Quran foods helping your health and curing many diseases

Many of us, specially mid-life men and  women, are being prescribed cholesterol-lowering drugs. Some doctors are even recommending the drugs be added to the water supply and no its not a joke.  
However, using statins or other prescribed drugs increase the risk of diabetes according to a study published by the Archives of Internal Medicine.

Statins are prescribed to reduce cholesterol and coronary heart disease. The science behind statins, however, is suspect. According to Dr. Hyman, studies have only found statins effective to prevent second heart attacks but not first heart attacks.
Although they have been prescribed to lower cholesterol, there are also serious questions as to whether cholesterol is even related to coronary heart disease and heart attacks. In fact, in older patients, lower cholesterol levels are associated with higher rates of death from all causes.
In 99 out of 100 men, says Dr. Hyman, the drugs have no therapeutic effect. They do, however, have significant side effects. In 15% of patients, reported side effects include muscle damage, muscle cramps, muscle weakness, sexual dysfunction, and liver and nerve damage.

Quran foods are the Alternatives to Statins
Safe and natural alternatives to statins are abundant including dietary choices. Including Quran foods in your diet will help reduce cholesterol and risk of coronary heart disease:

1. Salmon. Fatty fish containing Omega-3 fatty acids can reduce blood pressure and the risk of developing blood clots. Other good sources are mackerel, halibut, lake trout, herring, Albacore tuna and sardines.
2. Pomegranates are best to cure many heart disease and even prevent heart attacks
3. E mail us with any Questions    Shaikh@Quranfood.com

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Diabetes Treatment & Care

Treatment & Care

Diabetes is a common disease, yet every individual needs unique care. We encourage people with diabetes and their families to learn as much as possible about the latest medical therapies and approaches, as well as healthy lifestyle choices. Good communication with a team of experts can help you feel in control and respond to changing needs.

Blood Glucose Testing

Blood glucose (blood sugar) is an essential measure of your health. If you're struggling to manage your blood glucose levels, we can help! With the latest tools and strategies, you can take steps today to monitor your condition, prevent serious complications and feel better while living with diabetes.

Medication

Insulin & Other Injectables

Insulin is a naturally occurring hormone secreted by the pancreas. Many people with diabetes are prescribed insulin, either because their bodies do not produce insulin (type 1 diabetes) or do not use insulin properly (type 2 diabetes).

There are more than 20 types of insulin sold in the United States. These insulins differ in how they are made, how they work in the body, and how much they cost. Your doctor will help you find the right type of insulin for your health needs and your lifestyle.

What About Insulin?

Although it is a common practice to try pills before insulin, you may start on insulin based on several factors, including the following:

How long you have had diabetes

How high your blood glucose level is

What other medicines you take

Your overall health

Combination Therapy

Because diabetes pills seem to help the body use insulin better, some people take them along with insulin shots. The idea behind this "combination" therapy is to try to help insulin work better

Insulin Basics

There are different types of insulin depending on how quickly they work, when they peak, and how long they last.

Insulin is available in different strengths; the most common is U-100.

All insulin available in the United States is manufactured in a laboratory, but animal insulin can still be imported for personal use.

Inside the pancreas, beta cells make the hormone insulin. With each meal, beta cells release insulin to help the body use or store the blood glucose it gets from food.

In people with type 1 diabetes, the pancreas no longer makes insulin. The beta cells have been destroyed and they need insulin shots to use glucose from meals.

People with type 2 diabetes make insulin, but their bodies don't respond well to it. Some people with type 2 diabetes need diabetes pills or insulin shots to help their bodies use glucose for energy.

Insulin cannot be taken as a pill because it would be broken down during digestion just like the protein in food. It must be injected into the fat under your skin for it to get into your blood. In some rare cases insulin can lead to an allergic reaction at the injection site. Talk to your doctor if you believe you may be experiencing a reaction.

Types of Insulin

Rapid-acting insulin, begins to work about 15 minutes after injection, peaks in about 1 hour, and continues to work for 2 to 4 hours. Types: Insulin glulisine (Apidra), insulin lispro (Humalog), and insulin aspart (NovoLog)

Regular or Short-acting insulin usually reaches the bloodstream within 30 minutes after injection, peaks anywhere from 2 to 3 hours after injection, and is effective for approximately 3 to 6 hours. Types: Humulin R, Novolin R

Intermediate-acting insulin generally reaches the bloodstream about 2 to 4 hours after injection, peaks 4 to 12 hours later, and is effective for about 12 to 18 hours. Types: NPH (Humulin N, Novolin N)

Long-acting insulin reaches the bloodstream several hours after injection and tends to lower glucose levels fairly evenly over a 24-hour period. Types: Insulin detemir (Levemir) and insulin glargine (Lantus)

Premixed insulin can be helpful for people who have trouble drawing up insulin out of two bottles and reading the correct directions and dosages. It is also useful for those who have poor eyesight or dexterity and is convenient for people whose diabetes has been stabilized on this combination.

Characteristics of Insulin

Insulin has 3 characteristics:

Onset is the length of time before insulin reaches the bloodstream and begins lowering blood glucose.

Peaktime is the time during which insulin is at maximum strength in terms of lowering blood glucose.

Duration is how long insulin continues to lower blood glucose.

Insulin Strength

All insulins come dissolved or suspended in liquids. The standard and most commonly used strength in the United States today is U-100, which means it has 100 units of insulin per milliliter of fluid, though U-500 insulin is available for patients who are extremely insulin resistant.

U-40, which has 40 units of insulin per milliliter of fluid, has generally been phased out around the world, but it is possible that it could still be found in some places (and U-40 insulin is still used in veterinary care).

Insulin Routines

Insulin is required for people with type 1 diabetes and sometimes necessary for people with type 2 diabetes.

Syringe is the most common form of insulin delivery, but there are other options, including insulin pens and pumps.

Insulin should be injected in the same general area of the body for consistency, but not the exact same place.

Insulin delivery should be timed with meals to effectively process the glucose entering your system.

Insulin Therapy

With the help of your health care team, you can find an insulin routine that will keep your blood glucose near normal, help you feel good, and fit your lifestyle.

Type 1

People diagnosed with type 1 diabetes usually start with two injections of insulin per day of two different types of insulin and generally progress to three or four injections per day of insulin of different types. The types of insulin used depend on their blood glucose levels. Studies have shown that three or four injections of insulin a day give the best blood glucose control and can prevent or delay the eye, kidney, and nerve damage caused by diabetes.

Type 2

Most people with type 2 diabetes may need one injection per day without any diabetes pills. Some may need a single injection of insulin in the evening (at supper or bedtime) along with diabetes pills. Sometimes diabetes pills stop working, and people with type 2 diabetes will start with two injections per day of two different types of insulin. They may progress to three or four injections of insulin per day.

Fine-Tuning Your Blood Glucose

Many factors affect your blood glucose levels, including the following:

What you eat

How much and when you exercise

Where you inject your insulin

When you take your insulin injections

Illness

Stress

Self Monitoring

Checking your blood glucose and looking over results can help you understand how exercise, an exciting event, or different foods affect your blood glucose level. You can use it to predict and avoid low or high blood glucose levels. You can also use this information to make decisions about your insulin dose, food, and activity.

Insulin Delivery

Many people who take insulin use a syringe, but there are other options as well.

Insulin Pens

Some insulin pens contain a cartridge of insulin that is inserted into the pen and some are pre-filled with insulin and discarded after all the insulin has been used. The insulin dose is dialed on the pen, and the insulin is injected through a needle, much like using a syringe. Cartridges and pre-filled insulin pens only contain one type of insulin. Two injections must be given with an insulin pen if using two types of insulin.

Pump Therapy

Insulin pumps help you manage diabetes by delivering insulin 24 hours a day through a catheter placed under the skin.

Site Rotation

The place on your body where you inject insulin affects your blood glucose level. Insulin enters the blood at different speeds when injected at different sites. Insulin shots work fastest when given in the abdomen. Insulin arrives in the blood a little more slowly from the upper arms and even more slowly from the thighs and buttocks. Injecting insulin in the same general area (for example, your abdomen) will give you the best results from your insulin. This is because the insulin will reach the blood with about the same speed with each insulin shot.

Don't inject the insulin in exactly the same place each time, but move around the same area. Each mealtime injection of insulin should be given in the same general area for best results. For example, giving your before-breakfast insulin injection in the abdomen and your before-supper insulin injection in the leg each day give more similar blood glucose results. If you inject insulin near the same place each time, hard lumps or extra fatty deposits may develop. Both of these problems are unsightly and make the insulin action less reliable. Ask your health care provider if you aren't sure where to inject your insulin.

Timing

Insulin shots are most effective when you take them so that insulin goes to work when glucose from your food starts to enter your blood. For example, regular insulin works best if you take it 30 minutes before you eat.

Too much insulin or not enough?

High morning blood glucose levels before breakfast can be a puzzle. If you haven't eaten, why did your blood glucose level go up? There are two common reasons for high before-breakfast blood glucose levels. One relates to hormones that are released in the early part of sleep (called the Dawn Phenomenon). The other is from taking too little insulin in the evening. To see which one is the cause, set your alarm to self-monitor around 2 or 3 a.m. for several nights and discuss the results with your health care provider.

Explore: Insulin & Other Injectables

Insulin Storage and Syringe Safety

Follow these tips for storing insulin, using syringes, and keeping the supplies you need to your manage diabetes.

Insulin Pumps

Is an insulin pump right for you? Consider the pros and cons.

Advantages of Using an Insulin Pump

Disadvantages of Using an Insulin Pump

Although there are many good reasons to use an insulin pump, there are some disadvantages.

How Do Insulin Pumps Work?

Insulin pumps deliver rapid- or short-acting insulin 24 hours a day through a catheter placed under the skin.

Getting Started with an Insulin Pump

You don't need to be an expert on insulin pumps overnight. If you are uncertain about anything, you can go to your diabetes care team for help.

Other Injectable Medications

Oral Medication

The first treatment for type 2 diabetes blood glucose (sugar) control is often meal planning, weight loss, and exercising.

Sometimes these measures are not enough to bring blood glucose levels down near the normal range. The next step is taking a medicine that lowers blood glucose levels

Can Diabetes Pills Help Me?

Only people with type 2 diabetes can use pills to manage their diabetes, people with type 1 diabetes must use insulin.

These pills work best when used with meal planning and exercise. This way you have three therapies working together to lower your blood glucose levels.

Diabetes pills don't work for everyone. Although most people find that their blood glucose levels go down when they begin taking pills, their blood glucose levels may not go near the normal range.

Will They Help?

What are the chances that diabetes pills will work for you? Your chances are low if you have had diabetes for more than 10 years or already take more than 20 units of insulin each day. On the other hand, your chances are good if you developed diabetes recently or have needed little or no insulin to keep your blood glucose levels near normal.

Diabetes pills sometimes stop working after a few months or years. The cause is often unknown. This doesn't mean your diabetes is worse. When this happens, oral combination therapy can help.

Even if diabetes pills do bring your blood glucose levels near the normal range, you may still need to take insulin if you have a severe infection or need surgery. Pills may not be able to control blood glucose levels during these stressful times when blood glucose levels shoot up.

Also, if you plan to become pregnant, you will need to control your diabetes with diet and exercise or with insulin. It is not safe for pregnant women to take oral diabetes medications.

There is no "best" pill or treatment for type 2 diabetes. You may need to try more than one type of pill, combination of pills, or pills plus insulin.

My Medicine Tracker

My Medicine Tracker is a free medication monitoring service for patients brought to you by the American Diabetes Association.

It allows you to:

Track and print a list of all your medications, both prescription and over the counter

View safety information regarding side effects and when combining medications may not be advisable

Receive email alerts and updates on important safety information about medications

What Are My Options?

There are different types, or classes, of drugs that work in different ways to lower blood glucose (blood sugar) levels:

Sulfonylureas

Biguanides

Meglitinides

Thiazolidinediones

DPP-4 inhibitors

SGLT2 Inhibitors

Alpha-glucosidase inhibitors

Bile Acid Sequestrants

Sulfonylureas

Sulfonylureas stimulate the beta cells of the pancreas to release more insulin. Sulfonylurea drugs have been in use since the 1950s. Chlorpropamide (Diabinese) is the only first-generation sulfonylurea still in use today. The second generation sulfonylureas are used in smaller doses than the first-generation drugs. There are three second-generation drugs: glipizide (Glucotrol and Glucotrol XL), glyburide (Micronase, Glynase, and Diabeta), and glimepiride (Amaryl). These drugs are generally taken one to two times a day, before meals. All sulfonylurea drugs have similar effects on blood glucose levels, but they differ in side effects, how often they are taken, and interactions with other drugs.

Biguanides

Metformin (Glucophage) is a biguanide. Biguanides lower blood glucose levels primarily by decreasing the amount of glucose produced by the liver. Metformin also helps to lower blood glucose levels by making muscle tissue more sensitive to insulin so glucose can be absorbed. It is usually taken two times a day. A side effect of metformin may be diarrhea, but this is improved when the drug is taken with food.

Meglitinides

Meglitinides are drugs that also stimulate the beta cells to release insulin. Repaglinide (Prandin) and nateglinide (Starlix) are meglitinides. They are taken before each of three meals.

Because sulfonylureas and meglitinides stimulate the release of insulin, it is possible to have hypoglycemia (low blood glucose levels).

You should know that alcohol and some diabetes pills may not mix. Occasionally, chlorpropamide and other sulfonylureas, can interact with alcohol to cause vomiting, flushing or sickness. Ask your doctor if you are concerned about any of these side effects.

Thiazolidinediones

Rosiglitazone (Avandia) and pioglitazone (ACTOS) are in a group of drugs called thiazolidinediones. These drugs help insulin work better in the muscle and fat and also reduce glucose production in the liver. The first drug in this group, troglitazone (Rezulin), was removed from the market because it caused serious liver problems in a small number of people. So far rosiglitazone and pioglitazone have not shown the same problems, but users are still monitored closely for liver problems as a precaution. Both drugs appear to increase the risk for heart failure in some individuals, and there is debate about whether rosiglitazone may contribute to an increased risk for heart attacks. Both drugs are effective at reducing A1C and generally have few side effects.

DPP-4 Inhibitors

A new class of medications called DPP-4 inhibitors help improve A1C without causing hypoglycemia. They work by by preventing the breakdown of a naturally occurring compound in the body, GLP-1. GLP-1 reduces blood glucose levels in the body, but is broken down very quickly so it does not work well when injected as a drug itself. By interfering in the process that breaks down GLP-1, DPP-4 inhibitors allow it to remain active in the body longer, lowering blood glucose levels only when they are elevated. DPP-4 inhibitors do not tend to cause weight gain and tend to have a neutral or positive effect on cholesterol levels. Sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina) are the DPP-4 inhibitors currently on the market in the US.

SGLT2 Inhibitors

Glucose in the bloodstream passes through the kidneys, where it can either be excreted or reabsorbed.   Sodium-glucose transporter 2 (SGLT2) works in the kidney to reabsorb glucose, and a new class of medication, SGLT2 inhibitors, block this action, causing excess glucose to be eliminated in the urine. Canagliflozin (Invokana) and dapagliflozin (Farxiga) are SGLT2 inhibitors that have recently been approved by the FDA to treat type 2 diabetes.  Because they increase glucose levels in the urine, side effects can include urinary tract and yeast infections.

Alpha-glucosidase inhibitors

Acarbose (Precose) and miglitol (Glyset) are alpha-glucosidase inhibitors. These drugs help the body to lower blood glucose levels by blocking the breakdown of starches, such as bread, potatoes, and pasta in the intestine. They also slow the breakdown of some sugars, such as table sugar. Their action slows the rise in blood glucose levels after a meal. They should be taken with the first bite of a meal. These drugs may have side effects, including gas and diarrhea.

Bile Acid Sequestrants

The bile acid sequestrant (BAS) colesevelam (Welchol) is a cholesterol-lowering medication that also reduces blood glucose levels in patients with diabetes.  BASs help remove cholesterol from the body, particularly LDL cholesterol, which is often elevated in people with diabetes.  The medications reduce LDL cholesterol by binding with bile acids in the digestive system; the body in turn uses cholesterol to replace the bile acids, which lowers cholesterol levels. The mechanism by which colesevelam lowers glucose levels is not well understood. Because BASs are not absorbed into the bloodstream, they are usually safe for use by patients who may not be able to use other medications because of liver problems. Because of the way they work, side effects of BASs can include flatulence and constipation.

Oral combination therapy

Because the drugs listed above act in different ways to lower blood glucose levels, they may be used together. For example, a biguanide and a sulfonylurea may be used together. Many combinations can be used. Though taking more than one drug can be more costly and can increase the risk of side effects, combining oral medications can improve blood glucose control when taking only a single pill does not have the desired effects. Switching from one single pill to another is not as effective as adding another type of diabetes medicine.

My Medicine Tracker

My Medicine Tracker is a free medication monitoring service for patients brought to you by the American Diabetes Association.

It allows you to:

Track and print a list of all your medications, both prescription and over the counter

View safety information regarding side effects and when combining medications may not be advisable

Receive email alerts and updates on important safety information about medications

Interact with others to share experiences with medications

Is There a Danger of Interactions?

In general, diabetes pills are safe and work well. But like any other drug, they must be used with care.

All diabetes pills can interact with other medicines. Because of the chance of medication interactions, you need to tell your doctor about all medicines you are taking. While you're taking diabetes pills, you should check with your doctor before starting anything new — even over-the-counter items.

Any sulfonylurea or meglitinide can cause blood glucose levels to drop too low (hypoglycemia).

Metformin or the glitazones rarely cause hypoglycemia unless taken with insulin stimulators (sulfonylureas or repaglinide) or insulin injections.

Acarbose or miglitol, taken as prescribed, does not cause hypoglycemia. However, hypoglycemia can occur when acarbose or meglitol is taken in combination with other diabetes medications.

My Medicine Tracker

My Medicine Tracker is a free medication monitoring service for patients brought to you by the American Diabetes Association.

It allows you to:

Track and print a list of all your medications, both prescription and over the counter

View safety information regarding side effects and when combining medications may not be advisable

Receive email alerts and updates on important safety information about medications

Interact with others to share experiences with medications

Other Treatments

Aspirin, flu shots, dietary supplments, and more are covered in this section on treatments that people living with diabetes may find beneficial.

Mobile Prescription Therapy

Smartphones and tablet computers are a new way to deliver diabetes therapy. The Food and Drug Administration (FDA) calls this new type of therapy “mobile prescription therapy.”

Mobile prescription therapy (MPT) products tell you what to do to take care of your diabetes. The advice shows up on your smartphone or other device.

Herbs, Supplements and Alternative Medicines

Herbal Supplements

It is best to get vitamins and minerals from the foods you eat. In fact, research has not been able to prove that dietary or herbal supplements (including omega-3 supplements, cinnamon, and other herbs) help to manage diabetes. 

Still, more and more people use dietary supplements. And studies show that people with diabetes are more likely to use supplements than people without diabetes.

The National Health Interview Survey found that 22 percent of people with diabetes used some type of herbal therapy, while another study found that 31 percent used dietary supplements.

Certain ethnic groups, such as Hispanics, Native Americans, Asians, and African Americans are also more likely to use dietary supplements.

Using Supplements Safely

If you’re one of the many people taking dietary supplements, you’re probably concerned about doing the right thing for your body.

However, finding reliable information about the benefits and safety of these products is difficult. There are hundreds of dietary supplements—each purporting their own health benefits.

Unfortunately, the US does not have a system for testing the effectiveness of supplements.

Oral Health and Hygiene

There are more bacteria in your mouth right now than there are people on Earth. If those germs settle into your gums, you've got gum disease. Unfortunately, if you have diabetes, you are at higher risk for gum problems. Poor blood glucose control makes gum problems more likel

Diabetes and Oral Health Problems

The more severe form of gum disease is called periodontitis. When you reach this stage, your gums begin to pull away from your teeth. Pockets form between your teeth and gums. These fill with germs and pus, and deepen. When this happens, you may need gum surgery to save your teeth. If nothing is done, the infection goes on to destroy the bone around your teeth. The teeth may start to move or get loose. Your teeth may fall out or need to be pulled.

Is There an Association Between Gum Disease and Diabetes?

For the nearly 30 million Americans who have diabetes, many may be surprised to learn about an unexpected complication associated with this condition. Research shows that there is an increased prevalence of gum disease among those with diabetes, adding serious gum disease to the list of other complications associated with diabetes, such as heart disease, stroke and kidney disease.

Is There a Two-Way Street?

Emerging research also suggests that the relationship between serious gum disease and diabetes is two-way. Not only are people with diabetes more susceptible to serious gum disease, but serious gum disease may have the potential to affect blood glucose control and contribute to the progression of diabetes. Research suggests that people with diabetes are at higher risk for oral health problems, such as gingivitis (an early stage of gum disease) and periodontitis (serious gum disease). People with diabetes are at an increased risk for serious gum disease because they are generally more susceptible to bacterial infection, and have a decreased ability to fight bacteria that invade the gums.

The Surgeon General's Report on Oral Health states that good oral health is integral to general health. So be sure to brush and floss properly and see your dentist for regular checkups.

If I Have Diabetes, am I at Risk for Dental Problems?

If your blood glucose levels are poorly controlled, you are more likely to develop serious gum disease and lose more teeth than non-diabetics. Like all infections, serious gum disease may be a factor in causing blood sugar to rise and may make diabetes harder to control.

Other oral problems associated to diabetes include: thrush, an infection caused by fungus that grows in the mouth, and dry mouth which can cause soreness, ulcers, infections and cavities.

How Can I Help Prevent Dental Problems Associated with Diabetes?

First and foremost, control your blood glucose level. Then, take good care of your teeth and gums, along with regular checkups every six months. To control thrush, a fungal infection, maintain good diabetic control, avoid smoking and, if you wear them, remove and clean dentures daily. Good blood glucose control can also help prevent or relieve dry mouth caused by diabetes.

What Can I Expect at My Checkup? Should I Tell My Dental Professional About My Diabetes?

People with diabetes have special needs and your dentist and hygienist are equipped to meet those needs—with your help. Keep your dentist and hygienist informed of any changes in your condition and any medication you might be taking. Postpone any non-emergency dental procedures if your blood sugar is not in good control.

Gum Disease and Plaque

When you have gum disease, germs work to destroy your gums (gingiva) and the bone around your teeth. It starts with plaque. Plaque is a sticky film of food, saliva, and germs. Plaque loves to settle at the gum line. There, germs get busy making your gums red, tender, and likely to bleed.

The goal of your daily tooth brushing and flossing is to clean away plaque. When plaque stays put, it hardens into tartar. Tartar builds up under the gum line. More plaque forms over the tartar. Only your dentist or dental hygienist can get tartar off your teeth.

If plaque and tartar are not cleaned away, even gentle brushing can cause your gums to bleed. This is called gingivitis. It is the first stage of gum disease. You can fight gingivitis with:

daily good brushing and flossing habits, and

getting your teeth cleaned at least twice a year at your dentist's office.

If you ignore gingivitis, the gum disease gets worse.

The more severe form of gum disease is called periodontitis. When you reach this stage, your gums begin to pull away from your teeth. Pockets form between your teeth and gums. These fill with germs and pus, and deepen. When this happens, you may need gum surgery to save your teeth. If nothing is done, the infection goes on to destroy the bone around your teeth. The teeth may start to move or get loose. Your teeth may fall out or need to be pulled.

Warning Signs

As if this is not enough, diabetes can make things worse. Plaque is the main bad guy of gum disease. But diabetes can also be a culprit. Diabetes may weaken your mouth's germ-fighting powers. High blood sugar levels can help the gum disease get worse. At the same time, gum disease can make diabetes harder to control.

Often gum disease is painless. You may not even know you have it until you have some serious damage. Regular dentist visits are your best weapon.

While gum disease may not hurt, there are warning signs to watch for.

Bleeding gums when you brush or floss. This bleeding is not normal. Even if your gums don't hurt, get them checked.

Red, swollen, or tender gums.

Gums that have pulled away from teeth. Part of the tooth's root may show, or your teeth may look longer.

Pus between the teeth and gums (when you press on the gums).

Bad breath.

Permanent teeth that are loose or moving away from each other.

Changes in the way your teeth fit when you bite.

Changes in the fit of partial dentures or bridges

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Diabetes.Its Definition

Definition

Diabetes mellitus refers to a group of diseases that affect how your body uses blood sugar (glucose). Glucose is vital to your health because it's an important source of energy for the cells that make up your muscles and tissues. It's also your brain's main source of fuel.

If you have diabetes, no matter what type, it means you have too much glucose in your blood, although the causes may differ. Too much glucose can lead to serious health problems.

Chronic diabetes conditions include type 1 diabetes and type 2 diabetes. Potentially reversible diabetes conditions include prediabetes — when your blood sugar levels are higher than normal, but not high enough to be classified as diabetes — and gestational diabetes, which occurs during pregnancy but may resolve after the baby is delivered.

What is Diabetes?

Too Much Glucose in the Blood

Diabetes means your blood glucose (often called blood sugar) is too high. Your blood always has some glucose in it because your body needs glucose for energy to keep you going. But too much glucose in the blood isn't good for your health.

Anatomical illustration of the pancreas' location in the abdomen.

Glucose comes from the food you eat and is also made in your liver and muscles. Your blood carries the glucose to all of the cells in your body. Insulin is a chemical (a hormone) made by the pancreas. The pancreas releases insulin into the blood. Insulin helps the glucose from food get into your cells.

If your body does not make enough insulin or if the insulin doesn't work the way it should, glucose can't get into your cells. It stays in your blood instead. Your blood glucose level then gets too high, causing pre-diabetes or diabetes.

DEFINITION AND DESCRIPTION OF DIABETES MELLITUS

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.

Several pathogenic processes are involved in the development of diabetes. These range from autoimmune destruction of the ß-cells of the pancreas with consequent insulin deficiency to abnormalities that result in resistance to insulin action. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of hormone action. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycemia.

Symptoms of marked hyperglycemia include polyuria, polydipsia, weight loss, sometimes with polyphagia, and blurred vision. Impairment of growth and susceptibility to certain infections may also accompany chronic hyperglycemia. Acute, life-threatening consequences of uncontrolled diabetes are hyperglycemia with ketoacidosis or the nonketotic hyperosmolar syndrome.

Long-term complications of diabetes include retinopathy with potential loss of vision; nephropathy leading to renal failure; peripheral neuropathy with risk of foot ulcers, amputations, and Charcot joints; and autonomic neuropathy causing gastrointestinal, genitourinary, and cardiovascular symptoms and sexual dysfunction. Patients with diabetes have an increased incidence of atherosclerotic cardiovascular, peripheral arterial, and cerebrovascular disease. Hypertension and abnormalities of lipoprotein metabolism are often found in people with diabetes.

The vast majority of cases of diabetes fall into two broad etiopathogenetic categories (discussed in greater detail below). In one category, type 1 diabetes, the cause is an absolute deficiency of insulin secretion. Individuals at increased risk of developing this type of diabetes can often be identified by serological evidence of an autoimmune pathologic process occurring in the pancreatic islets and by genetic markers. In the other, much more prevalent category, type 2 diabetes, the cause is a combination of resistance to insulin action and an inadequate compensatory insulin secretory response. In the latter category, a degree of hyperglycemia sufficient to cause pathologic and functional changes in various target tissues, but without clinical symptoms, may be present for a long period of time before diabetes is detected. During this asymptomatic period, it is possible to demonstrate an abnormality in carbohydrate metabolism by measurement of plasma glucose in the fasting state or after a challenge with an oral glucose load.

The degree of hyperglycemia (if any) may change over time, depending on the extent of the underlying disease process (Fig. 1). A disease process may be present but may not have progressed far enough to cause hyperglycemia. The same disease process can cause impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) without fulfilling the criteria for the diagnosis of diabetes. In some individuals with diabetes, adequate glycemic control can be achieved with weight reduction, exercise, and/or oral glucose-lowering agents. These individuals therefore do not require insulin. Other individuals who have some residual insulin secretion but require exogenous insulin for adequate glycemic control can survive without it. Individuals with extensive ß-cell destruction and therefore no residual insulin secretion require insulin for survival. The severity of the metabolic abnormality can progress, regress, or stay the same. Thus, the degree of hyperglycemia reflects the severity of the underlying metabolic process and its treatment more than the nature of the process itself.

DEFINITION AND DESCRIPTION OF DIABETES MELLITUS

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.

Several pathogenic processes are involved in the development of diabetes. These range from autoimmune destruction of the ß-cells of the pancreas with consequent insulin deficiency to abnormalities that result in resistance to insulin action. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of hormone action. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycemia.

Symptoms of marked hyperglycemia include polyuria, polydipsia, weight loss, sometimes with polyphagia, and blurred vision. Impairment of growth and susceptibility to certain infections may also accompany chronic hyperglycemia. Acute, life-threatening consequences of uncontrolled diabetes are hyperglycemia with ketoacidosis or the nonketotic hyperosmolar syndrome.

Long-term complications of diabetes include retinopathy with potential loss of vision; nephropathy leading to renal failure; peripheral neuropathy with risk of foot ulcers, amputations, and Charcot joints; and autonomic neuropathy causing gastrointestinal, genitourinary, and cardiovascular symptoms and sexual dysfunction. Patients with diabetes have an increased incidence of atherosclerotic cardiovascular, peripheral arterial, and cerebrovascular disease. Hypertension and abnormalities of lipoprotein metabolism are often found in people with diabetes.

The vast majority of cases of diabetes fall into two broad etiopathogenetic categories (discussed in greater detail below). In one category, type 1 diabetes, the cause is an absolute deficiency of insulin secretion. Individuals at increased risk of developing this type of diabetes can often be identified by serological evidence of an autoimmune pathologic process occurring in the pancreatic islets and by genetic markers. In the other, much more prevalent category, type 2 diabetes, the cause is a combination of resistance to insulin action and an inadequate compensatory insulin secretory response. In the latter category, a degree of hyperglycemia sufficient to cause pathologic and functional changes in various target tissues, but without clinical symptoms, may be present for a long period of time before diabetes is detected. During this asymptomatic period, it is possible to demonstrate an abnormality in carbohydrate metabolism by measurement of plasma glucose in the fasting state or after a challenge with an oral glucose load.

The degree of hyperglycemia (if any) may change over time, depending on the extent of the underlying disease process (Fig. 1). A disease process may be present but may not have progressed far enough to cause hyperglycemia. The same disease process can cause impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) without fulfilling the criteria for the diagnosis of diabetes. In some individuals with diabetes, adequate glycemic control can be achieved with weight reduction, exercise, and/or oral glucose-lowering agents. These individuals therefore do not require insulin. Other individuals who have some residual insulin secretion but require exogenous insulin for adequate glycemic control can survive without it. Individuals with extensive ß-cell destruction and therefore no residual insulin secretion require insulin for survival. The severity of the metabolic abnormality can progress, regress, or stay the same. Thus, the degree of hyperglycemia reflects the severity of the underlying metabolic process and its treatment more than the nature of the process itself.


CLASSIFICATION OF DIABETES MELLITUS AND OTHER CATEGORIES OF GLUCOSE REGULATION

Assigning a type of diabetes to an individual often depends on the circumstances present at the time of diagnosis, and many diabetic individuals do not easily fit into a single class. For example, a person with gestational diabetes mellitus (GDM) may continue to be hyperglycemic after delivery and may be determined to have, in fact, type 2 diabetes. Alternatively, a person who acquires diabetes because of large doses of exogenous steroids may become normoglycemic once the glucocorticoids are discontinued, but then may develop diabetes many years later after recurrent episodes of pancreatitis. Another example would be a person treated with thiazides who develops diabetes years later. Because thiazides in themselves seldom cause severe hyperglycemia, such individuals probably have type 2 diabetes that is exacerbated by the drug. Thus, for the clinician and patient, it is less important to label the particular type of diabetes than it is to understand the pathogenesis of the hyperglycemia and to treat it effectively.

Type 1 diabetes (ß-cell destruction, usually leading to absolute insulin deficiency) Immune-mediated diabetes.
This form of diabetes, which accounts for only 5–10% of those with diabetes, previously encompassed by the terms insulin-dependent diabetes, type I diabetes, or juvenile-onset diabetes, results from a cellular-mediated autoimmune destruction of the ß-cells of the pancreas. Markers of the immune destruction of the ß-cell include islet cell autoantibodies, autoantibodies to insulin, autoantibodies to glutamic acid decarboxylase (GAD65), and autoantibodies to the tyrosine phosphatases IA-2 and IA-2ß. One and usually more of these autoantibodies are present in 85–90% of individuals when fasting hyperglycemia is initially detected. Also, the disease has strong HLA associations, with linkage to the DQA and DQB genes, and it is influenced by the DRB genes. These HLA-DR/DQ alleles can be either predisposing or protective.

In this form of diabetes, the rate of ß-cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults). Some patients, particularly children and adolescents, may present with ketoacidosis as the first manifestation of the disease. Others have modest fasting hyperglycemia that can rapidly change to severe hyperglycemia and/or ketoacidosis in the presence of infection or other stress. Still others, particularly adults, may retain residual ß-cell function sufficient to prevent ketoacidosis for many years; such individuals eventually become dependent on insulin for survival and are at risk for ketoacidosis. At this latter stage of the disease, there is little or no insulin secretion, as manifested by low or undetectable levels of plasma C-peptide. Immune-mediated diabetes commonly occurs in childhood and adolescence, but it can occur at any age, even in the 8th and 9th decades of life.

Autoimmune destruction of ß-cells has multiple genetic predispositions and is also related to environmental factors that are still poorly defined. Although patients are rarely obese when they present with this type of diabetes, the presence of obesity is not incompatible with the diagnosis. These patients are also prone to other autoimmune disorders such as Graves’ disease, Hashimoto’s thyroiditis, Addison’s disease, vitiligo, celiac sprue, autoimmune hepatitis, myasthenia gravis, and pernicious anemia.

Idiopathic diabetes.

Some forms of type 1 diabetes have no known etiologies. Some of these patients have permanent insulinopenia and are prone to ketoacidosis, but have no evidence of autoimmunity. Although only a minority of patients with type 1 diabetes fall into this category, of those who do, most are of African or Asian ancestry. Individuals with this form of diabetes suffer from episodic ketoacidosis and exhibit varying degrees of insulin deficiency between episodes. This form of diabetes is strongly inherited, lacks immunological evidence for ß-cell autoimmunity, and is not HLA associated. An absolute requirement for insulin replacement therapy in affected patients may come and go.

Type 2 diabetes (ranging from predominantly insulin resistance with relative insulin deficiency to predominantly an insulin secretory defect with insulin resistance)
This form of diabetes, which accounts for ~90–95% of those with diabetes, previously referred to as non-insulin-dependent diabetes, type II diabetes, or adult-onset diabetes, encompasses individuals who have insulin resistance and usually have relative (rather than absolute) insulin deficiency At least initially, and often throughout their lifetime, these individuals do not need insulin treatment to survive. There are probably many different causes of this form of diabetes. Although the specific etiologies are not known, autoimmune destruction of ß-cells does not occur, and patients do not have any of the other causes of diabetes listed above or below.

Most patients with this form of diabetes are obese, and obesity itself causes some degree of insulin resistance. Patients who are not obese by traditional weight criteria may have an increased percentage of body fat distributed predominantly in the abdominal region. Ketoacidosis seldom occurs spontaneously in this type of diabetes; when seen, it usually arises in association with the stress of another illness such as infection. This form of diabetes frequently goes undiagnosed for many years because the hyperglycemia develops gradually and at earlier stages is often not severe enough for the patient to notice any of the classic symptoms of diabetes. Nevertheless, such patients are at increased risk of developing macrovascular and microvascular complications. Whereas patients with this form of diabetes may have insulin levels that appear normal or elevated, the higher blood glucose levels in these diabetic patients would be expected to result in even higher insulin values had their ß-cell function been normal. Thus, insulin secretion is defective in these patients and insufficient to compensate for insulin resistance. Insulin resistance may improve with weight reduction and/or pharmacological treatment of hyperglycemia but is seldom restored to normal The risk of developing this form of diabetes increases with age, obesity, and lack of physical activity. It occurs more frequently in women with prior GDM and in individuals with hypertension or dyslipidemia, and its frequency varies in different racial/ethnic subgroups. It is often associated with a strong genetic predisposition, more so than is the autoimmune form of type 1 diabetes. However, the genetics of this form of diabetes are complex and not clearly defined.

Other specific types of diabetes Genetic defects of the ß-cell.

Several forms of diabetes are associated with monogenetic defects in ß-cell function. These forms of diabetes are frequently characterized by onset of hyperglycemia at an early age (generally before age 25 years). They are referred to as maturity-onset diabetes of the young (MODY) and are characterized by impaired insulin secretion with minimal or no defects in insulin action. They are inherited in an autosomal dominant pattern. Abnormalities at six genetic loci on different chromosomes have been identified to date. The most common form is associated with mutations on chromosome 12 in a hepatic transcription factor referred to as hepatocyte nuclear factor (HNF)-1a. A second form is associated with mutations in the glucokinase gene on chromosome 7p and results in a defective glucokinase molecule. Glucokinase converts glucose to glucose-6-phosphate, the metabolism of which, in turn, stimulates insulin secretion by the ß-cell. Thus, glucokinase serves as the “glucose sensor” for the ß-cell. Because of defects in the glucokinase gene, increased plasma levels of glucose are necessary to elicit normal levels of insulin secretion. The less common forms result from mutations in other transcription factors, including HNF-4a, HNF-1ß, insulin promoter factor (IPF)-1, and NeuroD1.

Point mutations in mitochondrial DNA have been found to be associated with diabetes mellitus and deafness The most common mutation occurs at position 3243 in the tRNA leucine gene, leading to an A-to-G transition. An identical lesion occurs in the MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like syndrome); however, diabetes is not part of this syndrome, suggesting different phenotypic expressions of this genetic lesion.

Genetic abnormalities that result in the inability to convert proinsulin to insulin have been identified in a few families, and such traits are inherited in an autosomal dominant pattern. The resultant glucose intolerance is mild. Similarly, the production of mutant insulin molecules with resultant impaired receptor binding has also been identified in a few families and is associated with an autosomal inheritance and only mildly impaired or even normal glucose metabolism.

Genetic defects in insulin action.

There are unusual causes of diabetes that result from genetically determined abnormalities of insulin action. The metabolic abnormalities associated with mutations of the insulin receptor may range from hyperinsulinemia and modest hyperglycemia to severe diabetes. Some individuals with these mutations may have acanthosis nigricans. Women may be virilized and have enlarged, cystic ovaries. In the past, this syndrome was termed type A insulin resistance. Leprechaunism and the Rabson-Mendenhall syndrome are two pediatric syndromes that have mutations in the insulin receptor gene with subsequent alterations in insulin receptor function and extreme insulin resistance. The former has characteristic facial features and is usually fatal in infancy, while the latter is associated with abnormalities of teeth and nails and pineal gland hyperplasia.

Alterations in the structure and function of the insulin receptor cannot be demonstrated in patients with insulin-resistant lipoatrophic diabetes. Therefore, it is assumed that the lesion(s) must reside in the postreceptor signal transduction pathways.

Diseases of the exocrine pancreas.

Any process that diffusely injures the pancreas can cause diabetes. Acquired processes include pancreatitis, trauma, infection, pancreatectomy, and pancreatic carcinoma. With the exception of that caused by cancer, damage to the pancreas must be extensive for diabetes to occur; adrenocarcinomas that involve only a small portion of the pancreas have been associated with diabetes. This implies a mechanism other than simple reduction in ß-cell mass. If extensive enough, cystic fibrosis and hemochromatosis will also damage ß-cells and impair insulin secretion. Fibrocalculous pancreatopathy may be accompanied by abdominal pain radiating to the back and pancreatic calcifications identified on X-ray examination. Pancreatic fibrosis and calcium stones in the exocrine ducts have been found at autopsy.

Endocrinopathies.

Several hormones (e.g., growth hormone, cortisol, glucagon, epinephrine) antagonize insulin action. Excess amounts of these hormones (e.g., acromegaly, Cushing’s syndrome, glucagonoma, pheochromocytoma, respectively) can cause diabetes. This generally occurs in individuals with preexisting defects in insulin secretion, and hyperglycemia typically resolves when the hormone excess is resolved.

Somatostatinoma- and aldosteronoma-induced hypokalemia can cause diabetes, at least in part, by inhibiting insulin secretion. Hyperglycemia generally resolves after successful removal of the tumor.

Drug- or chemical-induced diabetes.

Many drugs can impair insulin secretion. These drugs may not cause diabetes by themselves, but they may precipitate diabetes in individuals with insulin resistance. In such cases, the classification is unclear because the sequence or relative importance of ß-cell dysfunction and insulin resistance is unknown. Certain toxins such as Vacor (a rat poison) and intravenous pentamidine can permanently destroy pancreatic ß-cells. Such drug reactions fortunately are rare. There are also many drugs and hormones that can impair insulin action. Examples include nicotinic acid and glucocorticoids. Patients receiving a-interferon have been reported to develop diabetes associated with islet cell antibodies and, in certain instances, severe insulin deficiency. The list shown in Table 1 is not all-inclusive, but reflects the more commonly recognized drug-, hormone-, or toxin-induced forms of diabetes.

Infections.

Certain viruses have been associated with ß-cell destruction. Diabetes occurs in patients with congenital rubella, although most of these patients have HLA and immune markers characteristic of type 1 diabetes. In addition, coxsackievirus B, cytomegalovirus, adenovirus, and mumps have been implicated in inducing certain cases of the disease.

Uncommon forms of immune-mediated diabetes.

In this category, there are two known conditions, and others are likely to occur. The stiff-man syndrome is an autoimmune disorder of the central nervous system characterized by stiffness of the axial muscles with painful spasms. Patients usually have high titers of the GAD autoantibodies, and approximately one-third will develop diabetes.

Anti-insulin receptor antibodies can cause diabetes by binding to the insulin receptor, thereby blocking the binding of insulin to its receptor in target tissues. However, in some cases, these antibodies can act as an insulin agonist after binding to the receptor and can thereby cause hypoglycemia. Anti-insulin receptor antibodies are occasionally found in patients with systemic lupus erythematosus and other autoimmune diseases. As in other states of extreme insulin resistance, patients with anti-insulin receptor antibodies often have acanthosis nigricans. In the past, this syndrome was termed type B insulin resistance.

Other genetic syndromes sometimes associated with diabetes.

Many genetic syndromes are accompanied by an increased incidence of diabetes mellitus. These include the chromosomal abnormalities of Down’s syndrome, Klinefelter’s syndrome, and Turner’s syndrome. Wolfram’s syndrome is an autosomal recessive disorder characterized by insulin-deficient diabetes and the absence of ß-cells at autopsy. Additional manifestations include diabetes insipidus, hypogonadism, optic atrophy, and neural deafness. Other syndromes are listed in Table 1.

Gestational diabetes mellitus (GDM)

GDM is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. The definition applies regardless of whether insulin or only diet modification is used for treatment or whether the condition persists after pregnancy. It does not exclude the possibility that unrecognized glucose intolerance may have antedated or begun concomitantly with the pregnancy. GDM complicates ~4% of all pregnancies in the U.S., resulting in ~135,000 cases annually. The prevalence may range from 1 to 14% of pregnancies, depending on the population studied. GDM represents nearly 90% of all pregnancies complicated by diabetes.

Deterioration of glucose tolerance occurs normally during pregnancy, particularly in the 3rd trimester.

Impaired glucose tolerance (IGT) and impaired fasting glucose (IFG)
The Expert Committee (1,2) recognized an intermediate group of subjects whose glucose levels, although not meeting criteria for diabetes, are nevertheless too high to be considered normal. This group is defined as having fasting plasma glucose (FPG) levels =100 mg/dl (5.6 mmol/l) but <126 mg/dl (7.0 mmol/l) or 2-h values in the oral glucose tolerance test (OGTT) of =140 mg/dl (7.8 mmol/l) but <200 mg/dl (11.1 mmol/l). Thus, the categories of FPG values are as follows:

FPG <100 mg/dl (5.6 mmol/l) = normal fasting glucose;

FPG 100–125 mg/dl (5.6–6.9 mmol/l) = IFG (impaired fasting glucose);

FPG =126 mg/dl (7.0 mmol/l) = provisional diagnosis of diabetes (the diagnosis must be confirmed, as described below).

The corresponding categories when the OGTT is used are the following:

2-h postload glucose <140 mg/dl (7.8 mmol/l) = normal glucose tolerance;

2-h postload glucose 140–199 mg/dl (7.8–11.1 mmol/l) = IGT (impaired glucose tolerance);

2-h postload glucose =200 mg/dl (11.1 mmol/l) = provisional diagnosis of diabetes (the diagnosis must be confirmed, as described below).

Patients with IFG and/or IGT are now referred to as having “pre-diabetes” indicating the relatively high risk for development of diabetes in these patients. In the absence of pregnancy, IFG and IGT are not clinical entities in their own right but rather risk factors for future diabetes as well as cardiovascular disease. They can be observed as intermediate stages in any of the disease processes listed in Table 1. IFG and IGT are associated with the metabolic syndrome, which includes obesity (especially abdominal or visceral obesity), dyslipidemia of the high-triglyceride and/or low-HDL type, and hypertension. It is worth mentioning that medical nutrition therapy aimed at producing 5–10% loss of body weight, exercise, and certain pharmacological agents have been variably demonstrated to prevent or delay the development of diabetes in people with IGT; the potential impact of such interventions to reduce cardiovascular risk has not been examined to date.

Note that many individuals with IGT are euglycemic in their daily lives. Individuals with IFG or IGT may have normal or near normal glycated hemoglobin levels. Individuals with IGT often manifest hyperglycemia only when challenged with the oral glucose load used in the standardized OGTT.


DIAGNOSTIC CRITERIA FOR DIABETES MELLITUS

The criteria for the diagnosis of diabetes are shown in Table 2. Three ways to diagnose diabetes are possible, and each, in the absence of unequivocal hyperglycemia, must be confirmed, on a subsequent day, by any one of the three methods given in Table 2. The use of the hemoglobin A1c (A1C) for the diagnosis of diabetes is not recommended at this time.

Diagnosis of GDM

The criteria for abnormal glucose tolerance in pregnancy are those of Carpenter and Coustan (3). Recommendations from the American Diabetes Association’s Fourth International Workshop-Conference on Gestational Diabetes Mellitus held in March 1997 support the use of the Carpenter/Coustan diagnostic criteria as well as the alternative use of a diagnostic 75-g 2-h OGTT. These criteria are summarized below.

Testing for gestational diabetes.

Previous recommendations included screening for GDM performed in all pregnancies. However, there are certain factors that place women at lower risk for the development of glucose intolerance during pregnancy, and it is likely not cost-effective to screen such patients. Pregnant women who fulfill all of these criteria need not be screened for GDM.

This low-risk group comprises women who

are <25 years of age

are a normal body weight

have no family history (i.e., first-degree relative) of diabetes

have no history of abnormal glucose metabolism

have no history of poor obstetric outcome

are not members of an ethnic/racial group with a high prevalence of diabetes (e.g., Hispanic American, Native American, Asian American, African American, Pacific Islander)

Risk assessment for GDM should be undertaken at the first prenatal visit. Women with clinical characteristics consistent with a high risk of GDM (marked obesity, personal history of GDM, glycosuria, or a strong family history of diabetes) should undergo glucose testing (see below) as soon as feasible. If they are found not to have GDM at that initial screening, they should be retested between 24 and 28 weeks of gestation. Women of average risk should have testing undertaken at 24–28 weeks of gestation.

A fasting plasma glucose level >126 mg/dl (7.0 mmol/l) or a casual plasma glucose >200 mg/dl (11.1 mmol/l) meets the threshold for the diagnosis of diabetes. In the absence of unequivocal hyperglycemia, the diagnosis must be confirmed on a subsequent day. Confirmation of the diagnosis precludes the need for any glucose challenge. In the absence of this degree of hyperglycemia, evaluation for GDM in women with average or high-risk characteristics should follow one of two approaches.

One-step approach.

Perform a diagnostic OGTT without prior plasma or serum glucose screening. The one-step approach may be cost-effective in high-risk patients or populations (e.g., some Native-American groups).

Two-step approach.

Perform an initial screening by measuring the plasma or serum glucose concentration 1 h after a 50-g oral glucose load (glucose challenge test [GCT]) and perform a diagnostic OGTT on that subset of women exceeding the glucose threshold value on the GCT. When the two-step approach is used, a glucose threshold value >140 mg/dl (7.8 mmol/l) identifies ~80% of women with GDM, and the yield is further increased to 90% by using a cutoff of >130 mg/dl (7.2 mmol/l).

With either approach, the diagnosis of GDM is based on an OGTT. Diagnostic criteria for the 100-g OGTT are derived from the original work of O’Sullivan and Mahan (4) modified by Carpenter and Coustan (3) and are shown in the top of Table 3. Alternatively, the diagnosis can be made using a 75-g glucose load and the glucose threshold values listed for fasting, 1 h, and 2 h (Table 2, bottom); however, this test is not as well validated as the 100-g OGTT.

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