they learned of the diagnosis and what the signs and symptoms were at the time. Get records of past blood chemistries (fasting plasma glucose levels, A1C values, and fasting lipid levels) and of past blood pressure readings. Also get details of acute episodes of hyper- or hypoglycemia. Finally, chart a history of the way the diabetes has been managed up to the present.
What medications does the person take? Many drugs can cause increased plasma glucose levels, even in people without diabetes. Specifically, ask patients whether they take or have taken glucocorticoids (e.g., prednisone), anti-epileptics (e.g., phenytoin), antihypertensives (e.g., calcium channel blockers, diuretics, diazoxide, clonidine), antipsychotic drugs (e.g., clozapine, olanzapine), antiretroviral drugs (e.g., the protease inhibitors used to treat HIV infections), asthma drugs (beta 2 adrenergic agonists, epinephrine/adrenalin), pentamidine (long-term use), or H2-receptor blockers (e.g., cimetidine).
Have patients ever been diagnosed with diabetes or prediabetes? Have they ever been told they had high blood sugar or sugar in the urine? Do they have high blood pressure, glaucoma, or high cholesterol? Have they had retinal, kidney, nerve, foot, artery, or heart problems? Do they get frequent infections? Do skin sores heal slowly or not at all? Have they had gangrene or amputations?
For a woman in her reproductive years, has she been having sporadic (or no) menstrual periods? Does she get itchy vaginitis or frequent candida (yeast) infections? Has she delivered a baby who weighed more than 9 lbs (4.1 kg)? Did she have gestational diabetes, polyhydramnios (excess amniotic fluid), or pre-eclampsia? Has she had an unexplained miscarriage?
For a man, has he had difficulty having erections?
For the family history, ask specifically whether the patient has any close relatives who have (or had) diabetes? What type of diabetes was it? How early did it show up? Did the person need to take insulin? Was the person overweight? If the person is not alive, what was the cause of death? Does the patient have relatives who are overweight? Do heart or artery problems run in the family? Have any close relatives had strokes?
As a basis for planning the patient's proper diet, write down the typical daily diet. Ask: "What do you eat for breakfast? … lunch? … supper? Do you have snacks between breakfast and lunch? … lunch and supper? … supper and bedtime? What do you drink during the day?" (Buse et al., 2003). Ask how much exercise patients get each week. Ask whether they smoke or have ever smoked. Find out what they know about diabetes and diabetes self-care.
One common complication after many years of hyperglycemia is autonomic neuropathy (damage to the nerves that supply the internal organs, including the heart, stomach, and intestines). A thorough review of systems can help to identify damage to the autonomic nervous system. Be sure to ask whether the patient has been having any of these problems:
The physical exam should include a thorough search for signs of diabetic complications and for other problems, such as abdominal obesity or hypertension, that compound the risks posed by diabetes.
The most commonly used measure of obesity is the body mass index (BMI). This is measured using the formula
BMI = weight in kilograms / height in meters2
or
BMI = weight in pounds x 703 / height in inches2
The BMI has been shown to be a good indirect indication of the percentage of body fat, and it is the most commonly used measure of total body fat.
When weight is measured in kilograms and height in meters, the BMI obesity definitions for adults are as follows.
| Normal | 18.5–24.9 | |
| Overweight | 25.0–29.9 | |
| Obese | Class 1 | 30.0–34.9 |
| Class 2 | 35.0–39.9 | |
| Class 3 (extreme obesity) | >40.0 | |
As a broad generalization, the excess fat on people with type 2 diabetes tends to be central (in the face, neck, chest, and abdomen) rather than in the arms or legs. When there is excess of fat inside the abdomen, the person has a round, "apple" shape. This form of obesity is associated with metabolic syndrome. A diabetic person with intra-abdominal obesity has a high risk of developing atherosclerotic cardiovascular disease.
Intra-abdominal fat is visceral fat, which is the more dangerous type of fat. Studies have shown that simply measuring a person's waist circumference gives a good indication of the amount of visceral fat. To get a standard waist circumference, measure around the smallest (minimal) circumference anywhere in the waist region (below the ribs and above the top margins of the hip bones). A waist circumference of >37 in (94 cm) in men and >31.5 in (80 cm) in women is considered a warning sign, and a circumference of >40 in (102 cm) in men and >35 in (88 cm) in women puts a person in a high-risk category for developing cardiovascular disease.
Record the patient's resting blood pressure. In a person with diabetes, resting blood pressures (repeated on separate days) of >130/85 mm Hg are a warning sign of future problems. In addition, measure orthostatic blood pressure (i.e., just after the person has stood up). Diabetic autonomic neuropathy can slow a person's vasoconstrictive responses, and suddenly standing may produce notable hypotension. Autonomic neuropathy can also produce resting tachycardia, which you will pick up when checking the patient's heart rate.
Autonomic neuropathy can cause reduced sweating, which makes the skin (especially on hands and feet) dry and itchy. Diabetes also makes a person prone to infections and makes skin sores heal slowly. Look for ulcers and skin erosions, especially in places on the peripheral extremities that are bumped frequently, such as the pretibial regions and the feet. In patients using insulin, check the skin areas that are used as injection sites.
People with diabetes get retinopathies, cataracts, and glaucoma. Examine the optic fundi for retinal hemorrhages, which appear as small round red spots, for "cotton wool" patches, which are gray or white areas with fluffy borders, and for "hard" exudates, which are small whitish spots with sharp edges. Diabetic autonomic neuropathy can produce miotic pupils with sluggish light reflexes.
Dental diseases are more common in people with diabetes, so examine the patient's teeth and gums. Ketosis gives a fruity, acetone-like odor to a person's breath.
Macrovascular problems lead to poor peripheral circulation. Quantifying the strength of all the peripheral pulses provides a baseline for monitoring the patient's circulation. Be sure to record both the ankle and feet pulses. Note whether the feet are cool and pale, and check the capillary refill under the nails of the toes.
In diabetes, the feet and ankles can suffer from reduced micro- and macrovascular circulation, poor healing, and peripheral neuropathy (damage to the nerves outside of the brain and spinal cord). Study the skin on the feet for erosions, ulcers, and infections. Check for toenail problems. Examine the ankle and foot joints for deformities and injuries.
Diabetic neuropathies show up only after many years of hyperglycemia. Peripheral sensory and motor neuropathies injure the longest nerves first and show up in the feet before the hands. Over the years, peripheral neuropathies slowly move proximally. Sensory problems include paresthesias, numbness, and pain; motor problems include reduced deep tendon reflexes and muscle weakness.
Test the patient's toes, ankles, and fingers bilaterally for proprioception, vibration, and monofilament sensation (using a standardized diabetes monofilament). Try to quantify any deficits so that you can objectively follow the progression or appearance of problems. (See Nerve Problems in the section on Chronic Complications below for more details.)
An initial diabetes examination screens for abnormalities and also establishes baseline values that you will use to evaluate the treatment program and to follow the progress of the disease objectively.
Among the various measurements of the body's ability to produce and use glucose, the blood level of glucose after an 8-hour fast is the standard. After 8 or more hours without eating, the body should maintain plasma glucose levels in the range of 90 to 100 mg/dl.
In the United States, measurements of the concentration of molecules in the blood are traditionally given in terms of milligrams per deciliters, or mg/dl. Standard chemistry prefers millimoles per liter, mmol/l. Plasma glucose levels—the key laboratory values in evaluating diabetes—are sometimes given in each of the units. This graph shows how the concentration of plasma glucose translates from mg/dl to mmol/l.
People whose fasting blood level of glucose are frequently 100 to 125 mg/dl are not able to use glucose optimally and are said to have prediabetes; they are said to have impaired fasting glucose (IFG). When a person's fasting blood glucose levels are frequently ≥126 mg/dl, the continual hyperglycemia threatens his health, and he is said to have diabetes.
Fasting plasma glucose (FPG) is the preferred diagnostic test for diabetes, except in pregnant women. Formally, diabetes is diagnosed when a person's FPG is ≥126 mg/dl on at least two different days.. It is important to confirm high FPG values on a second day, because the FPG varies from day to day (ADA, 2007a).
| Glucose metabolism is categorized by level of fasting plasma glucose. | |
| Fasting Plasma Glucose Levels | |
| Normal | ≤100 mg/dl |
| Prediabetes | 100–125 mg/dl |
| Diabetes | ≥126 mg/dl |
A more complicated test, the oral glucose tolerance test, can also be used to diagnose diabetes. In an OGTT, the patient drinks a sugar-water solution (75 g glucose in 300 ml water), and the plasma glucose level is measured after 2 hours. For values, see table above. Again, high plasma glucose levels must be confirmed by a test on a second day. For an OGTT, constraints include:
Currently, fasting plasma glucose (FPG) measurements are the preferred test for diagnosing diabetes. Oral glucose tolerance tests are used mainly for research studies and to resolve borderline results from FPG tests (Buse et al., 2003).
The A1C test is also called the A1c, hemoglobin A1c, HbA1c, glycohemoglobin, glycated hemoglobin, and glycosylated hemoglobin test. This test is used to monitor a patient's blood glucose levels during treatment—it is not used to diagnosis diabetes (ADA, 2007a).
The A1C test measures the percent of hemoglobin to which glucose molecules have become attached—i.e., the percent of glycosylated hemoglobin. As a person's plasma glucose level rises, more hemoglobin molecules become glycosylated. Red blood cells (and their hemoglobin) are replaced after about 4 months, and the amount of glycosylated hemoglobin at any one time reflects the average plasma glucose level over the last 2 to 3 months.
Be aware that the exact level of "normal" for an A1C test varies somewhat from laboratory to laboratory. Another caveat is that the A1C test can be inaccurate when the patient has genetic mutations of the hemoglobin, conditions that change the amount of red blood cells in the circulation (eg, bleeding, hemolysis, anemia), renal failure, or alcoholism. The following graph shows the average plasma glucose levels that are indicated by various A1C values.
The overall average blood glucose level for the past 2 to 3 months as indicated by various A1C values.
A 1% change in an A1C value reflects a change of about 30 mg/dl in average plasma glucose. Normal levels of plasma glucose produce an A1C value of about 5%. As the A1C value increases, so does the likelihood of complications. The American Diabetes Association recommends that people with diabetes aim for A1C levels <7%, although this goal can be hard to achieve for many people with diabetes (ADA, 2007a).
A1C values are averages, and A1C values will lower (and therefore appear to be improved) if there are significant periods of excessively low plasma glucose levels (i.e., hypoglycemia). Also, the A1C values will not reflect short swings in plasma glucose levels, as happens with brittle diabetes (diabetes in which the blood glucose level easily swings from too low to too high and back again). To recognize hypoglycemic periods or short-term shifts in plasma glucose levels, patients should monitor their glucose levels regularly. The true level of glycemic control can be seen best through a combination of A1C tests and daily blood glucose readings (Buse et al., 2003; ADA, 2007a).
Dyslipidemia (i.e., an unhealthy level of blood lipids) increases a person's risk of developing a variety of health problems, most notably atherosclerotic cardiovascular disease. Type 2 diabetes is characteristically accompanied by dyslipidemia. This dyslipidemia, which is a component of metabolic syndrome and is associated with obesity, includes:
| Triglycerides | normal | <150 mg/dl |
| borderline high | 150–199 mg/dl | |
| high | ≥200 mg/dl | |
| HDL Cholesterol | low | <40 mg/dl |
| high | ≥60 mg/dl | |
| LDL Cholesterol | optimal | <100 mg/dl |
| borderline high | 130–159 mg/dl | |
| high | ≥160 /mg/dl |
The dyslipidemia of type 2 diabetes is not always improved by simply reducing the patient's hyperglycemia: dyslipidemia may need direct treatment (Masharani & German, 2004; Masharani, 2007).
Record a baseline set of values for liver functioning. Most of the medications used to lower blood glucose levels are deactivated in the liver. If the liver is not functioning properly or if it later develops problems, the dosages or types of medications may need to be adjusted.
At one time, diabetes treatment was monitored by measuring the amount of glucose in the urine. Finger-stick blood glucose measurements are more sensitive and more accurate, and they have replaced urine tests for monitoring daily plasma glucose levels.
In the kidneys, glucose that is initially filtered from the blood is almost fully reabsorbed before the urine is excreted. This reabsorption is very efficient, even when there is an excess of blood glucose up to levels of about 180 mg/dl. (Reabsorption is not absolute—normal urine does contain a small amount of glucose.)
Beyond 180 mg/dl, however, the kidney cannot reabsorb all the glucose that it filters. Therefore, at mild levels of hyperglycemia, some glucose begins to spill into the urine. Above a blood glucose level of about 275 mg/dl, all the excess glucose is spilled into the urine (Bonnardeaux & Bichet, 2004).
By the time measurable sugar appears in the urine, hyperglycemia is already at an unhealthy level. Nonetheless, urine testing is an easy and quick warning of mild hyperglycemia, and urine tests are sometimes used for screening. Commercial plastic or paper strips (eg, Clinistix, Diastix, Miltistix, Uristix) can be dipped in fresh urine and will change color in different concentrations of sugar (Silkensen & Kasiske, 2004).
Ketones are released into the blood when fatty acids are being used for energy instead of glucose. When significant amounts of ketones are found in the urine of a person with diabetes, his hyperglycemia is usually >300 mg/dl. Patients on insulin therapy who have not taken sufficient insulin have measurable ketones in the urine.
Protein (albumin) leaking into the urine of a person with diabetes usually indicates kidney damage. Significant kidney damage is preceded by a period during which only a small amount of albumin is found in the urine, an amount less than that detectable by regular reagent strips (e.g., Albustix). This early microalbuminuria can be qualitatively recognized using specialized reagent strips (Micral-Test) or tablets (Micro-Bumintest) (Silkensen & Kasiske, 2004).
Diabetes is the leading cause of endstage renal disease. Therefore, it is important to monitor indicators of kidney function. A periodic record should be kept of serum creatinine and blood urea nitrogen (BUN) levels, and a glomerular filtration rate (GFR) should be calculated with each blood test. The GFR can be estimated using a formula that requires the serum creatinine level and the age, weight, and sex of the patient (Oh, 2006).
People who do not know that they have diabetes may come to an office, clinic, or emergency room with hyperglycemia. Sometimes their hyperglycemia is discovered incidentally and with no other clues. On the other hand, these patients may have symptoms of diabetes, such as polydipsia, polyuria, weakness, fatigue, blurred vision, headache, dizziness, or dehydration. At times, such patients already have diabetic complications, for example, coronary artery disease, peripheral vascular problems, nonhealing wounds, or recurrent skin or genitourinary tract infections.
If patients not known to have diabetes present with mild hyperglycemia (<300 mg/dl), with no serious dehydration, and with no other significant disorders, they should be scheduled for a full diabetes evaluation. If they present with hyperglycemia of >200 mg/dl and classic symptoms of diabetes, they can be diagnosed as having diabetes and should be scheduled for a full diabetes evaluation. If they present with moderate to severe hyperglycemia (>400 mg/dl), they should be evaluated immediately and given insulin and fluids if necessary.
Moderate to severe hyperglycemia in a person not previously known to have diabetes is usually triggered by another recent problem, so in these cases, look for infections or acute cardiac or kidney problems.
Ideally, patients with diabetes should be treated by a team of healthcare professionals. The primary physician does not have the time to help each patient manage everyday care. The many necessary interactions with a patient, especially at the beginning of therapy, should be divided among a team of specialists—nurses, dietitians, physical therapists, and psychological counselors. Medical complications should be referred to specialty physicians, such as ophthalmologists, cardiologists, renal specialists, podiatrists, and psychiatrists.
Pregnant women pose special challenges for diabetes care and therefore need special caretakers. During pregnancy, weight-loss programs should be terminated, oral hypoglycemic medications are contraindicated, and insulin therapy should be intensified. Congenital malformations are more common in diabetic pregnancies when the diabetes is not well-controlled, and infants are often of larger than normal birthweight.
These and other potential complications make it important for diabetic women of reproductive age to understand the risks of a pregnancy, and their diabetes care teams should include nurse-midwives or obstetricians specializing in diabetes.
The primary physician, with help from the patient and the treatment team, formulates an initial plan from the various treatment options. The arsenal of treatment options ranges from lifestyle changes to medications.
The primary lifestyle changes used to treat type 2 diabetes are weight loss, increased physical activity, smoking cessation, and planned meals. The most effective ways to reduce the insulin resistance that underlies type 2 diabetes are weight loss and exercise.
Changing a lifestyle requires guidance and willpower. Losing weight takes encouragement, monitoring, and practical advice—even for people who are only mildly overweight. Moving from a sedentary pattern to a program of physical activity is also extremely challenging for newly diagnosed diabetes patients.
Time works against lifestyle changes. Lost weight is notorious for reappearing: people who diet on their own tend to regain the lost weight in less than a year. Organized dieting programs such as Weight Watchers, TOPS (Take Off Pounds Sensibly), and Overeaters Anonymous can help mildly overweight patients to maintain lower weights. For patients who are moderately or severely overweight, however, professional behavioral therapy may be necessary.
Lifestyle changes and medications work least often in severely obese patients. For these patients, bariatric surgery is an option. Surgery is considered if the patient has tried monitored dieting, exercise regimens, and medications.
Typically, surgery is only recommended for extremely obese patients, i.e., patients with a body mass index (BMI) ≥40 kg/m2 (extreme obesity). Less overweight patients—those with a BMI of 35.0–39.9 kg/m2—are considered for surgery when they have sleep apnea, type 2 diabetes, or components of metabolic syndrome.
The best hospitals for bariatric surgery are those that do a significant number of the surgeries and that use a team (physician, psychologist, and dietician) to treat patients. Even in the best of circumstance, however, slimming down to a person's ideal weight is not a realistic goal. With optimal treatment, bariatric patients are likely to lose 50% to 60% of their excess weight.
Smoking worsens insulin resistance and speeds up the appearance of diabetic complications. Explain the medical consequences to any patient who smokes, and strongly recommend that the patient stop smoking. It is difficult for smokers to quit on their own, so help them get into a program that includes support, counseling, and the availability of anti-smoking medications.
Even a modest weight loss makes a difference for an overweight or obese person, and losing 5% to 7% of the original weight and keeping the weight off is a realistic goal. The best weight loss results come from structured programs that include individualized counseling, meals with reduced calories and fats, regular physical activity, and frequent contacts with a professional advisor.
To lose weight, a person must eat fewer calories each day. The American Diabetes Association (ADA, 2007c) recommends that, even for weight loss, a daily diet should be balanced and moderate. Neither very low carbohydrate (i.e., <130 g/day) nor very high protein (i.e., >35% of total daily calories) diets are recommended in weight loss programs for a person with diabetes. Instead, low-fat, low-calorie diets are preferred.
| Source: ADA, 2007c. | |
| Carbohydrates | 45% to 65% of total daily calories |
| Fats | 20% to 35% of total daily calories |
| Proteins | 15% to 20% of total daily calories |
| Total daily calories are determined by the individual's specific weight loss goals. | |
Well-controlled research studies have confirmed the common experience that it is difficult to lose even modest amounts of weight and then to keep the weight off. One successful program uses reduced-calorie, low-fat diets designed to meet the limits shown below.
| Initial Weight | Total Daily Calories | Total Daily Fat |
|---|---|---|
| Source: ADA, 2007c. | ||
| 120–174 lb | 1200 | 33 g |
| 175–219 lb | 1500 | 42 g |
| 220–249 lb | 1800 | 50 g |
| >250 lb | 2000 | 55 g |
For overweight or obese patients with type 2 diabetes, dietary fat should be watched carefully. Reducing the overall calories in a person's diet will improve the lipid profile. Reducing the amount of fat improves the lipid profile even further. It is important to remove foods that are high in saturated fats, such as:
Fat-rich foods should be replaced with foods that have high water and fiber content, eg, fruits, vegetables, legumes, and low-fat soups.
It is best to tailor the foods of any diet program to the dieter, and it is ideal to have a nutritionist or dietician as part of the diabetes care team. In addition to food planning, these professionals can suggest patterns of eating that help in weight loss. For example, scheduling regular eating times helps a person to control eating. For people with type 2 diabetes, spacing meals roughly every 4 hours during the day is optimal (Buse et al., 2003).
Exercise not only contributes to losing weight but also to maintaining weight loss; nonetheless, exercise alone rarely leads to significant weight loss and a reduced-calorie diet is usually necessary. A regular exercise program has independent metabolic effects that reduce insulin resistance in people with type 2 diabetes. It also helps lower blood triglycerides, raise blood HDLs, and reduce hypertension. Exercise immediately reduces blood glucose levels, and regular exercise reduces a person's average level of hyperglycemia (i.e., it lowers A1C values).
Regular exercise may be the single most important lifestyle change for people with type 2 diabetes (Buse et al., 2003). Both moderate aerobic and moderate resistance exercises are recommended for most people with type 2 diabetes. The goal is at least 150 minutes of exercise per week, distributed over 3 to 4 days.
For most people with type 2 diabetes, the recommendation is to schedule a minimum of 2.5 hours of moderately intensive aerobic exercise a week. The exercise sessions should be spread over at least three days, without skipping more than two days in a row. Ideally, the person should exercise a full 30 minutes at a time, because a 30-minute session is about twice as beneficial as one lasting 20 minutes.
Aerobic exercises include walking, dancing, bicycling, jogging, swimming, water aerobics, and many sports. "Moderate intensity" means that the exercise brings a person's heart rate up to between 1/2 and 3/4 of his maximum rate—the rate at which a person is still able to carry on a conversation (ADA, 2007a).
Patients should try to add resistance exercises to their weekly schedule. Resistance exercises use muscular strength to push or pull a weight; these exercises include push-ups, pull-ups, weight lifting, and exercises on weight machines. The recommendation is to have resistance exercise sessions three days a week, and with three sets of 8 to 10 weight repetitions per session. It is suggested that people use a resistance weight that they can push (or pull) for only 8 to 10 repetitions without stopping to rest.
For exercise to have a substantial role in treating diabetes, the activities must be regular and long-term. Therefore, they must fit realistically into the patient's life. Exercise schedules must be practical, so it is important that the patient be involved in setting up the exercise regimen. An exercise specialist or physical therapist should sit down with each patient and to help create a manageable exercise plan. The professional should meet with patients regularly to monitor and advise them.
Many patients with type 2 diabetes live sedentary lives. For them, the exercise schedule should begin gradually, with short regular walks or brief exercise sessions. Over time, the length and the intensity of the exercise sessions should be increased. Trainers should present each increase as an accomplishment, as a goal met, not as the addition of a further burden.
The physician in a diabetes team should screen each patient for health problems that must be accommodated in the exercise program. Very few problems preclude adding more physical activity to the daily life of a person with diabetes, but certain problems put special constraints on those activities.
An exercise session uses up circulating glucose. If a patient takes insulin or insulin secretagogues, their effect may suddenly be too much for the lowered level of plasma glucose during exercise. In this case, the person becomes hypoglycemic. The general solution is for people who take insulin or insulin secretagogues to eat additional carbohydrates before exercising. See the section below on Insulin Therapy for a discussion of hypoglycemia.
Before a sedentary person with diabetes and cardiovascular risks starts a new exercise program, it is usually best to administer a stress test. (This is not always needed for young, otherwise healthy people with diabetes.) If the test shows cardiovascular problems, it is still possible to create a gradually increasing exercise plan, with the patient warned not to overexert and to watch for chest, jaw, or arm tightness or pain and for palpitations or shortness of breath.
The general rule is to bring a person's blood pressure into a healthy range before initiating an exercise program.
Proliferative diabetic retinopathy or severe nonproliferative retinopathy puts a patient at risk for vitreous hemorrhages or retinal detachment. There is controversy over whether vigorous exercise can cause these problems, so consult a retinal ophthalmologist before advising exercise programs for people with diabetic retinopathy.
A person who lacks the ability to fully sense injury to the feet, ankles, and legs can damage skin and joints without realizing it. Therefore, diabetic patients with peripheral neuropathy should limit themselves to low-impact exercises, such as swimming, bicycling, and arm exercises.
Damage to the autonomic nervous system can cause reduced or inappropriate responses to exercise. Diabetic patients who have autonomic neuropathy should be given a thorough cardiac examination before beginning a new exercise program.
Lifestyle changes and counseling are the first steps in treating obesity. When these steps do not lead to sufficient weight loss, medications can be tried. One drug used for obesity is the appetite suppressant sibutramine (Meridia), which works in the brain to make a person feel full earlier in a meal. Other central nervous system medications that have been used for obesity are fluoxetine (Prozac), diethylpropion (Tenuate), and bupropion (Wellbutrin, Zyban).
The anti-obesity drug orlistat (Xenical) works quite differently. Orlistat is a malabsorption agent that inhibits intestinal lipase and reduces the intestine's absorption of fat; thus Orlistat is helpful only for meals containing fat. A frequent side effect of this drug and its recent over-the-counter variant (Alli) is sudden bouts of diarrhea. Patients should be made aware of this when the medication is prescribed.
Weight that has been lost with the aid of medications is typically regained when the medication is stopped. For this reason, drug therapy works best when it is used as part of a treatment plan that includes lifestyle changes and counseling.
For most people with type 2, medications are part of their treatment programs. Oral hypoglycemics are the most commonly used medications, but many people with type 2 diabetes need insulin. Typically, treatment for a person with type 2 diabetes starts with a trial of lifestyle interventions. If these are not sufficient to improve the patient's metabolic problems, then oral hypoglycemic medications are tried, usually beginning with Metformin.
Oral medications for treating type 2 diabetes fall roughly into five classes. The two most commonly prescribed classes are insulin secretagogues (drugs that increase insulin secretion) and insulin sensitizers (drugs that decrease insulin resistance).
The three lesser-used classes are alpha-glucosidase inhibitors (drugs that slow glucose absorption in the intestines), incretin-related drugs, and glucagon suppressors. All the oral anti-diabetic medications should be used cautiously or not at all in people with significant liver or kidney problems (Masharani & German, 2004; Davis, 2005; Masharani, 2007).
Sulfonylureas stimulate beta cells to release insulin. Sulfonylureas cannot be used for type 1 diabetes because the beta cells are not functioning; on the other hand, sulfonylureas are the most-prescribed drugs for the treatment of type 2 diabetes. Sulfonylureas are secretagogues, and their main adverse effect is hypoglycemia, especially in older adults.
The sulfonylureas are divided into two groups. The first-generation drugs are:
The second-generation sulfonylureas, which are more potent releasers of insulin, are:
Meglitinides are another class of insulin secretagogues:
Metformin, a biguanide, is the classic insulin sensitizer. It counteracts insulin resistance by reducing the amount of glucose released by the liver and, to a lesser extent, by improving the ability of muscle cells to extract glucose from the circulation. Technically, metformin is anti-hyperglycemic, not hypoglycemic. It does not cause insulin to be released from the pancreas, and therefore, it rarely causes hypoglycemia, even in large doses:
The second class of insulin sensitizers is the thiazolidinediones:
Rosiglitazone has recently (May 2007) been associated with an increased risk of serious heart problems. Therefore, a diabetes specialist and/or a cardiologist should be involved if this drug is used (FDA, 2007; Nissen & Wolski, 2007).
Alpha-glucosidase inhibitors are glucose absorption retardants that slow the digestion and absorption of glucose; this lowers the hyperglycemic peak that occurs after a meal. These drugs work locally (in the intestine) and temporarily:
The incretins are gastrointestinal hormones that have a number of hypoglycemic effects including the stimulation of insulin secretion. One of the incretin-related drugs, exenatide, mimics incretin actions; the other incretin-related drug, sitagliptin, prolongs incretin actions:
Amylin is a natural hormone that suppresses the secretion of glucagon, delays the emptying of the stomach, and decreases appetite. Pramlintide is a synthetic analogue of amylin:
Over the years, the ability of pancreatic beta cells to secrete insulin continues to decrease in people with type 2 diabetes. When the pancreas can only secrete 20% to 30% of the normal amount of insulin, a person begins to need insulin therapy.
Typically, type 2 diabetes is diagnosed when a person has already lost about half of his normal insulin-producing ability, and the majority of people with type 2 diabetes begin to need insulin less than 10 years after their diagnosis (DeWitt & Hirsch, 2003).
The ability of beta cells to secrete insulin declines progressively in most patients with type 2 diabetes. Type 2 diabetes is typically diagnosed approximately 12 years into the disease, when the person has already lost about 50% of the normal insulin secretory ability (adapted from DeWitt & Hirsch, 2003).
Currently, insulin therapy is recommended when the combination of lifestyle changes and oral medications cannot reduce the A1C index below 8% (DeWitt & Hirsch, 2003). The idea of taking insulin injections can scare patients, but by reducing the levels and durations of their hyperglycemic episodes, patients can delay or prevent the otherwise inevitable debilitating complications of the disease. When insulin injections are incorporated into the treatment of poorly controlled diabetes, patients feel better and they report that their quality of life has improved (DeWitt & Hirsch, 2003).
Three things distinguish the available forms of insulin: how fast they act, when they peak, and how long they act.
Three insulin analogues plus inhaled insulin are rapid-acting (in 5–15 min), reach their peak of action in 1 hour, and act for only a short time (<5 hours):
When injected, regular insulin (short-acting, natural-acting) begins acting in 30–60 minutes, reaches its peak of action in 2–3 hours, and acts for 5–8 hours:
The intermediate-acting insulins begin acting in 2–4 hours, reach a peak of action in 4–10 hours, and act for 10–16 hours:
The effects of long-acting insulins can last for up to a day:
To match the daily changes in blood glucose levels (i.e., high after meals and low during the night), an insulin-dependent patient must mix a variety of insulins. Mixed injections have a rapid onset, give two peaks, and last for 10–16 hours. For convenience, insulins are available in a few dual-acting, pre-mixed formulations:
It has been estimated that almost half of the adults who have diabetes try alternative therapies: acupuncture, Ayurveda, biofeedback, chelation, chiropractic care, energy healing, herbs, homeopathy, hypnosis, massage, naturopathy, Reiki therapy, relaxation, unusual diets, or yoga (Garrow & Egede, 2006). Herbs and dietary supplements can be a problem for people with diabetes who are taking insulin or insulin secretagogues (such as sulfonylureas), because some herbs and supplements lower glucose levels. When used along with prescribed medications, the following compounds have the potential to cause unexpected bouts of hypoglycemia:
At each visit with your patient, ask whether they are trying any herbs or supplements to help treat their diabetes.
The most serious risk of insulin therapy is hypoglycemia. Hypoglycemia can cause unconsciousness, and if not corrected by the addition of glucose to the bloodstream, can eventually be fatal. A very low blood glucose level (<10 mg/dl) begins causing irreversible brain damage in as short as 30 minutes.
As a rule, hypoglycemia is less a risk for people with type 2 diabetes than for those with type 1, but it still occurs. All diabetes patients should learn to recognize the feelings caused by hypoglycemia. Initially, patients should test their plasma glucose levels in different situations to compare their subjective sensations with the actual glucose levels. They should also occasionally check blood glucose levels in the middle of the night to make sure they are not getting too hypoglycemic while sleeping.
For people on insulin therapy, missing a meal or exercising vigorously are the most common causes of hypoglycemia. Diabetic patients who take anti-sympathetic drugs, such as beta-blockers, should be warned that these medications blunt the symptoms of hypoglycemia, making a potentially life-threatening situation less obvious. Patients need to recognize the following:
Sugar is the treatment for hypoglycemia. Patients should be told to take 15 g of glucose (1/2 cup of fruit juice, 5 small pieces of hard candy, or 3 standard glucose tablets) if they feel hypoglycemic. If the symptoms persist for more than 10 to 15 minutes, they should repeat the 15-g dose of sugar. If both doses do not improve the symptoms, the patient should report to a physician, clinic, or hospital.
All patients who take critical medications, such as insulin or insulin secretagogues, should carry medical identification, such as a Medic-Alert tag. Patients on insulin therapy also need to be given specific instructions about how to handle hypoglycemic episodes. These patients should always have with them tablets of sugar or hard candy. At home, they should have an emergency glucagon kit, and family and friends should be taught how and when to give an intramuscular injection of glucagon (Masharani & German, 2004; Masharani, 2007).
For all types of diabetes, a fundamental part of treatment is controlling the composition and quantity of meals. People with type 2 diabetes who take fixed doses of insulin or insulin secretagogues must strictly schedule their meals and their medications to avoid periods of hypo- and hyperglycemia; for these people, as with people who have type 1 diabetes, counting carbohydrates and using exchange lists are important parts of their daily eating plan (Buse et al., 2003; ADA, 2007c).
Most people with type 2 diabetes do not take fixed doses of insulin. For these people, the top priority of a proper diet is striking a balance that minimizes hyperglycemia, encourages weight loss (when needed), reduces dyslipidemia, and lowers blood pressure. These goals can be accomplished when the person's meals have reduced calories, low saturated and trans fat, low cholesterol, and low amounts of sodium, with an appropriate overall mix of carbohydrates, fats, and proteins. Detailed carbohydrate counting of each meal is not necessary.
There is no exact mix of nutrients that comprises the optimal diet for people with type 2 diabetes. The recommended balance for all healthy adults is also the best guide for people with diabetes; however, when building a diet with this overall mix of macronutrients, there are some special recommendations for people with type 2 diabetes.
A person with diabetes should aim for approximately 130 gm of carbohydrates each day. Although diets high in carbohydrates can cause hyperglycemia, low-carbohydrate diets (i.e., <130 gm/day) are not recommended, because foods containing carbohydrates are important sources of energy, fiber, vitamins, and minerals. Fruits, vegetables, whole grains, legumes, and low-fat milk are all recommended. Foods with whole grains have been shown to reduce insulin sensitivity.
There is no need to avoid using sucrose as a sweetener (in moderation), and naturally occurring fructose is also not harmful. The standard reduced-calorie sweeteners—such as mannitol, sorbitol, and xylitol—are safe for people with diabetes and have about one-half the calories of equivalent amounts of sugar. Likewise, artificial (non-nutritive) sweeteners—such as acesulfame potassium, sucralose, and aspartame—are safe for people with diabetes, in moderation (ADA, 2007a).
The glycemic index is a standard way to compare the effects of different foods on the blood glucose level after a meal. Foods with a lower glycemic index value cause less of a spike in blood glucose after they are eaten. Low glycemic-index foods include oats, barley, bulgur, beans, lentils, legumes, pasta, pumpernickel (coarse rye) bread, apples, oranges, milk, yogurt, and ice cream. Theoretically, these foods should make blood glucose control easier for people with diabetes; in reality, studies show that diets with low glycemic index foods make glycemic control only slightly easier than diets with high glycemic index foods.
Limiting carbohydrates in the diet is a key part of controlling hyperglycemia. When regular doses of insulin or insulin secretagogues are needed to cope with the glucose load after meals, it is important to match the dose to the amount of carbohydrates that are eaten at each meal. Patients can estimate the carbohydrates in their meals by summing the approximate grams in each serving. The labels of most foods help patients to make these estimates.
Another way to keep track of carbohydrates is through a standardized set of foods and portions in the form of exchange lists. A single carbohydrate serving is considered to have 15 grams of carbohydrates, and a person with diabetes should have 8.5 to 9 servings of carbohydrates each day, divided among 4 meals. On an exchange list, specific foods are listed in terms of portions equivalent to one carbohydrate serving, so a person can choose preferred foods to fill out the daily allotment. See the table below for examples of carbohydrate equivalents.
| Starches | 1 slice of bread |
| 1/3 cup of cooked pasta | |
| 3/4 cup of dry cereal | |
| 4–6 crackers | |
| Fruits | 1 small piece of fruit |
| 1/2 cup of fruit juice | |
| Milk | 1 cup nonfat (skim) milk |
| 1/2 cup of yogurt | |
| Desserts | 2 small cookies |
| 1/2 cup of ice cream |
Exchange lists are co-published by The American Dietetic Association and the American Diabetes Association. Nutritionists, dieticians, and diabetes educators have these lists, and the websites of the two Associations (http://www.diabetes.org, http://www.eatright.org) tell how to get copies of "Exchange Lists for Meal Planning." The best way for a patient to learn how to estimate the carbohydrate content of his meals is through individualized training sessions with diabetes nutrition instructors (ADA, 2007c).
Dietary fats contribute to the total calories consumed, but the amount of fat in a meal has only a small affect on the level of blood glucose after the meal. The more important consideration for people with type 2 diabetes is their risk for developing coronary heart disease. Dietary fats play a major role in the formation of atherosclerotic plaque. To reduce the likelihood of atherosclerotic cardiovascular disease, a person—especially, a person with type 2 diabetes—should limit the saturated fatty acids, trans fatty acids, and cholesterol in meals.
Fats should make up 20% to 35% of a person's total daily calories. Saturated fats should be limited to less than 7% of total daily calories, trans fats minimized, and cholesterol limited to less than 200 mg per day. Most of the daily fat intake should be monounsaturated or polyunsaturated (a "Mediterranean" diet).
Two or more servings of fish per week (but not commercially fried fish filets) are recommended for their long polyunsaturated fatty acids. Other healthy fats are found in many seeds and nuts, olives, olive oil, and canola oil.
Plant sterols and stanols (types of natural vegetable fats) can lower blood cholesterol levels and are good substitutes for other fats. To increase the sterols and stanols in the diet, patients can replace other types of fat with commercial margarine spreads (eg, Benecol, Take Control) or dietary supplement capsules (eg, Benecol Softgels, Cholest-Off, Cholesterol Success Plus).
As with fats, proteins in a meal do not significantly raise after-meal glucose levels. Proteins (actually, the amino acids derived from the proteins) do increase insulin secretion, and in this way, eating protein with carbohydrates helps a person with type 2 diabetes to reduce the spike of blood glucose after a meal. For the same reason, however, proteins are not good snacks for preventing the hypoglycemia of vigorous exercise or hypoglycemic episodes in the middle of the night.
In a healthy diet, proteins should contribute about 15% to 20% of a day's total calories. The best sources of protein for a person with type 2 diabetes are poultry, veal, fish, eggs, milk, cheese, and soy products.
Some plant carbohydrates, such as cellulose, gums, and pectins, cannot be broken down and digested by humans. These are called dietary fiber. Insoluble dietary fiber, such as cellulose (eg, bran), speeds the movement of food through the digestive tract.
Soluble dietary fiber, such as gums and pectins (eg, oatmeal) slows the rate of absorption of digestible nutrients. A high quantity of soluble fiber in a patient's diet can reduce blood cholesterol and can modestly reduce hyperglycemia and insulin resistance.
The recommendation for the general public is 14 grams of fiber for every 1000 calories in a person's everyday diet. For people with diabetes, the recommendation is higher—a total of 50 grams of fiber per day, regardless of the total daily calories. Plants contain dietary fiber. Legumes, cereals with ≥5 gm fiber/serving, fruits, vegetables, and whole-grain products are recommended.
Micronutrients are the additional substances that people need to ingest in small amounts. As with the general population, people with diabetes need sufficient vitamins and minerals in their diets to meet the body's daily needs. Poorly controlled diabetes or weight loss diets can cause nutritional deficiencies, and the minimum daily vitamin and mineral needs may require the patient to take daily supplements. Other people with diabetes who may need supplements are older adults, pregnant women, lactating women, and strict vegetarians.
No scientific evidence currently exists that any vitamins or antioxidants have special beneficial effects for people with diabetes who do not have vitamin deficiencies. Although not absolutely necessary, some clinicians recommend that patients with type 2 diabetes take a daily supplement of 0.4–1.0 mg folic acid, 0.4 mg vitamin B12, and 10 mg pyroxidine (Buse et al., 2003).
Similarly, no mineral supplements have clear beneficial effects for diabetes beyond their role in general health. Deficiencies in chromium, potassium, magnesium, and zinc can worsen insulin resistance. Potassium and magnesium deficiencies are easily identified in tests of blood chemistry.
Chromium and zinc deficiencies are harder to measure. Chromium picolinate supplements have been used in an attempt to reduce insulin resistance, but the FDA has concluded that there is insufficient scientific evidence to recommend these supplements to all people with diabetes (Center for Food Safety and Applied Nutrition, 2005).
Caloric beverages tend to be sugary, so they should be replaced by artificially sweetened drinks. Most fruit juices contain more sugar than people realize, and juices should not be drunk by people with diabetes merely to quench their thirst.
Drinking a moderate amount of alcohol can reduce the risk of developing type 2 diabetes, coronary heart disease, and stroke. Drinking higher amounts of alcohol brings a host of health problems, including an increased risk for developing diabetes. Those people with diabetes who choose to drink should drink only moderately.
Mixed drinks can contain significant amounts of carbohydrates, so people with diabetes should pay attention to the content of their drinks. It is also best for people with diabetes to drink alcohol with food—especially at night, to avoid a later episode of hypoglycemia.
Moderate drinking means two drinks per day for men and one drink per day for women. Heavy drinking means three or more drinks per day for men and two or more drinks per day for women.
ONE DRINK (15 g of alcohol)
One drink is considered to be 15 grams of alcohol, and the equivalents are as follows.
Alcohol should not be drunk by pregnant women or by people with liver disease, pancreatitis, advanced neuropathy, or very high levels of blood triglycerides.
The American Diabetes Association and The American Dietetic Association make available many detailed recommendations about healthy eating for people with diabetes. Frequently, however, it is necessary for diabetes educators to translate the recommendations into terms that are practical and understandable for individual patients. For this task, a diabetes treatment team needs trained dietitians or nutritionists.
Diabetic patients are more likely than most nondiabetic patients to present with a variety of other problems. Therefore, the team of health professionals taking responsibility for the care of a person with diabetes must keep a careful watch on the health of the whole person.
Treatment of a person with type 2 diabetes begins with a thorough medical history and examination. From this, the physician generates a list of problems along with their degrees of severity. The example below would be typical.
Fred Jones, 65-year-old white male, 7-9-2007
The physician then chooses a plan from the available treatment options, making sure that the included treatments address all the major problems on the list. For diabetic hyperglycemia, the physician begins by choosing from lifestyle changes, proper diet, and medications. For diabetic complications, such as retinopathy, albumin in the urine, or nonhealing foot wounds, referrals are made to the appropriate specialists or specialty clinics. For women of reproductive age, diabetic family planning specialists are recommended.
For all patients with diabetes, the physician schedules a session of individualized diabetes education, because diabetes management requires the knowledgeable participation of patients in their own care. Finally, the plan includes a schedule of regular visits for monitoring the patient's progress.
The treatment for type 2 diabetes must be realistic. The initial plan is only a prototype, and it must be tailored to the specific patient. Diabetes is a chronic illness, and, except for people living in long-term care facilities, the day-to-day management of the disease is in the hands of the patient and family.
The most successful approach is for the physician to present the prototype to the patient and work together to craft it into a plan that the patient can realistically carry out. The other team members—nutritionists, physical therapists, nurses—should help to design the details of the diet, exercise, and medication schedules so that they fit most comfortably into the life of the particular patient. Team members have the shared responsibility for explaining the plan's rationale, so the patient can believe in it and be willing to make the effort necessary to carry it out.
Much detail is available on specific treatment guidelines. A good up-to-date source is the information provided by the American Association of Clinical Endocrinologists (AACE, 2007). Central to all treatment plans for people with type 2 diabetes is the same glycemic goal: patients should aim for an A1C <7% (AACE, 2007; ADA 2007a). In other words, people with diabetes should try to keep their average blood glucose levels below 170 mg/dl. This has been shown to be a realistic goal and a goal that will improve the health of a wide variety of people with type 2 diabetes.
A1C levels are checked at each visit to monitor the patient's progress. The A1C level is only an average value. To ensure that it has not been artificially lowered by periods of hypoglycemia, it is important to have the patient record blood glucose readings at key times each day (eg, first thing in the morning and 2 hours after meals) and then bring the records to each office visit.
Although the treatment plan for a patient with type 2 diabetes must be tailored to the individual, the usual progression begins with lifestyle interventions. Next, oral hypoglycemics are added. Finally, the treatment is changed to insulin therapy.
Weight loss, increased physical activity, and improved diet can all reduce hyperglycemia in a person with type 2 diabetes. These lifestyle changes will also improve many of the health problems that often accompany type 2 diabetes, notably, obesity, hypertension, and dyslipidemia.
Each of these lifestyle changes requires a long-term, steady effort. They are all hard changes to sustain, and the best successes come when they are carried out in supervised programs. Therefore, the first step for a patient with type 2 diabetes is to schedule or to enroll in a regular exercise program and to get help planning appropriate meals. Overweight or obese patients should also enroll in a weight-loss program.
Initially, lifestyle changes are given a 3- to 6-month trial. If they succeed in producing A1C values <7%, the lifestyle changes are continued and the patient is seen (and A1C levels are measured) every 3 to 6 months.
If the 3- to 6-month trial does not lead to an A1C value <7%, the patient should continue the lifestyle changes and add step 2.
At some point, the treatment for type 2 diabetes usually includes medications. In the United States, about 85% of the people being treated for diabetes take anti-diabetes drugs. People with type 1 diabetes need regular doses of insulin. Some people with type 2 diabetes also need insulin, but most people with type 2 diabetes are being treated with a mix of weight loss, proper diet, exercise, and oral medications.
Treatment with insulin and oral medications for people with diabetes (U.S., 1999–2001) (National Diabetes Fact Sheet, 2007).
When lifestyle changes become insufficient to keep A1C values low, it is time to add an oral hypoglycemic. There is currently insufficient scientific data to dictate a first choice. Metformin is usually recommended, however, because it is generic (and so is least expensive), it has proved to be effective when added to lifestyle changes, it can be paired with most other hypoglycemics if needed, and it rarely if ever causes hypoglycemia (Buse et al., 2003; ADA, 2007a). Metformin should not be given to people who are being treated for congestive heart failure.
The addition of metformin is given a 3- to 6-month trial. If this succeeds in producing A1C values <7%, the regimen is continued, and the patient is seen (and A1C levels are measured) every 3 to 6 months.
If the 3- to 6-month trial does not lead to an A1C value <7%, the patient should continue the lifestyle changes and add step 3 (Buse et al., 2003).
The next step in treating type 2 diabetes is more individualized. In general, another type of oral hypoglycemic is added to the metformin treatment and the lifestyle changes. When choosing the additional drug, it is useful to have records of first-thing-in-the-morning blood glucose levels. If these levels are low (most of them <130 mg/dl) and if A1C is >7%, it is likely that there is a significant hyperglycemic peak after meals. Therefore, the best choices for the second anti-diabetes medication are usually drugs that lower after-meal glucose peaks, such as:
In contrast, if morning blood glucose levels are high (most of them >200 mg/dl), it is usually necessary to directly increase insulin levels. This means adding sulfonylureas, glinides, or insulin injections. Experience and detailed information about the individual patient are needed for this decision (Buse et al., 2003).
When the combination of lifestyle changes and hypoglycemics cannot reduce A1C values below about 8%, it is time to consider insulin therapy. Insulin therapy often begins with a two-drug regimen: metformin plus a daily bedtime injection of insulin glargine. Patients prefer simple treatment regimens, but over time, most patients require a more complex schedule of insulin injections (DeWitt & Hirsch, 2003). Mooradian and colleagues (2006) present an excellent discussion on the way to begin insulin therapy in patients with type 2 diabetes.
In addition to the treatment steps, the overall program for a person with diabetes should include a patient education program. It is the patients who must carry out the treatment. They will be the frontline member of the treatment team, and they must understand and believe in their particular plan. Specifically, the patient must understand:
Patient education should be an entire program of its own, with trained counselors who meet with the patient regularly and who are available for questions between visits (Buse et al., 2003; Joslin Diabetes Center, 2006; ADA, 2007a). To help set up diabetes education programs, The American Association of Diabetes Educators (telephone: 800-TEAM-UP4) provides the names of local diabetes educators and contact information for education programs throughout the country.
A key part of the education program is teaching patients how to check their blood glucose levels. Patients should measure their blood glucose levels for two reasons:
All diabetic patients should check their blood glucose levels at a variety of times. This makes the abstract numbers (eg, mg/dl) more real to the patient. It also builds a detailed record of the daily variation of glucose levels, which is especially useful while the initial treatment plan is being adjusted. Moreover, if patients watch their blood glucose levels over an extended period of time, they will learn to recognize the feeling of hypoglycemia and help to distinguish it from other uncomfortable sensations.
The frequency with which a patient checks the glucose level is an individual decision. Patients beginning insulin therapy are usually asked to monitor their blood glucose 4 times a day until an optimal regimen of meals, exercise, and injections is established. After they have established a stable pattern, patients can reduce the number of blood tests to 2 or 3 times a day. When their life pattern changes, when they get symptoms of hypoglycemia, or when they develop another illness, patients are advised to test more frequently.
Patients with type 2 diabetes who do not take insulin usually settle into a schedule of checking blood glucose levels once a day. Typically, they are asked to vary the test times so that within each week they check levels:
Occasionally, they should set an alarm and check their blood glucose level in the middle of the night. In addition, they should measure their blood glucose level when they get symptoms of hypoglycemia and when they develop another illness.
In all cases, patients should be given a target range of glucose values and told to report by telephone or email to a member of their diabetes team when a home test value falls out of the range. Patients are also instructed to bring a log of all the interim blood glucose values to each office visit.
Glucose monitors are pocket-sized, handheld electronic devices. Most home monitors measure the glucose concentration in a drop of whole capillary blood from a finger prick. Clinical laboratories, however, measure the glucose concentration in plasma (blood without the cells) from venous blood. Glucose is about 15% more concentrated in plasma than in whole blood. The newer home monitors make this correction, so the home numbers can be compared directly to the published standards. On the other hand, some older home monitors give the whole-blood glucose levels; therefore, patients should read the information on the box of test strips for their monitor to see if they are getting plasma glucose levels or whole-blood glucose levels.
Old or new, home monitors must be calibrated occasionally to ensure the reliability of their readings. One method for checking the accuracy of patients' monitors is to ask them to bring their monitor each time blood is being drawn for a laboratory test. The patient takes a reading using the monitor within 1 to 2 minutes of when the lab technician draws a blood sample. In this way, the monitor can be compared directly with the clinical test results.
Home testing supplies come with a variety of features, and they are changing and improving continually. Each January, the American Diabetes Association publishes an updated guide to basic products (blood and urine testing equipment, oral hypoglycemics, insulins, insulin delivery devices, and hypoglycemic treatments) used by people with diabetes. The most recent guide can be read online at http://www.diabetes.org/diabetes-forecast/back-issues.jsp.
After an initial 6 to 12 months of trying out and modifying a program of therapy, the skeleton of a long-term program takes shape. Patients should have a schedule of regular visits with the physician and with other members of the diabetes care team. At each visit, the team reviews A1C values and daily blood glucose records, screens for the development and/or progression of diabetic complications, and offer advice and help with problems in daily healthcare routines. When lab values or the clinical picture suggest the treatment routine needs to be changed, the patient should meet with healthcare workers more frequently until health is again stabilized.
Two sets of data should be used to follow a patient's glycemic control: A1C values and daily blood glucose records.
The A1C values show the average level of hyperglycemia in the preceding 2 to 3 months. (See earlier graph to translate A1C values into average plasma glucose levels.) The target for adults with diabetes is an A1C of less than 7%, or about 170 mg/dl. Although the ideal would be an A1C of less than 6% (about 135 mg/dl), it is difficult for most people with diabetes to get these low A1C values without having significant periods of hypoglycemia.
In addition to following A1C values, the patient's daily glucose levels are examined. The American Diabetes Association suggests aiming for a majority of pre-meal glucose values to be in the range of 90 to 130 mg/dl and the majority of glucose values 1 to 2 hours after a meal to be <180 mg/dl (ADA, 2007a).
Patients whose blood glucose values are close to the targets should be re-examined every 6 months. Patients whose blood glucose values are out of the target ranges or whose medications have changed are re-examined every 3 months.
People with type 2 diabetes are at risk for developing cardiovascular disease, therefore blood pressure and lipid profiles are monitored. Target goals are:
The liver is the major site of the degradation of most anti-diabetes drugs, including insulin. Liver dysfunction can lead to abnormally high or prolonged levels of these drugs in the blood, thus liver function should be monitored by checking liver enzymes periodically.
Kidney damage is a classic complication of diabetes. Among the values to be monitored are serum creatinine levels and urine albumin levels. Estimates of glomerular filtration rates (GFR) should be calculated from the creatinine values.
At each visit, the patient's feet should be examined for skin or joint damage, and his ability to sense stimuli in his feet should be assessed.
People with diabetes should have regular eye exams, checking for glaucoma, cataracts, and retinal damage.
People with diabetes face two kinds of ongoing health threats. On the one hand, they sometimes develop acute complications, the two most common of which are diabetic ketoacidosis and hyperglycemic hyperosmolar state. (Another possible emergency—hypoglycemia—is discussed in the section on Insulin Therapy, above.) On the other hand, diabetes continually injures tissues microscopically, and as these microscopic injuries accumulate, they lead to observable problems such as heart disease or kidney failure.
Before the discovery of insulin, most people with diabetes died of a condition known as diabetic coma, which came on suddenly and was fatal by the second or third day. Typically, this fatal condition was characterized by dehydration and precipitated by the occurrence of some other disease. Today, diabetic coma is called diabetic ketoacidosis.
Diabetic ketoacidosis and hyperglycemic hyperosmolar state are two emergency conditions that threaten diabetics. Both conditions involve a high level of blood glucose that leads to dehydration beyond the body's ability to cope. The person becomes tired and weak, is thirsty and urinates excessively, and often has an altered mental state, ranging from confusion to coma. Dehydration causes hypotension and acute renal failure, and without IV fluids and insulin, the condition leads to serious electrolyte abnormalities, brain injury, and death.
Diabetic ketoacidosis develops when there is so little insulin that the body begins to use fat as a major fuel. Diabetic ketoacidosis is seen primarily in people with type 1 diabetes, although some people with type 2 diabetes develop the condition.
Diabetic ketoacidosis is characterized by acidic ketones (the result of fat metabolism) in the blood and the urine, and ketones can be smelled on the patient's breath, giving a fruity or acetone-like odor. The resulting acidosis—a drop in blood pH below 7.3 (normal pH is 7.38–7.44)—causes the body to adopt a deep, sighing pattern of respiration, called Kussmaul breathing or air hunger. Diabetic ketoacidosis, which usually comes on quickly (within a day or two), also produces nausea, vomiting, and abdominal pain.
Hyperglycemic hyperosmolar state develops when there is sufficient insulin for the body to use glucose as a fuel but there is not enough insulin to keep blood glucose levels in a safe range. Hyperglycemic hyperosmolar state is primarily seen in older adults with type 2 diabetes.
Unlike diabetic ketoacidosis, hyperglycemic hyperosmolar state produces no ketones. The condition is caused directly by very high blood glucose levels, typically greater than 600 mg/dl and often higher than 1000 mg/dl. Without acidic ketones, there is no Kussmaul breathing and usually no abdominal distress. Hyperglycemic hyperosmolar state tends to develop slowly, over days or weeks, and by the time it is apparent the patient may already be confused or stuporous.
Both diabetic ketoacidosis and hyperglycemic hyperosmolar state are precipitated by sudden stresses that change the body's balance of insulin and glucose. The stress can be a new illness, such as a serious infection, a heart attack, or a stroke, or the stress can be an injury. Alternately, the stress can be the addition of a new drug, such as a corticosteroid, thiazide, anticonvulsant, or sympathomimetic. Diabetic ketoacidosis, which is almost always a condition of insulin-dependent diabetics, can also develop when a patient does not take prescribed insulin.
Both conditions are emergencies and are treated in the same way. The patient is given insulin to lower the hyperglycemia and fluids to reverse the dehydration. The blood electrolyte levels are corrected, and for diabetic ketoacidosis, the pH balance of the body is shifted back toward normal. Typically, both conditions are precipitated by another recent stressor, so this problem, too, must be identified and corrected. The patient is usually monitored in an intensive care unit.
Because continual hyperglycemia is the cause of the chronic complications of diabetes, any reduction of average blood glucose levels (i.e., A1C values) reduces the chances of developing chronic complications. Prolonged hyperglycemia has a number of deleterious effects. Two types of microscopic cell and tissue damage seem to be involved in most of the long-term complications of diabetes (Davis, 2005; Powers, 2005).
When there is excess glucose in the bloodstream, glucose molecules stick indiscriminately to proteins, in a process called glycosylation. (For example, excess glucose binds to hemoglobin, and this is the basis of the A1C index of hyperglycemia.) Higher blood glucose levels produce more glycosylated proteins, and these glycosylated proteins tend to cross-link (bind together) into abnormal complexes. The complexes then add to atherosclerotic plaque, damage kidneys, and disrupt the structure of extracellular matrices.
Excess glucose also amplifies the amount of certain rarely produced chemicals in the body. These chemicals include sorbitol, diacylglycerol, and fructose-6-phosphate, all of which, in sufficient quantities, are detrimental to the normal functioning of cells.
Both types of molecular problem damage blood capillaries, endothelial cells of larger blood vessels, and nerves. The accumulation of these microscopic injuries leads to the macroscopic damages that are the long-term complications of diabetes.
Over the years, the continual hyperglycemia of diabetes takes its toll on tissues everywhere in the body. The chronic complications of diabetes are the macroscopic damage that finally shows up after the accumulation of 10 to 20 years of microscopic damage. In type 2 diabetes, hyperglycemia has gone on for many years before the disease is recognized. Therefore, many people with type 2 diabetes already have macroscopic damage when they are first seen by a physician.
In the United States, the major long-term health problems from diabetes are:
The most common long-term complications of diabetes are damage to arteries, kidneys, eyes, nerves, and feet.
People with type 2 diabetes get atherosclerotic heart and artery disease more frequently than people without diabetes. Atherosclerosis causes heart attacks, congestive heart failure, strokes, and insufficient circulation to the feet. Today, 80% of the people with type 2 diabetes die from some form of cardiovascular disease.
Patients with type 2 diabetes should be screened annually for signs, symptoms, and risk factors of cardiovascular disease. It is still not clear how aggressively a physician should search for unrecognized ("silent") heart ischemia in people with type 2 diabetes. Most recommendations suggest using cardiac stress tests for diabetic patients who also have:
It is best to consult a cardiologist when considering stress tests for a patient.
By controlling their blood glucose levels, people with type 2 diabetes reduce the likelihood of having heart and artery problems. The risk of cardiovascular disease can be reduced still farther by reducing high blood pressure, correcting dyslipidemia, and taking aspirin prophylactically. These three tasks should be added to the long-term treatment plan for all people with type 2 diabetes.
The majority of people with type 2 diabetes develop hypertension. The two problems are somehow tied together, because people with hypertension are 2.5 times more likely to develop type 2 diabetes than people with normal blood pressures.
The combination of diabetes and hypertension doubles a person's risk of cardiovascular disease (Buse et al., 2003). Hypertension plays such a large role in causing cardiovascular disease that reducing the blood pressure of a person with diabetes is more preventive of cardiovascular disease than controlling blood glucose levels (Cydulka & Pennington, 2006).
Systolic blood pressure of ≤130 mm Hg and diastolic blood pressure of ≤80 mm Hg are the recommended targets for people with type 2 diabetes.
The lifestyle changes recommended for treating type 2 diabetes will also improve a patient's blood pressure. Specifically, weight loss and maintaining a healthy weight, eating a low-fat diet of fruits, vegetables, and low-fat dairy products, avoiding excess alcohol, not smoking, and exercising regularly will reduce hypertension. For genetically predisposed people, low-salt diets will also improve blood pressures.
Even with lifestyle changes, most people with type 2 diabetes and hypertension need anti-hypertensive medications (often two or more drugs) to reduce their blood pressures to ≤130/80 mm Hg. For these people, the first drug to try is either an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB). (Both drugs can also delay the development of diabetic kidney damage.) If a second drug is needed, a thiazide diuretic is recommended (ADA, 2007a).
Dyslipidemia increases a person's chances of developing cardiovascular diseases. The fasting lipid levels of people with type 2 diabetes should be screened yearly, and unhealthy lipid levels treated.
In terms of reducing cardiovascular risk, the primary goal is a fasting LDL-cholesterol level of ≤100 mg/dl. Secondary goals are fasting triglyceride levels of ≤150 mg/dl and fasting HDL-cholesterol levels of ≥40 mg/dl in men and ≥50 mg/dl in women. People who already have some form of cardiovascular disease should aim for a lower LDL-cholesterol level, namely ≤70 mg/dl (ADA, 2007a).
As with hypertension, the lifestyle changes recommended for treating type 2 diabetes will also improve a patient's dyslipidemia. The addition of a statin drug is recommended for patients who do not meet the lipid target goals after changing their lifestyles. (Pregnant women should not take statins.)
In the prothrombotic state—a condition in which the blood clots inside blood vessels more easily than normal—unnecessarily high levels of clotting molecules in the bloodstream increase a person's risk for developing coronary artery disease and stroke. A low dose (75–162 mg/day) of enteric-coated aspirin is recommended for most people with type 2 diabetes to help prevent cardiovascular disease. (Patients with aspirin allergies, bleeding disorders, recent gastrointestinal bleeding, or liver disease should not take aspirin.)
Fifteen to twenty percent of people with type 2 diabetes develop a characteristic kidney damage called diabetic nephropathy. Diabetic nephropathy can progress to endstage renal disease, and 80% of all people with endstage renal disease have type 2 diabetes.
Diabetes injures those cell membranes in the kidney that are responsible for filtration and absorption of fluids and molecules. One of the earliest indicators of membrane damage is seen in the kidney glomeruli, the first of the filtration sites, which become slightly leaky and allow small amounts of protein into the urine. The small amount (30–300 mg/24 hr) of protein that abnormally appears in the urine is termed microalbuminuria.
A cross-section of the kidney showing ischemic pyramids and sclerotic arteries and arterioles. Illustration by Jason McAlexander. Copyright © 2007 Wild Iris Medical Education.
Without treatment, the ability of the glomeruli to keep protein out of the urine declines, and eventually the person has albuminuria—the excretion of a significant amount (>300 mg/24 hr) of protein. While glomeruli are loosing their ability to exclude large molecules, such as proteins, from the urine, they are also becoming less able to filter fluid, and the glomerular filtration rate (GFR) declines. At the same time, blood pressure begins to rise.
These three problems—albuminuria, declining GFR, and hypertension—are the symptoms of diabetic nephropathy, which will continue to damage the kidneys until they must be replaced by a transplant or dialysis (Parving et al., 2004).
The American Diabetes Association (ADA, 2007a) recommends that patients with type 2 diabetes should have two indicators of kidney functioning checked annually:
In addition, blood pressure should be measured at each check-up.
By controlling all three major risk factors—blood glucose levels, blood pressure, and blood lipid levels—people with type 2 diabetes can delay the development of kidney problems. Those people with diabetes who already have microalbuminuria can slow its progression to diabetic nephropathy by the same interventions. When kidney problems have progressed to albuminuria and a declining GFR, it is best to consult a kidney specialist.
By itself, good control of serum glucose levels will not prevent kidney problems in people with type 2 diabetes. On the other hand, when part of a regimen that targets all the major risk factors, glycemic control does slow the onset and progression of diabetic neuropathy.
Controlling blood pressure is an effective way to delay or prevent kidney problems in people with type 2 diabetes. Hypertension accelerates the development of kidney damage as well as atherosclerosis, and all these problems feed on and worsen each other. The American Diabetes Association (ADA, 2007a) recommends that hypertension be treated with ACE inhibitors, which appear to have a beneficial effect on the kidneys beyond the effect of lowered blood pressure.
Some studies suggest that angiotensin-receptor blockers (ARBs) can delay the progression of kidney problems in people with type 2 diabetes who do not have hypertension (i.e., whose blood pressures are <140/90) but who already have microalbuminuria. Currently, there are no agreed-upon recommendations for using either ACE inhibitors or ARBs in normotensive people with type 2 diabetes.
People with type 2 diabetes who have kidney problems usually also have high levels of serum cholesterol. Although it is not certain that high cholesterol levels cause or accelerate nephropathy, the American Diabetes Association (ADA, 2007a) advises that long-term treatment should aim for a blood LDL-cholesterol level of <100 mg/dl.
In diabetic patients with nephropathy, reducing the amount of protein in their diets slows the deterioration of the functioning of their kidneys. The American Diabetes Association (ADA, 2007a) suggests lowering protein intake from 15% to 20% of the daily calories to 10% to 15% of the daily calories, but diets with less protein than this are detrimental to the patient's health.
People with diabetes get cataracts earlier and with a higher frequency than people without diabetes. The most serious eye damage, however, results from long-term (>5 yr) diabetic injury to capillaries and small blood vessels of the retina.
The retina viewed through a scope showing damage due to diabetes including light exudate splotches, mini-hemorrhages, and areas of neovascularization. Illustration by Jason McAlexander. Copyright © 2007 Wild Iris Medical Education.
Diabetic retinopathy begins with tiny aneurysms, small ("dot") hemorrhages, and swelling of the retinal tissue. This early retinopathy leads to areas of ischemia and infarct, which are called cotton-wool spots. Eventually, the continuous injury causes new blood vessels to grow along the retina, accompanied by fibrous connective tissue. Once new blood vessels begin to grow (neovascularization), the problem is called proliferative diabetic retinopathy, which is the number one cause of new blindness in the United States.
Fortunately, the number of cases of severe vision loss can be reduced by a full treatment program that includes controlling blood glucose and blood pressure levels and regular eye examinations by an ophthalmologist. Today, ophthalmologists have laser therapy and vitrectomy procedures that can slow and sometimes stop the progressive loss of vision (Rosenblatt & Benson, 2004).
For effective treatment, catching retinal damage early is critical. People with diabetes should have a full (dilated) eye examination by an ophthalmologist or a trained optometrist when they are first diagnosed and every year thereafter (unless a less frequent schedule is recommended by an ophthalmologist). A diabetic patient who already has kidney damage, almost always has retinopathy, so kidney damage is a warning that the patient should be seen by an ophthalmologist (ADA, 2007a).
Nerve damage is a common complication for people with diabetes. The damage can decrease a patient's ability to sense actual pain, and at the same time, it can cause phantom burning pain, especially at night. Sometimes, motor nerves are affected, and muscles or reflexes are weakened. When autonomic nerves are damaged, the patient can have symptoms ranging from impotence to digestive problems to dizziness on standing.
Diabetic neuropathies can take many forms. The two most common are generalized nerve injuries (called diabetic distal symmetrical polyneuropathy) and diabetic autonomic neuropathy.
Symptoms of DSPN show up at the ends of the longest nerves first. Typically, DSPN begins with unusual sensations such as tingling and numbness in the toes and feet. Over time, the paresthesias and numbness slowly move upward, until they are distributed like socks on the feet, ankles, and legs. Before the problem reaches the knees, long nerves elsewhere in the body become affected, beginning at the fingers.
Eventually, the hands and lower arms have sensory reductions in a distribution like a pair of gloves. These "socks and gloves" sensory deficits are followed by decreased reflexes in the feet and ankles and by weakness in the muscles that spread the toes (Ferrante, 2003).
When diabetes damages the autonomic nerves, the symptoms vary and can affect any of the internal organs. Possible symptoms include:
At each visit, check for distal polyneuropathy. Test the ability of the patient to sense the vibration of a tuning fork in the toes of both feet and also the ability to sense the pressure of a standardized 10-g diabetes monofilament on the bottoms of the toes. Check the Achilles tendon reflexes at the ankles. Then examine each foot for skin lesions, soft tissue injuries, and joint damage.
To screen for autonomic neuropathy, ask patients whether they have each of the cardiovascular, gastrointestinal, genitourinary, and skin symptoms listed above. Check the resting heart rate and compare sitting blood pressure with blood pressure after standing (ADA, 2007a).
By improving glycemic control, neurologic symptoms can sometimes be reduced, but there are no cures for the nerve damage of diabetes: treatments for diabetic neuropathy only alleviate symptoms. Symptoms of diabetic neuropathy are treated individually.
Poor sensation in the feet is treated by educating the patient about foot care, by limiting impact exercises, by referring for special footwear or walking supports (such as a cane) when needed, and by foot exams every 3 to 6 months. (See upcoming section on Foot Problems for more information.)
Pain from neuropathy should be treated by a specialist who will choose a medication (or other regimen) appropriate to the particular patient.
Orthostatic hypotension should be evaluated by a neurologist. Therapy usually includes having the patient sleep with the head of the bed elevated, avoid sudden posture changes by sitting or standing slowly, and wear full-length elastic stockings.
Diarrhea from autonomic neuropathy should be evaluated by a specialist. Sometimes, the diarrhea resolves on its own but, if not, it may respond to anti-diarrheal medications or to antibiotic therapy. In other cases, diarrhea can be caused by impaired neural control of sphincters and the consequent fecal incontinence.
Constipation can usually be treated with a stimulant laxative, such as senna.
Gastroparesis (decreased stomach motility), bladder dysfunction, and impotence can usually be improved by medications.
It has been estimated that 20% of the hospital admissions of diabetic patients are for foot problems. Over the years, damage to capillaries and small blood vessels reduces the ability of the microscopic circulation to deliver oxygen to the feet of people with diabetes. In addition, many people with diabetes develop atherosclerotic peripheral vascular disease, which impedes the overall circulation to their feet.
People with diabetic neuropathy can have muscle weakness and a poor sense of position. For these reasons, they tend to injure their feet, ankles, and legs. Any damage to their sensory nerves will make these frequent small injuries less likely to be noticed. To compound the problem, diabetic ischemia of the lower legs slows the healing of injuries and encourages infections.
The results of all these leg and foot problems are damaged and deformed joints and nonhealing skin ulcers. When soft tissues or bones become infected, the destruction can become severe enough to require amputation. The highest risk of amputations is in people who have had diabetes for more than 10 years and in whom microscopic tissue damage has already shown itself as eye or kidney problems (Cydulka & Pennington, 2006).
Decreased sensation from peripheral neuropathy can lead to ulcers. Daily inspections are important to address small abrasions and sores before they develop into ulcers. Illustration by Jason McAlexander. Copyright © 2007 Wild Iris Medical Education.
Examine the nails, skin, and joints of both of the patient's feet at each visit. Test the foot and ankle pulses and the ability to feel vibration and light touch in the toes. Watch the patient walk, looking for uneven gait, and check shoes for uneven wear and for locations of excess pressure. Ask whether there are other problems walking, such as intermittent claudication, weakness, or imbalance. Determine whether the patient can safely trim toenails (Joslin Diabetes Center, 2006; ADA, 2007a).
Patients with diabetes should be warned about the extra risks that foot injuries pose for them. They should be encouraged to examine their feet every day, and they should be counseled on how to care for their skin and toenails and how to choose appropriate footwear. If they have difficulty examining and caring for their feet, someone else (a family member, a nurse, a podiatrist) should be enlisted to help. Foot care should be part of the initial education of all patients diagnosed with diabetes (Dillingham, 2002).
The most common cause of foot injury is excess pressure on the skin under the bony bumps of the soles of the feet. To ease pressure points, well-fitted athletic shoes are better than dress shoes or shoes with hard soles. For feet with insufficient circulation or poor sensation, special shoes with individualized internal molds are needed so that the pressure of walking is distributed evenly; these patients should see a podiatrist (Dillingham, 2002; Cydulka & Pennington, 2006).
Wounds on feet with neuropathy or poor circulation cannot be treated casually. Even small wounds should be thoroughly examined, cleaned, and debrided; they should be re-examined daily. Antibiotics should be used at the first signs of infection. Walking and other foot pressures should be minimized while the wounds are healing. Soft-tissue infections have to be treated aggressively with hospitalization and IV antimicrobial therapy.
When a diabetic foot becomes pale, pulseless, and painful, it is an emergency, and a surgeon should be consulted.
In many cases, the onset of type 2 diabetes can be delayed or even prevented. People whose bodies do not handle blood sugar optimally have a condition called prediabetes, and these people have a high risk of developing type 2 diabetes. A program of weight loss and increased physical activity can improve the problems underlying prediabetes and, many times, lifestyle changes alone can prevent people with prediabetes from going on to develop diabetes.
Prediabetes can be recognized through the same screening tests used to diagnosis diabetes. The simplest test is the fasting plasma glucose level—in prediabetes, fasting plasma glucose is in the impaired range—100–125 mg/dl—in measurements taken on two different days. (Alternately, a glucose tolerance test in the impaired range—140–199 mg/dl at 2 hours, again on two different days— can be used to diagnose prediabetes.)
DEFINITION OF PREDIABETES
The diagnosis of prediabetes is made by a finding, on two different days, of either:
In addition to signaling a person's risk for developing type 2 diabetes, prediabetes warns that the person also has a higher risk for heart disease and stroke.
The American Association of Clinical Endocrinologists suggests screening people over the age of 29 for prediabetes every 1 to 3 years if they have any of these risk factors:
The most cost-effective way to screen people is to include a fasting glucose test at regular intervals (every 1–3 yr) in the person's other healthcare visits.
The best diabetes preventatives are the standard lifestyle changes used to treat diabetes—weight loss (when appropriate), increased exercise, and controlled meals (type 2 diabetic diet). As in diabetes treatment, these interventions should be tailored to the individual and are most effective when part of a supervised program. Some people (ages 25–40 yr who are 50–80 lb overweight) benefit from the addition of metformin to the lifestyle changes of their diabetes prevention program.
Nurses and other professionals who advise patients over the telephone should know straightforward answers to basic questions. Here are a few important questions and answers about type 2 diabetes.
How do you know if you have type 2 diabetes?
People with type 2 diabetes can have the disease for many years before symptoms appear. When symptoms eventually show up, they can include:
The only sure way to know if you have type 2 diabetes, however, is to have a physician check the level of sugar in your blood.
I have type 2 diabetes, and I've heard that I can faint from low blood sugar. What should I do to prevent this?
A low blood sugar level is called hypoglycemia. Diabetes is a disease of high blood sugar levels. In some situations, however, the medications that are used to lower high blood sugar levels overshoot the mark, and the person's blood sugar level gets too low. This happens most often when insulin is the medication that a person with diabetes is taking. Your physician can advise you if you need to be especially careful about hypoglycemia with your specific medications.
The symptoms of hypoglycemia are:
The treatment for hypoglycemia is eating sugar. It doesn't take much: 1/2 cup of fruit juice, 5 small pieces of hard candy, or 3 glucose tablets, which you can buy in any drugstore. If this doesn't make you feel better in 10 to 15 minutes, take the same amount of sugar a second time. If this still doesn't fix the problem, get someone to take you to a hospital.
Just as you've heard, hypoglycemia can make you faint. If you think you're feeling hypoglycemic, eat some form of sugar. It's better to be safe than to pass out.
If you are too dizzy to eat or if you pass out, someone must get you to an emergency room immediately. This condition justifies calling 911.
I have type 2 diabetes. Do I have to do anything special when I get sick?
Illnesses stress your body, and your body reacts by putting extra sugar into your bloodstream. In a person with diabetes, the extra sugar makes it harder to keep blood glucose levels from getting too high. High blood glucose can make a person with type 2 diabetes get dangerously dehydrated. If the illness makes you vomit or gives you diarrhea, you will get dehydrated even faster.
To protect yourself, you need a plan. Talk with your physician or diabetes nurse. They will probably recommend checking your blood glucose levels more frequently when you are ill. It is possible that they will tell you to take more medication if you find your blood sugar levels getting too high. They will also tell you what signs and symptoms mean that you should call them for advice—be sure to get telephone numbers that you can call day and night.
Even from the beginning of an illness, drink lots of noncaloric liquids—and be prepared by having plenty of these beverages on hand. If you can, try to stick to your normal eating pattern. If it is hard to eat your regular foods, use the equivalent soft or liquid foods, such as soups, puddings, and applesauce. Try to always have some of these foods in your cupboard. Diabetes recipe books usually have a section on easy-to-eat snacks for when you are ill.
My diabetes pills are expensive—any suggestions?
Talk with your physician. Ask if there is a generic version of the medication you're taking. The American Diabetes Association says that single tablets of one dosage are often less expensive than two smaller tablets of half the dosage (a 500 mg tablet can cost less than two 250 mg tablets). Ask your physician to prescribe the largest tablet strength suitable for the dose you are taking. Then you can use a pill cutter to break the pill into halves or quarters to get the specific dose you need.
What is type 2 diabetes?
The main form of sugar in your blood is glucose. Diabetes is a disease in which your body uses glucose inefficiently. Too much glucose is left in your blood after you eat, and the concentration of glucose in your blood remains too high—a condition called hyperglycemia.
Type 2 diabetes is the result of two specific problems. First, the tissues in your body don't absorb glucose as easily as they should. Second, your pancreas doesn't produce as much insulin as it should. (Insulin is the hormone that keeps glucose from piling up in your bloodstream.)
Diabetes can occur at any age, but type 2 diabetes usually shows up in people older than 40. People who are overweight or who have close family members with diabetes are more likely to develop type 2 diabetes.
What can be done for type 2 diabetes?
The three most basic treatments are:
These can be difficult challenges, but for some people with type 2 diabetes, these three changes in their lifestyles will control their blood sugar levels. Other people need to add medications to these lifestyle changes.
You can't manage your diabetes on your own. You need to find a diabetes physician. Your physician will set up a program that includes advisors who will help you to plan meals and exercise routines. You will have regular checkups, and there will be experts to whom you can ask questions between the visits. If the diabetes leads to problems with your heart, kidneys, eyes, or nerves, you will be referred to specialists in treating these complications.
What is a good way to get trustworthy information about diabetes?
The American Diabetes Association has helpful information and advice on its website at: http://www.diabetes.org. You can email them with questions at: AskADA@diabetes.org. Or, you can call them at: 1-800-DIABETES (1-800-342-2383), Monday to Friday, 8:30 a.m. to 8 p.m. Eastern Time.
I've heard that people with diabetes eventually have to get their feet amputated. Is this true?
People with diabetes are far more likely to have a foot or part of a leg amputated than other people. The reason is that diabetes can lower the blood flow to your feet. Without enough blood circulation, your feet don't heal well when they get injured, and any infections get worse more quickly than normal. Infected wounds can get so bad that the tissues can't be revived by medications and rest, and the only protection for the remaining good tissue is amputation of the dying area.
These problems can be prevented by paying special attention to your feet. Diabetes can make your feet less sensitive to injuries, so you have to watch for injuries with your eyes. Be aware of bumps, cuts, and bruises. Look over your feet every morning before you put on your socks. If your shoes are making sore spots, see a podiatrist or shoe specialist. If you think a cut isn't healing well, see a physician. If you are having trouble trimming your nails without cutting yourself, get help from a family member or go to a podiatrist for regular nail care. And, most important, stop smoking. Smoking is bad for your circulation, and many of the people with diabetes who end up with amputations are smokers.
What is metabolic syndrome?
To say someone has metabolic syndrome means that they have a specific group of health problems: they have too much stomach fat, too much sugar and fat circulating in their bloodstream, and high blood pressure. Having all these problems at once makes a person more likely to get heart disease and type 2 diabetes.
Are chromium supplements helpful for people with diabetes?
Chromium supplements have not been conclusively shown to be beneficial in diabetes (ADA, 2007a).
Should I take extra vitamin C or E for my diabetes?
These vitamins have not been shown to help people with diabetes (ADA, 2007a).
I have diabetes. I don't drink, but I've heard that wine is good for diabetes. Should I start drinking wine with dinner every night?
A moderate amount of alcohol in your diet can reduce your risk of developing high blood pressure and other heart and artery problems. A moderate amount means the equivalent of 4 to 8 oz of wine (12–24 oz of beer, or 1.5–3 oz of liquor) per day. (The lower amount is best for women, while the higher amount is best for men.) On the other hand, too much alcohol has the opposite effect, and excess alcohol can produce serious problems for people with diabetes (Kaplan, 2005).
At the moment, the medical profession does not recommend that nondrinkers with diabetes should begin drinking. It strongly recommends against drinking for people who have had problems with excess alcohol or who are pregnant. It also recommends against drinking for people with certain diseases, such as liver disease, pancreatitis, neuropathies, or high triglyceride levels.
Nonetheless, there is no general reason that people with diabetes cannot drink a small amount of alcohol regularly. We suggest talking with your physician about your specific situation. If you do decide to add a glass of wine to your diet, drink it with a meal. Don't take a drink by itself as a nightcap, because this can cause an episode of low blood sugar later that night (ADA, 2007c).
My physician says I'm getting diabetes. I think she's being a worrywart. Aren't most physicians too cautious, maybe because they're afraid of lawsuits?
No one wants to be sick. It's more than annoying, it's depressing and scary and everyone hopes their physician is wrong when they are diagnosed with a disease. This is the normal reaction.
It's not likely that your physician is wrong. But, it can take a while for you to feel okay with the news. Let the idea sink in for a few days. Talk with friends and family. Complain to them.
Then, don't let the diabetes win. Decide that you are going to get control of the problem so that you can get on with the important things in your life.
Diabetes is now part of your life—fine. Shift the worry to your physician's shoulders. Make an appointment. Ask for help to plan a lifestyle that will best treat the diabetes. Then follow the plan, live your life, and leave the worrying to your physician.
American Diabetes Association
http://www.diabetes.org
American Dietetic Association
http://www.eatright.org
American Heart Association
http://www.americanheart.org/
American Obesity Association
http://www.obesity.org
Centers for Disease Control and Prevention
http://www.cdc.gov/diabetes
Cleveland Clinic
http://www.clevelandclinic.org/
Joslin Diabetes Center, 2006 Diabetes Center
http://www.Joslin.org
Juvenile Diabetes Research Foundation International
http://www.jdrf.org
National Institute of Diabetes & Digestive & Kidney Diseases
http://www2.niddk.nih.gov
MedicAlert Foundation
phone: 800-ID-ALERT
http://www.medicalert.org
Mayo Clinic
http://www.mayoclinic.com/
Shape Up America!
http://www.shapeup.org
South Dakota Diabetes Prevention & Control Program
http://diabetes.sd.gov/cookbook.htm
University of Illinois Extension
http://www.urbanext.uiuc.edu/diabetesrecipes/
American Association of Clinical Endocrinologists (AACE). (2007). Medical Guidelines for Clinical Practice for the Management of Diabetes Mellitus. Retrieved June 2007 from http://www.aace.com/pub/guidelines/.
American Diabetes Association (ADA). (2007a). Standards of medical care in diabetes. Prevention and management of diabetes complications. Diabetes Care 30(Suppl 1): S4–S41. Online at http://www.guideline.gov/summary/summary.aspx?doc_id=10401.
American Diabetes Association (ADA). (2007b). Diagnosis and classification of diabetes mellitus. Diabetes Care 30(Suppl 1):S42–47.
American Diabetes Association (ADA). (2007c). Nutrition recommendations and interventions for diabetes: A position statement of the American Diabetes Association. Diabetes Care 30: S48–S65.
American Diabetes Association (ADA). [n.d.]. Diabetes Dictionary. Retrieved June 2007 from http://www.diabetes.org/diabetesdictionary.jsp?WTLPromo=FOOTER_dictionary&vms=234355644560.
American Diabetes Association (ADA), Executive Committee. (2007). Clinical practice recommendations. Diabetes Care 30(suppl 1). Online at http://care.diabetesjournals.org/content/vol30/suppl_1/.
American Optometric Association. (2002). Care of the Patient with Diabetes Mellitus, 3rd ed. St. Louis: Author. Online at http://www.guideline.gov/summary/summary.aspx?doc_id=4600.
Bender DA, Mayes PA. (2006). Carbohydrates of physiologic significance. In RK Murray, DK Granner, and VW Rodwell (Eds.), Harper's Illustrated Biochemistry, 27th ed. New York: McGraw-Hill, Ch. 14.
Bechmann JA, Libby P, Creager MA. (2005). Diabetes mellitus, the metabolic syndrome, and atherosclerotic vascular disease. In DP Zipes et al. (Eds.), Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed. Philadelphia: Saunders, Ch. 40.
Bonnardeaux A, Bichet DG. (2004). Inherited disorders of the renal tubule. In BM Brenner (Ed.), Brenner & Rector's The Kidney, 7th ed., Philadelphia: Saunders, Ch. 36.
Buse JB, Polonsky KS, Burant CF. (2003). Type 2 Diabetes Mellitus. In PL Larsen, et al. (Eds.), Williams: Textbook of Endocrinology, 10th ed. Philadelphia: Saunders, Ch. 29.
Center for Food Safety and Applied Nutrition. (2005). Chromium Picolinate and Insulin Resistance. Retrieved June 2007 from http://www.cfsan.fda.gov/~dms/qhccr.html.
Cydulka RK, Pennington J. (2006). Diabetes mellitus and disorders of glucose homeostasis. In JA Marx, et al., (Eds.), Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed. Philadelphia: Mosby, Ch. 124.
Davis SN. (2005). Insulin, oral hypoglycemic agents, and the pharmacology of the endocrine pancreas. In LL Brunton, JS Lazo, and KL Parker (Eds.), Goodman & Gilman's The Pharmacological Basis of Therapeutics, 11th ed. New York: McGraw-Hill, Ch. 60.
DeWitt DE, Hirsch IB. (2003). Outpatient insulin therapy in type 1 and type 2 diabetes mellitus. Journal of the American Medical Association 289(17): 2254–64.
Dillingham TR. (2002). Diabetic and peripheral vascular foot disease. In WR Frontera and JK Silver (Eds.), Essentials of Physical Medicine and Rehabilitation, 1st ed. Philadelphia: Hanley and Belfus, Ch. 106.
Eckel RH, Grundy SM, Zimmet PZ. (2005). The metabolic syndrome. Lancet 365(9468): 1415–28.
Eisenbarth S, Polonsky KS, Buse JB, et al. (2003). Type 1 diabetes mellitus. In PL Larsen PL et al. (Eds.), Williams: Textbook of Endocrinology, 10th ed. Philadelphia: Saunders, Ch. 30.
U.S. Food and Drug Administration (FDA). (2007). Rosiglitazone maleate information. Retrieved June 2007 from http://www.fda.gov/cder/drug/infopage/rosiglitazone/default.htm.
Ferrante MA. (2003). Endogenous metabolic disorders. In CG Goetz (Ed.), Textbook of Clinical Neurology, 2nd. ed. Philadelphia: Saunders, Ch. 38.
Garrow D, Egede LE. (2006). Association between complementary and alternative medicine use, preventive care practices, and use of conventional medical services among adults with diabetes. Diabetes Care 29(1): 15–19.
Joslin Diabetes Center. (2006). Clinical guideline for adults with diabetes. Boston: Author. Online at http://www.guideline.gov/summary/summary.aspx?doc_id=10573.
Joslin Diabetes Center, 2006 Diabetes Center. (2006). Clinical guideline for adults with diabetes. Boston: Authors. Online at http://www.guideline.gov/summary/summary.aspx?doc_id=10573.
Kaplan NM. (2005) Systemic hypertension: Therapy. In DP Zipes et. al, (Eds.), Braunwald's Heart Disease. A Textbook of Cardiovascular Medicine, 7th ed. Philadelphia: Saunders.
Landon MB, Catalano PM, Gabbe SG. (2002). Diabetes mellitus. In SG Gabbe, JR Niebyl, and JL Simpson (Eds.), Obstetrics. Normal and Problem Pregnancies, 4th ed. Philadelphia: Churchill Livingstone, Ch. 32.
Lorenzo C, Williams K, Hunt KJ, Haffner SM. (2007). The National Cholesterol Education Program—Adult Treatment Panel III, International Diabetes Federation, and World Health Organization definitions of the metabolic syndrome as predictors of incident cardiovascular disease and diabetes. Diabetes Care 30(1): 8–13.
Masharani U. (2007). Diabetes mellitus and hypoglycemia. In SJ McPhee, MA Papadakis, and LM Tierney Jr (Eds.), Current Medical Diagnosis & Treatment, 47th ed. New York: McGraw-Hill.
Masharani U, German MS. (2004). Pancreatic hormones and diabetes mellitus. IN DG Gardner and D Shoback (Eds.), Greenspan's Basic & Clinical Endocrinology, 8th ed. New York: McGraw-Hill, Ch. 18.
Mooradian AD, Bernbaum M, Albert SG. (2006). Narrative review: A rational approach to starting insulin therapy. Annals of Internal Medicine 145(2): 125–34.
National Diabetes Fact Sheet. (2007). Online at http://www.cdc.gov/diabetes/pubs/estimates.htm. Also available at http://www.cdc.gov/diabetes/pubs/general.htm#what.
Natural Standard. (2007). Herbs and supplements. Retrieved June 2007 from http://www.naturalstandard.com.
Nissen SE, Wolski K. (2007). Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. New England Journal of Medicine 356(24): 2457–71.
Nussey S, Whitehead S. (2001). Endocrinology. An Integrated Approach. Oxford: BIOS Scientific Publishers [London: Taylor & Francis]. Also found online at http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=endocrin.TOC&depth=1.
Oh MS. (2006). Evaluation of renal function, water, electrolytes and acid-base balance. In RA McPherson and MR Pincus (Eds.), McPerson & Pincus: Henry's Clinical diagnosis and Management by Laboratory Methods, 21st ed. Philadelphia: Saunders, Ch. 14.
Parving H-H, Mauer M, Ritz E. (2004). Diabetic nephropathy. In BM Brenner (Ed.), Brenner & Rector's The Kidney, 7th ed. Philadelphia: Saunders, Ch. 38.
Powers AC. (2005). Diabetes mellitus. In DL Kasper et al. (Eds.), Harrison's Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, Ch. 323.
Rasouli N, Molavi B, Elbein SC, Kern PA. (2007). Ectopic fat accumulation and metabolic syndrome. Diabetes, Obesity and Metabolism 9(1): 1–10.
Ropper AH, Brown RH. (2005). The acquired metabolic disorders of the nervous system. Adams and Victor's Principles of Neurology, 8th ed. New York: McGraw-Hill, Ch. 40.
Rosenblatt BJ, Benson WE. (2004). Diabetic retinopathy. In M Yanoff, et al. (Eds.), Ophthalmology, 2nd ed. Philadelphia: Mosby, Ch. 117.
Rush MD, Louie WWS. (2004). Emergency management of disorders of carbohydrate metabolism. In CK Stone and RL Humphries (Eds.), Current Emergency Diagnosis & Treatment, 5th ed. New York: McGraw-Hill.
Sierpina VS. (2003). Diabetes mellitus. In D Rakel (Ed.), Integrative Medicine, 1st ed. Philadelphia: Saunders, Ch. 27.
Silkensen JR, Kasiske BL. (2004). Laboratory assessment of kidney disease: Clearance, urinalysis, and kidney biopsy. In BM Brenner (Ed.), Brenner & Rector's The Kidney, 7th ed. Philadelphia: Saunders, Ch. 24.
Wassink AMJ, Olijhoek JK, Visseren FLJ. (2007). The metabolic syndrome: Metabolic changes with vascular consequences. European Journal of Clinical Investigation 37(1): 8–17.
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