Diabetes

Introduction

Of the 15 million Americans who have Type II diabetes, more than a third are unaware of it. Another 21 million Americans have a greater than 50/50 chance of developing the disease because they have impaired blood-sugar metabolism. This year alone more than 187,000 people will die of Type II diabetes, also called non-insulin-dependent diabetes mellitus (NIDDM), making it the sixth leading cause of death by disease. Each day, over 2,200 people are diagnosed with this chronic life debilitating, expansive, and pro-aging disease.

What is Diabetes?

Glucose is a simple sugar found in food. It is an essential nutrient that provides energy for the proper functioning of the body cells. After meals, food is digested in the stomach and the intestines into glucose and other nutrients. The glucose in digested food is absorbed by the intestinal cells into the bloodstream, and is carried by blood to all the cells in the body. However, glucose cannot enter the cells alone. It needs assistance from insulin in order to penetrate the cell walls. Insulin therefore acts as a regulator of glucose metabolism in the body.

Insulin is called the "hunger hormone". As the blood sugar level increases following a carbohydrate rich meal, the corresponding insulin level rises with the eventual lowering of the blood sugar level and glucose is transported from the blood into the cell for energy. When the blood glucose levels are lowered, the insulin release from the pancreas is turned off. When the blood sugar level drops below a certain level, hunger is felt. This often occurs a few hours after the meal. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. Cravings for sweets frequently form part of this cycle, which can lead to snacking, often for more carbohydrates. If the cravings are not fulfilled, sensations such as hunger, dizziness, moodiness, and a state of "collapse" can result.

This system of auto regulation and homeostasis is the function of the pancreas and it works around the clock. Dysfunction of this auto regulation system - either inability of the pancreas to secrete any or insufficient insulin, or pancreas overload from too much sugar ingested over a long period of time, or over compensatory mechanism, or a combination of these, results in the lack of insulin, and hence high blood sugar. This is the hallmark of diabetes mellitus (commonly called diabetes)

Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels, which result from defects in insulin secretion, or action, or both. Diabetes mellitus, commonly referred to as diabetes (as it will be in this article) was first identified as a disease associated with “sweet urine," and excessive muscle loss in the ancient world. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine, hence the term sweet urine. Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas to normalize the glucose level. In patients with diabetes, the absence or insufficient production of insulin causes hyperglycemia. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.

What is the impact of diabetes?

Over time, diabetes can lead to blindness, kidney failure, and nerve damage. These types of damage are the result of damage to small vessels, referred to as microvascular disease. Diabetes is also an important factor in accelerating the hardening and narrowing of the arteries (atherosclerosis), leading to strokes, coronary heart disease, and other large blood vessel diseases. This is referred to as macrovascular disease. Diabetes affects approximately 17 million people (about 8% of the population) in the United States. In addition, an estimated additional 12 million people in the United States have diabetes and don't even know it. From an economic perspective, the total annual cost of diabetes in 1997 was estimated to be 98 billion dollars in the United States. The per capita cost resulting from diabetes in 1997 amounted to $10,071.00; while healthcare costs for people without diabetes incurred a per capita cost of $2,699.00. During this same year, 13.9 million days of hospital stay were attributed to diabetes, while 30.3 million physician office visits were diabetes related. Remember, these numbers reflect only the population in the United States. Globally, the statistics are staggering.

Diabetes is the third leading cause of death in the United States after heart disease and cancer.

What causes diabetes?

Insufficient production of insulin (either absolutely or relative to the body's needs), production of defective insulin (which is uncommon), or the inability of cells to use insulin properly and efficiently leads to hyperglycemia and diabetes. This latter condition affects mostly the cells of muscle and fat tissues, and results in a condition known as "insulin resistance." This is the primary problem in type 2 diabetes. The absolute lack of insulin, usually secondary to a destructive process affecting the insulin producing beta cells in the pancreas, is the main disorder in type 1 diabetes. In type 2 diabetes, there also is a steady decline of beta cells that adds to the process of elevated blood sugars. For more, please read the Insulin Resistance article. Essentially, if someone is resistant to insulin, the body can, to some degree, increase production of insulin and overcome the level of resistance. After time, if production decreases and insulin cannot be released as vigorously, hyperglycemia develops.

Glucose is a simple sugar found in food. Glucose is an essential nutrient that provides energy for the proper functioning of the body cells. Carbohydrates are broken down in the small intestine and the glucose in digested food is then absorbed by the intestinal cells into the bloodstream, and is carried by the bloodstream to all the cells in the body where it is utilized. However, glucose cannot enter the cells alone and needs insulin to aid in its transport into the cells. Without insulin, the cells become starved of glucose energy despite the presence of abundant glucose in the bloodstream. In certain types of diabetes, the cells' inability to utilize glucose gives rise to the ironic situation of "starvation in the midst of plenty". The abundant, unutilized glucose is wastefully excreted in the urine.

Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia).

What are the different types of diabetes?

There are two major types of diabetes, called type 1 and type 2. Type 1 diabetes was also called insulin dependent diabetes mellitus (IDDM), or juvenile onset diabetes mellitus. In type 1 diabetes, the pancreas undergoes an autoimmune attack by the body itself, and is rendered incapable of making insulin. Abnormal antibodies have been found in the majority of patients with type 1 diabetes. Antibodies are proteins in the blood that are part of the body's immune system. The patient with type 1 diabetes must rely on insulin medication for survival.

In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood. Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. These antibodies can be measured in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.

At present, the American Diabetes Association does not recommend general screening of the population for type 1 diabetes, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age, however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Of all the patients with diabetes, only approximately 10% of the patients have type 1 diabetes and the remaining 90% have type 2 diabetes.

Type 2 diabetes was also referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells). In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.

While it is said that type 2 diabetes occurs mostly in individuals over 30 years old and the incidence increases with age, we are seeing an alarming number patients with type 2 diabetes who are barely in their teen years. In fact, for the first time in the history of humans, type 2 diabetes is now more common than type 1 diabetes in childhood. Most of these cases are a direct result of poor eating habits, higher body weight, and lack of exercise.

While there is a strong genetic component to developing this form of diabetes, there are other risk factors - the most significant of which is obesity. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes, and this holds true in children as well as adults. It is estimated that the chance to develop diabetes doubles for every 20% increase over desirable body weight.

Regarding age, data shows that for each decade after 40 years of age regardless of weight there is an increase in incidence of diabetes. The prevalence of diabetes in persons 65 to 74 years of age is nearly 20%. Type 2 diabetes is also more common in certain ethnic groups. Compared with a 6% prevalence in Caucasians, the prevalence in African Americans and Asian Americans is estimated to be 10%, in Hispanics 15%, and in certain Native American communities 20% to 50%. Finally, diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy (gestational diabetes - see below).

Diabetes can occur temporarily during pregnancy. Significant hormonal changes during pregnancy can lead to blood sugar elevation in genetically predisposed individuals. Blood sugar elevation during pregnancy is called gestational diabetes. Gestational diabetes usually resolves once the baby is born. However, 25-50% of women with gestational diabetes will eventually develop Type 2 diabetes later in life, especially in those who require insulin during pregnancy and those who remain overweight after their delivery. Patients with gestational diabetes are usually asked to undergo an oral glucose tolerance test about 6 weeks after giving birth to determine if their diabetes has persisted beyond the pregnancy, or if any evidence (such as impaired glucose tolerance) is present that may be a clue to the patient's future risk for developing diabetes.

"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas. Diabetes can also result from other hormonal disturbances, such as excessive growth hormone production (acromegaly) and Cushing's syndrome. In acromegaly, a pituitary gland tumor at the base of the brain causes excessive production of growth hormone, leading to hyperglycemia. In Cushing's syndrome, the adrenal glands produce an excess of cortisol, which promotes blood sugar elevation.

In addition, certain medications may worsen diabetes control, or "unmask" latent diabetes. This is seen most commonly when steroid medications (such as prednisone) are taken and also with medications used in the treatment of HIV infection (AIDS).

Two Types of Diabetes Mellitus

• Type I diabetes mellitus is also called insulin dependent diabetes mellitus (IDDM), or juvenile onset diabetes mellitus. It is an autoimmune disease in which the pancreas produces no insulin at all, and the patient relies on insulin medication for survival. Type I diabetes tends to occur in young, lean individuals, usually before 30 years of age. Approximately 10% of the patients with diabetes mellitus have IDDM. There is no cure for this type.
  
• Type II diabetes mellitus is also referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult onset diabetes mellitus (AODM). It is a metabolic disorder resulting from the body's inability to make enough, or properly use, insulin. 90% of all Diabetes Mellitus are of Type II. Type II diabetes mellitus occurs mostly in individuals over 40 years old. The incidence of type II diabetes increases with age. Unlike type I diabetes mellitus, 80% of type II diabetic patients are obese. Type II diabetes mellitus also has a strong genetic tendency.
  
  It is nearing epidemic proportions, due to an increased number of elderly people, a greater prevalence of obesity and a sedentary lifestyle. In type II diabetes, patients can still produce insulin, but do so inadequately. The pancreas in these patients not only produces an insufficient amount of insulin, but also releases insulin late in response to increased glucose levels. Some type II diabetics have body cells that are resistant to the action of insulin (Insulin Resistance). Finally, the liver in these patients continues to produce glucose despite elevated glucose levels.
  
  Type II diabetes once hardly ever struck before middle age, and the older you are the more at risk you are. Now it is striking younger people.

Symptoms of NIDDM

The early symptoms of untreated diabetes mellitus are related to elevated blood sugar levels, and excretion of it to the urine. High amounts of glucose in the urine can cause increased urine output and lead to dehydration. Dehydration causes increased thirst and water consumption. Some untreated diabetic patients also complain of fatigue, nausea, and vomiting. Patients with diabetes are prone to developing infections of the bladder, skin, and vaginal areas. Fluctuations in blood glucose levels can lead to blurred vision. Extremely elevated glucose levels can lead to lethargy and coma (diabetic coma).

The most unrecognized symptom of NIDDM is weight gain. High insulin levels prohibit the release of serotonin, a neurotransmitter in the brain that informs the body to slow down eating. Without serotonin, there is a tendency to overeat, which then leads to a spiral of excessive sugar intake. A viscous cycle of hyper-insulinemia resulting in insulin resistance is set up. This in turn creates a "carbohydrate addict" whose craving for a higher sugar intake continues to increase. The same dietary factors that cause NIDDM lead to obesity. Eating refined carbohydrates such as sugar, or carbohydrates that easily converts into sugar such as yam, potato, or rice, creates more glucose than the body can handle. Excess glucose then gets stored as fat. As diabetes sets in, so does lethargy and inactivity, contributing further to the vicious cycle of weight gain and worsening of diabetes.
What are diabetes symptoms?

The early symptoms of untreated diabetes are related to elevated blood sugar levels, and loss of glucose in the urine. High amounts of glucose in the urine can cause increased urine output and lead to dehydration. Dehydration causes increased thirst and water consumption. The inability of insulin to perform normally has effects on protein, fat and carbohydrate metabolism. Insulin is an anabolic hormone, that is, one that encourages storage of fat and protein. A relative or absolute insulin deficiency eventually leads to weight loss despite an increase in appetite. Some untreated diabetes patients also complain of fatigue, nausea and vomiting. Patients with diabetes are prone to developing infections of the bladder, skin, and vaginal areas. Fluctuations in blood glucose levels can lead to blurred vision. Extremely elevated glucose levels can lead to lethargy and coma.

How is diabetes diagnosed?

The fasting blood glucose (sugar) test is the preferred way to diagnose diabetes. It is easy to perform and convenient. After the person has fasted overnight (at least 8 hours), a single sample of blood is drawn and sent to the laboratory for analysis. This can also be done accurately in a doctor's office using a glucose meter.

Normal fasting plasma glucose levels are less than 100 milligrams per deciliter (mg/dl). Fasting plasma glucose levels of more than 126 mg/dl on two or more tests on different days indicate diabetes. A random blood glucose test can also be used to diagnose diabetes A blood glucose level of 200 mg/dl or higher indicates diabetes.

When fasting blood glucose stays above 100mg/dl, but in the range of 100-126mg/dl, this is known as impaired fasting glucose (IFG). While patients with IFG do not have the diagnosis of diabetes, this condition carries with it its own risks and concerns, and is addressed elsewhere.

The oral glucose tolerance test

Though not routinely used anymore, the oral glucose tolerance test (OGTT) is a gold standard for making the diagnosis of type 2 diabetes. It is still commonly used for diagnosing gestational diabetes. With an oral glucose tolerance test, the person fasts overnight (at least eight but not more than 16 hours). Then first, the fasting plasma glucose is tested. After this test, the person receives 75 grams of glucose (100 grams for pregnant women). There are several methods employed by obstetricians to do this test, but the one described here is standard. Usually, the glucose is in a sweet-tasting liquid that the person drinks. Blood samples are taken at specific intervals to measure the blood glucose.

For the test to give reliable results, the person must be in good health (not have any other illnesses, not even a cold). Also, the person should be normally active (not lying down, for example, as an inpatient in a hospital) and should not be taking medicines that could affect the blood glucose. For three days before the test, the person should have eaten a diet high in carbohydrates (150- 200 grams per day). The morning of the test, the person should not smoke or drink coffee.

The classic oral glucose tolerance test measures blood glucose levels five times over a period of three hours. Some physicians simply get a baseline blood sample followed by a sample two hours after drinking the glucose solution. In a person without diabetes, the glucose levels rise and then fall quickly. In someone with diabetes, glucose levels rise higher than normal and fail to come back down as fast.

People with glucose levels between normal and diabetic have impaired glucose tolerance (IGT). People with impaired glucose tolerance do not have diabetes, but are at high risk for progressing to diabetes. Each year, 1-5% of people whose test results show impaired glucose tolerance actually eventually develop diabetes. Weight loss and exercise may help people with impaired glucose tolerance return their glucose levels to normal. In addition, some physicians advocate the use of medications, such as metformin (Glucophage), to help prevent/delay the onset of overt diabetes. Recent studies have shown that impaired glucose tolerance itself may be a risk factor for the development of heart disease. In the medical community, most physicians are now understanding that impaired glucose tolerance is nor simply a precursor of diabetes, but is its own clinical disease entity that requires treatment and monitoring.

Evaluating the results of the oral glucose tolerance test

Glucose tolerance tests may lead to one of the following diagnoses:

• Normal response: A person is said to have a normal response when the 2-hour glucose level is less than 140 mg/dl, and all values between 0 and 2 hours are less than 200 mg/dl.
• Impaired glucose tolerance: A person is said to have impaired glucose tolerance when the fasting plasma glucose is less than 126 mg/dl and the 2-hour glucose level is between 140 and 199 mg/dl.
• Diabetes: A person has diabetes when two diagnostic tests done on different days show that the blood glucose level is high.
• Gestational diabetes: A woman has gestational diabetes when she has any two of the following: a 100g OGTT, a fasting plasma glucose of more than 95 mg/dl, a 1-hour glucose level of more than 180 mg/dl, a 2-hour glucose level of more than 155 mg/dl, or a 3-hour glucose level of more than 140 mg/dl.

Complications of Diabetes

Type 1 Diabetes:

Insulin is vital to patients with type I diabetes. Without insulin, patients with type I diabetes can develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the breakdown of fat cells, with the release of ketones into the blood. Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic acidosis can rapidly go into shock, coma, and even death. With proper treatment, the symptoms can be reversed rapidly, and patients can recover remarkably well.


Type 2 Diabetes:

Short term complications are normally due imbalance of sugar level in the body as a result of:

A. Severely high blood sugar levels due to a lack of insulin. Symptoms are similar to that of Type 1 Diabetes described above.

B. Abnormally low blood sugar levels due to too much insulin or other glucose-lowering medications. Low blood sugar can lead to nervous system symptoms such as dizziness, confusion, weakness, and tremors. Untreated, severely low blood sugar levels can lead to coma and irreversible brain death.

Long-term complications are related to blood vessel diseases. Diabetes causes diseases of the small vessels, which can damage the eyes, kidneys, nerves, and heart. Four major areas are involved:

A. EYE. Each year about 24,000 people lose their sight because of diabetes. Diabetes is the main cause of blindness in adult. Eye complications of diabetes (diabetic retinopathy) occur in patients who have had diabetes for at least 5 years. Disease in these blood vessels also causes the formation of small aneurysms (micro aneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision. Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% of diabetics have retinopathy after 15 years of the disease.

B. Kidney damage from diabetes is called diabetic nephropathy. Kidney disease usually occurs approximately 10 years after the onset of diabetes. Each year, about 28,000 people initiated treatment for end stage renal disease (kidney failure) because of diabetes. The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels.

C. Nerve damage in diabetes (diabetic neuropathy) is also caused by small blood vessel disease. Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Diabetic nerve damage can affect the nerves, which are important for penile erection, causing impotence. Diabetic neuropathy can also affect nerves to the intestines, causing nausea, weight loss, and diarrhea. About 60-70% of people with diabetes have mild to sever form of diabetic nerve damage. The risk of a leg amputation is 15-40 times greater for a person with diabetes. Each year, more than 56,000 amputations are performed among people with diabetes.

D. Heart Disease and Strokes. Patients with diabetes are 2-4 times more likely to have heart disease, which is present in 75 percent of diabetes-related death (more than 75,000 deaths due to heart disease annually). Diabetic patients are also 2 to 4 times more likely to suffer a stroke. Diabetes also accelerates the hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply.

Diabetic men were more than twice as likely to die of all causes compared with men without diabetes. As blood glucose increased, the risk of dying climbed higher regardless of age, weight, blood pressure, cholesterol and smoking status.

Researchers estimated that a reduction in blood glucose by just 0.1 per cent could reduce mortality rates by about five per cent in western countries.

Importance of Tight Blood Sugar Control

An aggressive and intensive control of elevated levels of blood sugar in patients with diabetes is absolutely essential. Studies have shown that in intensively treated patients, diabetic eye disease decreased by 76%, kidney disease decreased by 54%, and nerve disease decreased by 60%.

Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 180 mg/dl after meals; and a near normal hemoglobin A1C levels.

Not only will you feel better, stay healthy, and have more energy. You will also live longer.

Type II Diabetes - Curable?

Diabetes is a disease that has become prevalent only in the past 100 years. Before then, when everyone ate whole foods and sugar intake was moderate, diabetes was hardly a problem. It's a simple of matter of supply and demand. If the ingestion of grain products and refined sugars exceed the demand, the body is put into high gear to rid itself of the excess sugar. Diabetes is resulted when this process carries on for an extended period of time and ultimately fails. No other disease state can be cured as easily as NIIDM.

All you have to do is to reduce the supply of sugar to the body to a moderate level without sacrificing energy production. The secret lies not in avoiding carbohydrates as the most common source of sugar. The key is knowing what kind of carbohydrate to eat and which kind to avoid

Why is blood sugar checked at home?

Home blood sugar (glucose) testing is an important part of controlling blood sugar. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Blood glucose levels are usually tested before and after meals, and at bedtime. The blood sugar level is typically determined by pricking a fingertip with a lancing device and applying the blood to a glucose meter, which reads the value. There are many meters on the market, for example, Accu-Check Advantage, One Touch Ultra, Sure Step and Freestyle. Each meter has its own advantages and disadvantages (some use less blood, some have a larger digital readout, some take a shorter time to give you results, etc). The test results are then used to help patients make adjustments in medications, diets, and physical activities.

There are some interesting developments in blood glucose monitoring. Currently, at least three continuous glucose sensors are being considered for approval in the United States (Dexcom, Medtronic and Navigator). The new continuous glucose sensor systems involve an implantable cannula placed just under the skin in the abdomen or in the arm. This cannula allows for frequent sampling of blood glucose levels. Attached to this is a transmitter that sends the data to a pager-like device. This device has a visual screen that allows the wearer to see, not only the current glucose reading, but also the graphic trends. In some devices, the rate of change of blood sugar is also shown. There are alarms for low and high sugar levels. Certain models will alarm if the rate of change indicates the wearer is at risk for dropping or rising blood glucose too rapidly. The Medtronic version is specifically designed to interface with their insulin pumps. However, at this time the patient still must manually approve any insulin dose (the pump cannot blindly respond to the glucose information it receives, it can only give a calculated suggestion as to whether the wearer should give insulin, and if so, how much). All of these devices need to be correlated to fingersticks for a few hours before they can function independently. The devices can then provide readings for 3-5 days.

Diabetes experts feel that these blood glucose monitoring devices give patients a significant amount of independence to manage their disease process; and they are a great tool for education as well. It is also important to remember that these devices can be used intermittently with fingersticks. For example, a well-controlled patient with diabetes can rely on fingerstick glucose checks a few times a day and do well. If they become ill, if they decide to embark on a new exercise regimen, if they change their diet and so on, they can use the sensor to supplement their fingerstick regimen, providing more information on how they are responding to new lifestyle changes or stressors. This kind of system takes us one step closer to closing the loop, and to the development of an artifical pancreas that senses insulin requirements based on glucose levels and the body's needs and releases insulin accordingly - the ultimate goal.

Hemoglobin A1c (A1c)

To explain what an A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these cells, it gives us an idea of how much sugar is around for the preceding three months. In most labs, the normal range is 4-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%).>

While there are no guidelines to use A1c as a screening tool, it gives a physician a good idea that someone is diabetic if the value is elevated. Right now, it is used as a standard tool to determine blood sugar control in patients known to have diabetes.

A1c(%)	Mean blood sugar (mg/dl)
6	135
7	170
8	205
9	240
10	275
11	310
12	345

The American Diabetes Association currently recommends an A1c goal of less than 7.0%. Other Groups such as the American Association of Clinical Endocrinologists feel that an A1c of <>

Of interest, studies have shown that there is about a 10% decrease in relative risk for microvascular disease for every 1 % reduction in A1c. So, if a patient starts off with an A1c of 10.7 and drops to 8.2, though there are not yet at goal, they have managed to decrease their risk of microvascular complications by about 20%. The closer to normal the A1c, the lower the absolute risk for microvascular complications. Data also suggests that the risk of macrovascular disease decreases by about 24% for every 1% reduction in A1c values.

It should be mentioned here that there are a number of conditions in which an A1c value may not be accurate. For example, with significant anemia, the red blood cell count is low, and thus the A1c is falsely low as is similarly in cases of sickle cell disease and other hemoglobinopathies. For more, please read the Hemoglobin A1c article.

What are the acute complications of diabetes?

1. Severely elevated blood sugar levels due to an actual lack of insulin or a relative deficiency of insulin.

2. Abnormally low blood sugar levels due to too much insulin or other glucose-lowering medications.

Insulin is vital to patients with type 1 diabetes - they cannot live with out a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death.

Diabetic ketoacidosis can be caused by infections, stress, or trauma all which may increase insulin requirements. In addition, missing doses of insulin is also an obvious risk factor for developing diabetic ketoacidosis. Urgent treatment of diabetic ketoacidosis involves the intravenous administration of fluid, electrolytes, and insulin, usually in a hospital intensive care unit. Dehydration can be very severe, and it is not unusual to need to replace 6-7 liters of fluid when a person presents in diabetic ketoacidosis. Antibiotics are given for infections. With treatment, abnormal blood sugar levels, ketone production, acidosis, and dehydration can be reversed rapidly, and patients can recover remarkably well.

In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to exist, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in DKA.

Hypoglycemia means abnormally low blood sugar (glucose). In patients with diabetes, the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications, to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. When low blood sugar levels occur because of too much insulin, it is called an insulin reaction. Sometimes, low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion.

Blood glucose is essential for the proper functioning of brain cells. Therefore, low blood sugar can lead to central nervous system symptoms such as dizziness, confusion, weakness, and tremors. The actual level of blood sugar at which these symptoms occur varies with each person, but usually it occurs when blood sugars are less than 65 mg/dl. Untreated, severely low blood sugar levels can lead to coma, seizures, and, in the worse case scenario, irreversible brain death. At this point, the brain is suffering from a lack of sugar, and this usually occurs somewhere around levels of <40>

The treatment of low blood sugar consists of administering a quickly absorbed glucose source. These include glucose containing drinks, such as orange juice, soft drinks (not sugar-free), or glucose tablets in doses of 15-20 grams at a time (for example, the equivalent of half a glass of juice). Even cake frosting applied inside the cheeks can work in a pinch if patient cooperation is difficult. If the individual becomes unconscious, glucagon can be given by intramuscular injection.

Glucagon causes the release of glucose from the liver (i.e., it promotes gluconeogenesis). Glucagon can be lifesaving and every patient with diabetes who has a history of hypoglycemia (particularly those on insulin) should have a glucagon kit. Families and friends of those with diabetes need to be taught how to administer glucagon, since obviously the patients will not be able to do it themselves in an emergency situation. Another lifesaving device that should be mentioned is very simple; a medic alert bracelet should be worn by all patients with diabetes.

What are the chronic complications of diabetes?

These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication). For more information, please read the following articles: Stroke, Angina, and Heart Attack.

Eye Complications

The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision.

To treat diabetic retinopathy a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels. Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% of diabetics have retinopathy after 15 years of the disease. Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes. For more, please read the Diabetic Eye Disease article.

Cataracts and glaucoma are also more common among diabetics. It is also important to note that since the lens of the eye lets water through, if blood sugar concentrations vary a lot, the lens of the eye will shrink and swell with fluid accordingly. As a result, blurry vision is very common in poorly controlled diabetes. Patients are usually discouraged from getting a new eyeglass prescription until their blood sugar is controlled. This allows for a more accurate assessment of what kind of glasses prescription is required.

Kidney damage

Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered. For more about dialysis, please read the Kidney Dialysis article.

The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in diabetic patients.

Nerve damage

Nerve damage in diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.

Diabetic nerve damage can affect the nerves that are important for penile erection, causing erectile dysfunction (ED, impotence). Erectile dysfunction can also be caused by poor blood flow to the penis from diabetic blood vessel disease.

Diabetic neuropathy can also affect nerves to the stomach and intestines, causing nausea, weight loss, diarrhea, and other symptoms of gastroparesis (delayed emptying of food contents from the stomach into the intestines, due to ineffective contraction of the stomach muscles).

The pain of diabetic nerve damage may respond to traditional treatments with gabapentin (Neurontin), phenytoin (Dilantin), carbamazepine (Tegretol), desipramine (Norpraminine), amitriptyline (Elavil), or with topically-applied capsaicin (an extract of pepper). Neurontin, Dilantin and Tegretol are medications that are traditionally used in the treatment of seizure disorders. Elavil and Norpraminine are medications that are traditionally used for depression. While many of these medications are not FDA indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly. The pain of diabetic nerve damage may also improve with better blood sugar control, though unfortunately blood glucose control and the course of neuropathy do not always go hand in hand. Newer medications for nerve pain have recently come to market in the US. Pregabalin (Lyrica) which has an indication for diabetic neuropathic pain and duloxetine (Cymbalta) are newer agents used in the treatment of diabetic neuropathy. For more, please read the Diabetic Neuropathy article.

What can be done to slow diabetes complications?

Findings from the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) have clearly shown that aggressive and intensive control of elevated levels of blood sugar in patients with type 1 and type 2 diabetes decreases the complications of nephropathy, neuropathy, retinopathy, and may reduce the occurrence and severity of large blood vessel diseases. Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 160 mg/dl after meals; and a near normal hemoglobin A1C levels (see below).

Studies in type 1 patients have shown that in intensively treated patients, diabetic eye disease decreased by 76%, kidney disease decreased by 54%, and nerve disease decreased by 60%. More recently the EDIC trial has shown that type 1 diabetes is also associated with increased heart disease, similar to type 2 diabetes. However, the price for aggressive blood sugar control is a two to three fold increase in the incidence of abnormally low blood sugar levels (caused by the diabetes medications). For this reason, tight control of diabetes to achieve glucose levels between 70-120 mg/dl is not recommended for children under 13 years of age, patients with severe recurrent hypoglycemia, patients unaware of their hypoglycemia, and patients with far advanced diabetes complications. To achieve optimal glucose control without an undue risk of abnormally lowering blood sugar levels, patients with type 1 diabetes must monitor their blood glucose at least four times a day and administer insulin at least three times per day. In patients with type 2 diabetes, aggressive blood sugar control has similar beneficial effects on the eyes, kidneys, nerves and blood vessels.

How is diabetes treated?

Please see the Diabetes Treatment article.

Diabetes At A Glance

• Diabetes is a chronic condition associated with abnormally high levels of sugar (glucose) in the blood.
• Insulin produced by the pancreas lowers blood glucose.
• Absence or insufficient production of insulin causes diabetes.
• The two types of diabetes are referred to as type 1 (insulin dependent) and type 2 (non-insulin dependent).
• Symptoms of diabetes include increased urine output, thirst and hunger as well as fatigue.
• Diabetes is diagnosed by blood sugar (glucose) testing.
• The major complications of diabetes are both acute and chronic.
• Acutely: dangerously elevated blood sugar, abnormally low blood sugar due to diabetes medications may occur.
• Chronically: disease of the blood vessels (both small and large) which can damage the eye, kidneys, nerves, and heart may occur
• Diabetes treatment depends on the type and severity of the diabetes. Type 1 diabetes is treated with insulin, exercise, and a diabetic diet. Type 2 diabetes is first treated with weight reduction, a diabetic diet, and exercise. When these measures fail to control the elevated blood sugars, oral medications are used. If oral medications are still insufficient, insulin medications are considered.

1. Key Nutritional Supplements

A VARIETY OF NUTRIENTS AND HERBS can help offset the toll diabetes takes on your body. Supplements cannot, however, reverse the disease by themselves. Incorporating these minerals and vitamins can help to normalize blood sugar. If you already have diabetes or suspect you might have it, consult a health care practitioner before taking any supplements.


A. Chromium:.

Chromium is an essential trace mineral nutrient. Like iron, zinc, selenium, copper, and several other essential trace minerals, chromium plays a critical role in maintaining normal health and well-being.

Chromium helps insulin work efficiently. Many well controlled clinical studies through the years and the majority show blood glucose improvements in the patients tested.

Important studies include one from the Human Nutrition Research Center of the United States Department of Agriculture conducted in 1996. Researchers in the study randomized 180 adult-onset diabetics into 3 groups of 60 each: one group received placebo twice per day, the second received 100 mcg twice daily of chromium as chromium picolinate and the third received 500 mcg of chromium as chromium picolinate twice daily. Their blood work was examined at baseline, at 2 months and at 4 months. The patients were told to remain on their anti-diabetic medications and continue with their diets and activity levels as before. The results were impressive: blood glucose, insulin levels, cholesterol and Hemoglobin A1C all decreased, with the higher dose generally (but not always) more effective than the 200 mcg.


Dietary Intake of Chromium

Few foods are rich sources of chromium in the Western diet, the best being organic meats, mushrooms, wheat germ, broccoli and processed meats. Data from U. S. Government sources show that the great majority of Americans get less chromium in their daily diets than the amount recommended by nutrition experts. The RDA Committee recommends 50-200 mcg of chromium/day; the vast majority of Americans get less than 50 mcg/day. It is estimated that as many as 80% of all Americans are deficient in this mineral and may not know it.

Unfortunately, it is not possible to get enough chromium by food alone without excessive calories and obesity. To obtain 200 mcg by food alone, one has to take in over 8,000 calories a day. A large part of the problem has to do with processed food and the increase consumption of sugar. The modern American consumes an average of 120 pounds of sugar per year from all sources. These ingested sugars (such as table sugar and products made with it) bring insulin and chromium into the blood and cause chromium to be excreted in the urine after it's through working with the insulin on the increase in blood sugar.

Inadequate chromium intake from processed food, increased chromium losses due to increased sugar consumption, decreasing chromium tissue levels as we age are the main reasons why the majority of Americans and diabetics are deficient in chromium. Studies show an improvement in blood sugar in significant numbers of diabetics and pre-diabetics with modest chromium supplementation. It should, however, take place alongside the two other proven ways of normalizing sugar: low-fat, high complex-carbohydrate of low glycemic index type diets for weight loss/weight maintenance and regular exercise.

Assessment of Chromium Status

Deciding whether or not someone is chromium deficient cannot be done easily. Routine blood tests are generally not accurate. The only generally accepted method for the assessment of chromium status is to supplement an individual who has abnormalities of either blood sugar, cholesterol, triglycerides or all three with the trace element. If the laboratory values improve, then chromium insufficiency is presumed.


Safety of Chromium

Chromium comes in various forms. The dietary form is called chromium tri-valent. This is non-toxic and necessary for essential bodily functions. Chromium in its hexa-valent form is used in industries and that is highly toxic.

It is extremely difficult to poison laboratory animals with oral dietary tri-valent forms of chromium. For example, cats fed 1,000 mg of trivalent chromium per day showed no signs of toxicity. The equivalent daily dose for a 150 lb person would be approximately 35,000 mg per day or 3.5 million mcg per day. In terms of the number of 200 mcg tablets, this would be 175,000 tablets per day for a human.

"Trivalent chromium has such a low order of toxicity that deleterious effects from excessive intake of this form of chromium do not occur readily. Trivalent chromium becomes toxic only at extremely high amounts - chromium then acts as a gastric irritant rather than as a toxic element interfering with essential metabolism or biochemistry." Modern Nutrition In Health and Disease, Eighth Ed., 1994. Shils, Olson and Shike, eds.

The safety issue had been questioned by a study published in December 1995, which attempted to link chromosomal damage in the test tube to oral supplementation of chromium picolinate. Researchers in this study added unnaturally high amounts of chromium picolinate to cultured Chinese hamster ovarian cancer. Some of these cells showed chromosomal damage. This was not particularly surprising, since this concentration applied was 3,000 times the blood level of people who are ingesting chromium picolinate as supplements. It is interesting to note that another form of chromium, chromium polynicotinate, did not have this toxic effect.

It is important to note that very few essential minerals tested in this way would be found to be without toxicity. For example, merely doubling the blood concentration of the mineral calcium is fatal to humans.

A further study was conducted by Dr. Richard Anderson, the lead scientist for trace minerals at the U.S. Department of Agriculture's Human Nutrition Research Center, Beltsville, Md., His research team fed rats a stock diet . Added to the diet was 0, 5, 25, 50 or 100 micrograms (mcg) of chromium per gram of feed for a period of six months. The supplements were added to the feed in the form of chromium chloride or chromium picolinate. The highest supplemented level measured approximately 1500 mcg/day per kilogram of body weight. Translated to a human equivalent would mean that a 150 lb (70 kg) individual would have to consume 1.05 million micrograms, or more than 5,000 tablets containing 200 mcg of chromium each daily for six months to equal the rat intake. This study found no harmful effects in animals supplemented with two widely used forms of dietary chromium: chromium chloride and chromium picolinate.

Forms of Chromium

There are various forms of dietary chromium. These vary in bioavailability (absorption and retention) and biological activity (ability to potentate and harmonize insulin). Inorganic chromium such as chromium chloride is unfortunately poorly absorbed (0.5-2%) and has little effect on insulin because it must first be converted into a biologically active form, which the body has a limited ability to do.

The two most popular forms of organic chromium are niacin-bound chromium (also called chromium polynicotinate) and chromium picolinate. Although picolinate and polynicotinate sound alike, there are significant differences between the two compounds.

Chromium Polynicotinate is actually a family of niacin-bound chromium compounds. Niacin-bound chromium strongly potentiates insulin - chromium's most vital function - while chromium picolinate is less effective comparatively speaking.

Niacin-bound chromium such as chromium polynciotinate is also more bioavailable than chromium picolinate. An Animal study at the University of California found that chromium polynicotinate is better absorbed and retained up to 311% better than chromium picolinate and 672% better than chromium chloride. Such high bioavailability means that chromium polynicotinate can deliver more of the benefits that chromium has to offer.

B. VITAMIN C:

As a strong antioxidant, this vitamin enhances capillary strength, which improves blood flow. Dietary sources including leafy greens, broccoli, peppers, oranges, and grapefruit are the primary source of dietary vitamin C, followed by commercial supplements.

Vitamin C administration has beneficial effects on sugar and fat metabolism in NIIDM. In a randomized double-blind cross-over study, in which 56 diabetic patients participated, it has been established that a supplementation of high doses of ascorbic acid (2 grams a day) markedly improves the blood sugar regulation in patients with NIDDM. It was recorded that the vitamin C supplementation in the NIDDM group resulted in a statistically significant decrease of the fasting blood sugar of 10.1 to 9.1 mmol/liter. In this group the vitamin C supplement also succeeded in lowering the level of LDL cholesterol and of triglycerides in the blood. The greater the amount of vitamin C taken, the greater reduction in LDL cholesterol and plasma free radicals. The plasma free radicals are also lower compared to the placebo group. This was reported in the Journal of the American College of Nutrition (Aug. 1995).

Vitamin C also reduces the potential of complications arising from persistent high sugar environment in the body. Specifically, vitamin C prevents accumulation of sorbitol (a sugar equivalent) in cells and protect against most complications resulting from oxidation. A large population based study found that patients with high blood levels of Vitamin C had a lower HbA1C.

Furthermore, patients with diabetes have low levels of Vitamin C in their cells, which can result in impaired wound healing. High dose supplements have been shown to prevent sorbitol accumulation and glycosilation of proteins, both of which are important factors in the development of diabetic complications such as cataracts. 1 to 2 gram daily of Vitamin C is recommended for diabetic patients.

C. VITAMIN E:

Vitamin E reduces oxidative stress, thus improving membrane physical characteristics and related activities in glucose transport.

This antioxidant promotes healing of diabetes-related lesions, whose cause is undetermined. Researchers have extensively investigated the possible effects of vitamin E supplementation on the cardiac autonomic nervous system in patients with type 2 diabetes and cardiac autonomic neuropathy. It was reported in the American Journal of Clinical Nutrition that daily vitamin E supplementation (600 mg) for 4 months improved the ratio of cardiac sympathetic to parasympathetic tone in patients with NIIDM. This effect might be mediated by a decline in oxidative stress. In short, Vitamin E (800 to 1200 I.U.) improves insulin action and prevents a host of long-term complications of diabetes including neuropathy.

In another study, 21 NIIDM patients with microangiopathic complications were divided into 2 groups, in which 11 patients took 900 mg of vitamin E daily and the other group of 10 diabetic patients took a placebo daily for 6 months. The vitamin E was provided in tablets containing 100 mg of dl-alpha-tocopheryl acetate. The mean age of these subjects was 58 years. This study showed that these diabetic patients had impaired erythrocyte osmotic fragility, and that pharmacological doses of vitamin E increased the resistance of erythrocytes to osmotic hemolysis in patients with microangiopathy.

Vitamin E also appears to play a significant role in the prevention of diabetes. Studies have shown that a low vitamin-E concentration was associated with a 3.9 times greater risk of developing diabetes.

Diabetic Low Glycemic Index Diet:

Dietary control of diabetes comes down to 2 simple principles:

a. Eat less (fewer calories) to maintain ideal body weight.
b. Eat low glycemic index foods that do not turn into sugar quickly

The Glycemic Index (GI)

The glycemic index represents the magnitude of the increase in blood glucose that occurs after ingestion of the food. This index measures how much your blood sugar increases in the two or three hours after eating.

When you make use of the glycemic index to prepare healthy meals, it helps to keep your blood sugar levels under control. GI tends to be lower for foods that are present in relatively large particles, minimally processed, and are ingested along with fat and protein.

Below are the general guidelines to what is considered high or low Glycemic Index (GI) foods.

High GI Foods

The following foods are considered unacceptable:

· Foods containing sugar, honey, molasses, & corn syrup.
· Breads - all white breads, all white flour products, corn breads
· Grains - rice, rice products, millet, corn, corn products
· Cereals - all cereals except those on the Low GI List below
· Pasta - thick, large pasta shapes
· Fruits - bananas, watermelon, pineapple, raisins
· Vegetables - potatoes, corn, carrots, beets, turnips, parsnips
· Snacks - potato chips, corn chips, popcorn, rice cakes, pretzels
· Alcohol - beer, liqueurs, all liquor except red wine

Low GI Foods

Look at what you can have:

· Breads - whole rye, pumpernickel, whole wheat pita
· Grains - barley, bulgur, kasha
· Cereals - Special K, All Bran, Fiber One, regular oatmeal
· Pasta - whole-wheat pasta, bean threads
· All meats
· All dairy products (no sugars)
· Whole Fruits - all except the High GI fruits above
· Green leafy Vegetables - all except the High GI vegetables listed above
· Snacks - nuts, olives, cheese, pita chips, fried pork rinds
· Alcohol - red wine
· Misc. - olives, eggs, peanut butter (no sugar)


Anti-Aging Food Pyramid for Diabetes

This Diet consists of 50-55% complex carbohydrates of low glycemic type (whole fruits, above ground vegetables, whole grains), 20-25% protein (preferably from plant sources), 25-30% fat. The normal 5% sweets, candies and dessert should be avoided.

There are three major layers to the Anti-Aging Food Pyramid. They are divided into daily, 2-3 times a week, and weekly layers. Imagine a pyramid with three layers, each layer getting much narrower as it gets closer to the tip.

The daily broad base layers of the pyramid starts with 10 glasses of pure filtered water a day and complex carbohydrates supplying up to 55% of the calories These carbohydrates are those of low glycemic index type - barley, cereal, legumes, and above ground vegetables. A limited amount of nuts, which is a fatty food, is also included in this first base layer. Three servings of vegetables should be eaten daily. High glycemic index complex carbohydrates such as wheat, rice, and corn should be restricted. Moderate amounts are acceptable if they are mixed with fat and protein.

Eggs also form part of the base layers. It is a good protein source. One egg per day is acceptable (including those used in cooking and baking). Organic eggs are the best.

Olive oil and fats from fish; nuts are part of this daily layer. 25-30% of the calories in your comes from fats. The fats in the diet should come mainly from olive oil, which is high in monounsaturated fats and also a good source of antioxidant. Some come from the fish, poultry and meat consumed.

The second layer is a much smaller layer containing protein food from fish and poultry. You should eat from this group 2-3 times a week. Fish should be those that live in deep and cold water, such as salmon and tuna. Poultry should preferably come from free-range chickens.

The third layer, which is very small, contains foods that one should eat 1 time a week. These include sweets, red meat (lean). If blood sugar is severely impaired, sweets should be avoided altogether.


Diet Tips for Diabetes Mellitus

a. Reduce overall fat, especially trans- fat commonly found in fried food so the overall calories is immediately reduced, as a result, weight loss is inevitable. Use oils or foods that are high in Omega-3 fatty acid, such as olive oil, rapeseeds oil, flaxseed and flaxseed oil, for they lower insulin requirements.

b. Eliminate refined carbohydrates and sugar from your diet, as they increase the blood sugar immediately. Substitute complex carbohydrates that have lots of fiber. Beware that sweet snacking is a frequent behavior at times of stress. Fruit should be the major source of sweetness in your diet, as they are low in calories, high in fibers, and many other minerals and vitamins which are essential for keeping the body healthy.

c. Watch the glycemic Index (a rating system to measure food's effects on blood sugar levels) of the carbohydrates that you consume. The higher the glycemic index, the more pronounced the food will have on your blood sugar, and scientific studies have shown that leads to excessive food intake in obese subjects.

d. Celery, Bitter Melon, Onion, Garlic, Globe Artichoke, Jerusalem artichoke, Asparagus and Spinach are vegetables that alleviate Diabetes Mellitus.

f. Refrain from excessive protein in your diet. Try meat substitutes or non-animal protein foods such as legumes tofu. Eat more fish, chicken and very little red meats (12-16 oz. per month). Legumes are excellent insulin regulators.

g. Split your menu into 6 small meals per day, rather than the traditional 3 square meals. This way, you will maintain a balance in your blood sugar and the level of nutrients in your body throughout the day.

4 . Exercise

No diabetes program is complete without a well-balanced exercise program. While most people think of exercise as a way to reduce body weight (especially since 80% of diabetes are obese), exercise does much more, including reducing insulin resistance and impotence. Numerous studies have confirmed that exercise can cause a reduction in insulin resistance and thus diabetes. For example, a study was conducted on 5,159 men aged 40 to 59 years with no history of coronary heart disease, type 2 diabetes or stroke. During an average follow-up period of 16.8 years, there were 616 cases of major coronary heart disease cases and 196 incident cases of type 2 diabetes. Risk decreased progressively for type 2 diabetes, according to the Archives of Internal Medicine 2000 (160:2108-2116).

A well-balanced exercise must include three components:

a. Flexibility training
b. Cardiovascular training.
c. Strength training.

Ideally, about 2000 calories should be burned per week. Working out with 30 minutes of aerobics exercise at moderate intensity 5 times a week plus 15-20 minutes of strength training 3 times a week will accomplish this goal.


5. Prescription Medications

If the above protocol fails, drugs and insulin have to be used. Oral Medications commonly prescribed fall into one of 4 categories:

A. Medications that Increase the Insulin Output by the Pancreas, such as chlorpropamide and tolbutaminde, glyburide, glipizide, and glimepiride.

B. Medications that decrease the amount of glucose coming from the liver such as metformin (Glucophage). Metformin does not alter concentrations of insulin in the blood and, therefore, rarely causes low blood glucose levels.

C. Medications that increase the sensitivity of cells to insulin, such as Troglitazone (Rezulin) which was taken off the market in March 2000 due to liver toxicity, or rosiglitazone (Avandia) whose long-term safety profile is not known.


D. Medications that Decrease the Absorption of Carbohydrates from the Intestine such as Precose. Precose has significant gastrointestinal side effects. Abdominal pain, diarrhea, and gas are common and are seen in up to 75% of patients.

Angiotensin Converting Enzyme (ACE) Inhibitors

Pharmacy Author: Omudhome Ogbru, Pharm.D.
Medical Editor: Jay W. Marks, M.D.

What are ACE inhibitors, and how do they work?

Angiotensin II is a very potent chemical that causes the muscles surrounding blood vessels to contract and thereby narrows the blood vessels. The narrowing of the vessels increases the pressure within the vessels and can cause high blood pressure (hypertension). Angiotensin II is formed from angiotensin I in the blood by the enzyme, angiotensin converting enzyme (ACE). ACE inhibitors are medications that slow (inhibit) the activity of the enzyme, which decreases the production of angiotensin II. As a result, the blood vessels enlarge or dilate, and the blood pressure is reduced. This lower blood pressure makes it easier for the heart to pump blood and can improve the function of a failing heart. In addition, the progression of kidney disease due to high blood pressure or diabetes is slowed.

For what conditions are ACE inhibitors used?

ACE inhibitors are used for controlling blood pressure, treating heart failure and preventing kidney damage in people with hypertension or diabetes. They also benefit patients who have had heart attacks. In studies, individuals with hypertension, heart failure, or prior heart attacks who were treated with an ACE inhibitor lived longer than patients who did not take an ACE inhibitor. Because they prevent early death resulting from hypertension, heart failure or heart attacks, ACE inhibitors are one of the most important group of drugs. Some individuals with hypertension do not respond sufficiently to ACE inhibitors alone. In these cases, other drugs are used in combination with ACE inhibitors.

Are there any differences among the different types of ACE inhibitors?

ACE inhibitors are very similar. However, they differ in how they are eliminated from the body and their doses. Some ACE inhibitors need to be converted into an active form in the body before they work. In addition, some ACE inhibitors may work more on ACE that is found in tissues than on ACE that is present in the blood. The importance of this difference or whether one ACE inhibitor is better than another, has not been determined.

What are the side effects of ACE inhibitors?

ACE inhibitors are relatively well-tolerated by most individuals. Nevertheless, they are not free of side effects, and some patients should not use ACE inhibitors. ACE inhibitors usually are not prescribed for pregnant patients because they may cause birth defects. Individuals with severe kidney problems and people who have had a severe reaction to ACE inhibitors probably should avoid them. The most common side effects are cough, elevated blood potassium levels, low blood pressure, dizziness, headache, drowsiness, weakness, abnormal taste (metallic or salty taste), and rash. It may take up to a month for coughing to subside, and if one ACE inhibitor causes cough it is likely that the others will too. The most serious, but rare, side effects of ACE inhibitors are kidney failure, allergic reactions, a decrease in white blood cells, and swelling of tissues (angioedema).

With which drugs do ACE inhibitors interact?

ACE inhibitors have few interactions with other drugs. Since ACE inhibitors may increase blood levels of potassium, the use of potassium supplements, salt substitutes (which often contain potassium), or other drugs that increase the body's potassium may result in excessive blood potassium levels. ACE inhibitors also may increase the blood concentration of lithium (Eskalith) and lead to an increase in side effects from lithium. There have been reports that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDS) such as ibuprofen, indomethacin, and naproxen may reduce the effects of ACE inhibitors; however, there is no conclusive evidence that this interaction, if it exists, is important.

What ACE inhibitors are available?

The following is a list of the ACE inhibitors that are available in the United States:

captopril (Capoten), benazepril (Lotensin), enalapril (Vasotec), lisinopril (Prinivil, Zestril) fosinopril (Monopril), ramipril (Altace), perindopril (Aceon), quinapril (Accupril), moexipril (Univasc), and trandolapril (Mavik).

GENERIC NAME: lisinopril

BRAND NAME: Zestril, Prinivil

DRUG CLASS AND MECHANISM: Lisinopril is an angiotensin converting enzyme (ACE) inhibitor. Angiotensin is a chemical that is made by the body continuously. It narrows blood vessels and thereby maintains (elevates) blood pressure. When the enzyme is blocked by lisinopril, angiotensin cannot be converted into its active form. As a result, blood vessels dilate and blood pressure falls.

PRESCRIPTION: Yes

GENERIC AVAILABLE: Yes

PREPARATIONS: 2.5, 5, 10, 20, and 40 mg oral tablets.

STORAGE: Lisinopril should be stored in a dry place at 15–30°C (59–86 °F).

PRESCRIBED FOR: Lisinopril is used to treat elevated blood pressure, heart failure and to improve survival after a heart attack (myocardial infarction).

DOSING: Lisinopril should be taken at doses specifically directed by the physician. Lisinopril can be taken with or without food. Lisinopril should be taken at the same time each day to maintain consistent blood levels of lisinopril. Lisinopril should not be taken within two hours of taking an antacid since the antacid binds lisinopril and prevents its absorption. The dose of lisinopril is often lowered slowly when discontinuing.

The starting dose of lisinopril is 5 mg daily, and the effective dose range for treating heart failure is 5–40 mg daily. The dose can be increased by 10 mg every 2 weeks to achieve the maximum effect. The maximum dose is 40 mg daily.

The starting dose of lisinopril for treating high blood pressure is 10 mg daily. The usual dose range is 20–40 mg daily. A dose of 80 mg is not much more effective than 40 mg.

Treatment of heart attack (myocardial infarction) is started with 5 mg followed by 5 mg after 24 hours, 10 mg after 48 hours and then 10 mg daily. Treatment is continued for 6 weeks.

DRUG INTERACTIONS: In general, lisinopril should not be taken with potassium supplements or diuretics that conserve potassium [for example, hydrochlorothiazide/triamterene (Dyazide)], since blood potassium levels may rise to dangerous levels.

PREGNANCY: Lisinopril should not be taken during pregnancy because fetuses and neonates have died when lisinopril was administered during pregnancy.

NURSING MOTHERS: It is not known whether lisinopril is excreted in breast milk.

SIDE EFFECTS: First doses of lisinopril can cause dizziness due to a drop in blood pressure. Lisinopril can cause nausea, headaches, anxiety, insomnia, drowsiness, nasal congestion and sexual dysfunction. Lisinopril should be stopped if there are symptoms or signs of an allergic reaction including feelings of swelling of the face, lips, tongue or throat. Severe allergic reactions (anaphylaxis) and hives occasionally occur. Rarely, lisinopril may cause a drop in red blood cells, white blood cells, and platelets.

Lisinopril can impair the function of the kidneys, and every person taking this medication should have their kidney function checked.

GENERIC NAME: metformin

BRAND NAME: Glucophage, Glucophage XR, Glumetza, Fortamet, Riomet

DRUG CLASS AND MECHANISM: Metformin is an oral medication that lowers blood glucose (sugar) and is used for treating type 2 diabetes. Insulin is a hormone produced by the pancreas that controls glucose levels in blood by reducing the amount of glucose made by the liver and by increasing the removal of glucose from the blood by muscle and fat tissues. As a result, blood glucose levels fall. Diabetes caused by a decrease in production of insulin that causes increased production of glucose by the liver, and reduced uptake (and effects) of insulin on fat and muscle tissues. Metformin acts by increasing the sensitivity of liver, muscle, fat, and other tissues to the uptake and effects of insulin. These actions lower the level of sugar in the blood.

Unlike glucose–lowering drugs of the sulfonylurea class, for example glyburide (Micronase; DiaBeta) or glipizide (Glucotrol), metformin does not increase the concentration of insulin in the blood and, therefore, does not cause excessively low blood glucose levels (hypoglycemia) when used alone. In scientific studies, metformin reduced the complications of diabetes such as heart disease, blindness and kidney disease. Metformin was approved by the FDA in December 1994.

PRESCRIPTION: Yes

GENERIC AVAILABLE: Yes

PREPARATIONS: Tablets: 500, 850, and 1000 mg. Tablets (extended release): 500, 750, and 1000 mg. Solution: 500 mg/5 ml

STORAGE: Metformin should be stored at room temperature between 20–25°C (68–77°F).

PRESCRIBED FOR: Metformin is used for treating type 2 diabetes in adults and children. It may be used alone or in combination with other diabetic medications. Metformin also has been used to prevent the development of diabetes in people at risk for diabetes, treatment of polycystic ovaries, and weight gain due to medications used for treating psychoses.

DOSING: For treating type 2 diabetes in adults, metformin (immediate release) usually is begun at a dose of 500 mg twice a day or 850 mg once daily. The dose is gradually increased by 500 mg weekly or 850 mg every two weeks as tolerated and based on the response of the levels of glucose in the blood. The maximum daily dose is 2550 mg given in three divided doses. If extended tablets are used, the starting dose is 500 mg or 1000 mg daily with the evening meal. The dose can be increased by 500 mg weekly up to a maximum dose of 2000 mg (2500 mg of Fortamet) once daily or in two divided doses. Glumetza tablets are given once daily. Metformin should be taken with meals.

For pediatric patients 10–16 years of age, the starting dose is 500 mg twice a day. The dose can be increased by 500 mg weekly up to a maximum dose of 2000 mg. Glucophage XR has not been studied in children.

DRUG INTERACTIONS: Cimetidine (Tagamet), by decreasing the elimination of metformin from the body, can increase the amount of metformin in the blood by 40%. This may increase the frequency of side effects from metformin.

PREGNANCY: There are no adequate studies in pregnant women. Most experts agree that insulin is the best treatment for pregnant women with diabetes.

NURSING MOTHERS: Metformin is excreted into breast milk and can therefore be transferred to the nursing infant. Nursing mothers should not use metformin.

SIDE EFFECTS: The most common side effects with metformin are nausea, vomiting, gas, bloating, diarrhea and loss of appetite. These symptoms occur in one out of every three patients. These side effects may be severe enough to cause therapy to be discontinued in one out of every 20 patients. These side effects are related to the dose of the medication and may decrease if the dose is reduced.

A serious but rare side effect of metformin is lactic acidosis. Lactic acidosis occurs in one out of every 30,000 patients and is fatal in 50% of cases. The symptoms of lactic acidosis are weakness, trouble breathing, abnormal heartbeats, unusual muscle pain, stomach discomfort, light–headedness and feeling cold. Patients at risk for lactic acidosis include those with reduced function of the kidneys or liver, congestive heart failure, severe acute illnesses, and dehydration.

GENERIC NAME: insulin

BRAND NAME: various

DRUG CLASS AND MECHANISM: Insulin is a naturally-occurring hormone secreted by the pancreas. Insulin is required by the cells of the body in order for them to remove and use glucose from the blood. From glucose the cells produce the energy that they need to carry out their functions. Researchers first gave an active extract of the pancreas containing insulin to a young diabetic patient in 1922, and the FDA first approved insulin in 1939. Currently, insulin used for treatment is derived from beef and pork pancreas as well as recombinant (human) technology. The first recombinant human insulin was approved by the FDA in 1982.

Patients with diabetes mellitus have an inability to take up and use glucose from the blood, and, as a result, the glucose level in the blood rises. In type 1 diabetes, the pancreas cannot produce enough insulin. Therefore, insulin therapy is needed. In type 2 diabetes, patients produce insulin, but cells throughout the body do not respond normally to the insulin. Nevertheless, insulin also may be used in type 2 diabetes to overcome the resistance of the cells to insulin. By increasing the uptake of glucose by cells and reducing the concentration of glucose in the blood, insulin prevents or reduces the long-term complications of diabetes, including damage to the blood vessels, eyes, kidneys, and nerves. Insulin is administered by injection under the skin (subcutaneously). The subcutaneous tissue of the abdomen is preferred because absorption of the insulin is more consistent from this location than subcutaneous tissues in other locations.

Regular (rapid onset of action, short duration of action) and NPH (slower onset of action, longer duration of action) human insulin are the most commonly-used preparations. Regular insulin has an onset of action (begins to reduce blood sugar) within 30 minutes of injection, reaches a peak effect at 1-3 hours, and has effects that last 6-8 hours.

NPH insulin is an insulin with an intermediate duration of action. It has an onset of action starting about 2 hours following injection. It has a peak effect 4-12 hours after injection, and a duration of action of 18-26 hours.

Lente insulin also is an insulin with an intermediate duration of action. It has an onset of action 2-4 hours after injection, a peak activity 6-12 hours after injection, and a duration of action of 18 to 26 hours. Ultralente insulin is a long-acting insulin with an onset of action 4-8 hours after injection, a peak effect 10-30 hours after injection, and a duration of action of more than 36 hours.

An ultra rapid-acting insulin, insulin lispro is a chemically-modified, natural insulin. It was approved by the FDA in June, 1996. As compared to regular insulin, insulin lispro has a more rapid onset of action, an earlier peak effect, and a shorter duration of action. It reaches peak activity 0.5-2.5 hours after injection. Therefore, insulin lispro should be injected 15 minutes before a meal as compared to regular insulin which is injected 30-60 minutes before a meal.

Insulin aspart and insulin glargine are both human insulin that have had their chemical composition slightly altered. The chemical changes provide insulin aspart with a faster onset of action (20 minutes) and a shorter duration of action (3-5 hours) than regular human insulin. It reaches peak activity 1-3 hours after injection. Insulin glargine has a slower onset of action (70 minutes) and a longer duration of action (24 hours) than regular human insulin. Its activity does not peak.

GENERIC: no

PRESCRIPTION: yes

PREPARATIONS: Insulin comes in three different forms-vials, prefilled syringes, and cartridges. The cartridges are to be used in a pen-like device that simplifies injection. Human recombinant insulin, insulin lispro, insulin aspart, and insulin glargine are the commonly-used insulins. Beef and pork insulin are infrequently used. Regular human insulin (Novolin R, Humulin R) is available in vials, cartridges, and prefilled syringes.

NPH human insulin (Novolin N, Humulin N) is available in vials, cartridges and prefilled syringes. A mixture of 70% NPH human insulin and 30% regular human insulin (Novolin 70/30, Humulin 70/30) is available in vials, cartridges and pre-filled syringes.

A mixture of 50% NPH human insulin and 50% regular human insulin (Humulin 50/50) is available in vials.

Lente human insulin (Novolin L, Humulin L) is available in vials.

Ultralente human insulin (Humulin U) is available in vials.

Insulin lispro (Humalog) is available in vials and cartridges.

Insulin aspart (Novolog) is available in vials and cartridges.

Insulin glargine (Lantus) is available in vials and cartridges.

STORAGE: Unopened insulin should be stored in a refrigerator between 2 and 8°C (36 and 46°F); it should not be placed in a freezer. Insulin vials that are being used can be kept at room temperature for up to a month. All vials should be protected from light and excessive heat. Unused insulin should be thrown away after the expiration date. The vials should never be shaken.

PRESCRIBED FOR: Insulin is prescribed for the treatment of type 1 and type 2 diabetes mellitus.

DOSING: The abdomen is the preferred site for insulin injection, but the sites of injection must be rotated in order to prevent erosion of the fat beneath the skin, a condition called lipodystrophy.

DRUG INTERACTIONS: Several drugs augment the action of insulin and may lower blood glucose to a dangerous level (hypoglycemia). To prevent hypoglycemia when these drugs are used, the dose of insulin may need to be reduced. Such drugs include alcohol, MAO inhibitors like phenelzine (Nardil), beta-blockers like propranolol (Inderal), salicylates like aspirin (Bayer) or salsalate (Disalcid), and anabolic steroids like methyltestosterone (Android).

Diabetes: Blood Glucose Control

The chart below gives you an idea of what your blood glucose level should be. Your goal blood glucose range may be different from another person's and will change throughout the day. Your health care provider will tell you what range is good for you.

Recommended Blood Glucose Range for People With Diabetes*

Time of Test	Goal plasma glucose
Before meals	90-130 mg/dL (milligrams per deciliter)
Before bedtime snack (1-2 hours after a meal/postprandial)	less than 180mg/dL
Every three months HgA1c	less than 7%

*Source: American Diabetes Association, 2003

For women with gestational diabetes, experts recommend the following goals for diabetes management:

• A fasting glucose less than 105 mg/dL (plasma) or less than 95 mg/dL (whole blood)
• A 2 hour post meal less than 130mg/dL (plasma) or less than 120 md/dL (whole blood)

When to Call the Doctor

If your blood glucose is less than 70 mg/dL and you have more than one unexplained low blood glucose reaction in one week, call your health care provider.

If your blood glucose is more than 180 mg/dL for more than a week, or if you have two consecutive readings greater than 300 mg/dL, call your health care provider.

In most cases, your health care provider will suggest changes in your diabetes management.

Reviewed by Certified Diabetes Educators in the Department of Patient Education and Health Information and by physicians in the Department of Endocrinology at The Cleveland Clinic .
Edited by Brunilda Nazario , MD, WebMD, October 2004.