If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin insensitivity or insulin resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by the body cells that require it, and it will not be stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.[60]
By the time a person is diagnosed with type 2 diabetes, up to 50% of the beta cells in the pancreas have usually been damaged. In fact, these cells may have been declining for up to 10 years before the diagnosis. Along with raised blood pressure and elevated cholesterol levels, this predisposes the person to arterial damage years before diabetes is diagnosed. So, at the time of diagnosis, the person is already at risk for cardiovascular disease (CVD).
You are more likely to develop type 2 diabetes if you are not physically active and are overweight or obese. Extra weight sometimes causes insulin resistance and is common in people with type 2 diabetes. The location of body fat also makes a difference. Extra belly fat is linked to insulin resistance, type 2 diabetes, and heart and blood vessel disease. To see if your weight puts you at risk for type 2 diabetes, check out these Body Mass Index (BMI) charts.
Diabetes mellitus (DM) is best defined as a syndrome characterized by inappropriate fasting or postprandial hyperglycemia, caused by absolute or relative insulin deficiency and its metabolic consequences, which include disturbed metabolism of protein and fat. This syndrome results from a combination of deficiency of insulin secretion and its action. Diabetes mellitus occurs when the normal constant of the product of insulin secretion times insulin sensitivity, a parabolic function termed the “disposition index” (Figure 19-1), is inadequate to prevent hyperglycemia and its clinical consequences of polyuria, polydipsia, and weight loss. At high degrees of insulin sensitivity, small declines in the ability to secrete insulin cause only mild, clinically imperceptible defects in glucose metabolism. However, irrespective of insulin sensitivity, a minimum amount of insulin is necessary for normal metabolism. Thus, near absolute deficiency of insulin must result in severe metabolic disturbance as occurs in type 1 diabetes mellitus (T1DM). By contrast, with decreasing sensitivity to its action, higher amounts of insulin secretion are required for a normal disposition index. At a critical point in the disposition index curve (see Figure 19-1), a further small decrement in insulin sensitivity requires a large increase in insulin secretion; those who can mount these higher rates of insulin secretion retain normal glucose metabolism, whereas those who cannot increase their insulin secretion because of genetic or acquired defects now manifest clinical diabetes as occurs in type 2 diabetes (T2DM).
Although many of the symptoms of type 1 and type 2 diabetes are similar, they present in very different ways. Many people with type 2 diabetes won’t have symptoms for many years. Then often the symptoms of type 2 diabetes develop slowly over the course of time. Some people with type 2 diabetes have no symptoms at all and don’t discover their condition until complications develop.
Diabetic peripheral neuropathy is a condition where nerve endings, particularly in the legs and feet, become less sensitive. Diabetic foot ulcers are a particular problem since the patient does not feel the pain of a blister, callous, or other minor injury. Poor blood circulation in the legs and feet contribute to delayed wound healing. The inability to sense pain along with the complications of delayed wound healing can result in minor injuries, blisters, or callouses becoming infected and difficult to treat. In cases of severe infection, the infected tissue begins to break down and rot away. The most serious consequence of this condition is the need for amputation of toes, feet, or legs due to severe infection.
According to the National Institutes of Health, the reported rate of gestational diabetes is between 2% to 10% of pregnancies. Gestational diabetes usually resolves itself after pregnancy. Having gestational diabetes does, however, put mothers at risk for developing type 2 diabetes later in life. Up to 10% of women with gestational diabetes develop type 2 diabetes. It can occur anywhere from a few weeks after delivery to months or years later.

Pre-clinical diabetes refers to the time during which destruction of pancreatic insulin-producing cells is occurring, but symptoms have not yet developed. This period may last for months to years. Normally, 80-90% of the pancreatic beta cells must be destroyed before any symptoms of diabetes develops. During this time, blood tests can identify some immunological markers of pancreatic cell destruction. However, there is currently no known treatment to prevent progression of pre-clinical diabetes to true diabetes mellitus.
There is evidence that certain emotions can promote type 2 diabetes. A recent study found that depression seems to predispose people to diabetes. Other research has tied emotional stress to diabetes, though the link hasn't been proved. Researchers speculate that the emotional connection may have to do with the hormone cortisol, which floods the body during periods of stress. Cortisol sends glucose to the blood, where it can fuel a fight-or-flight response, but overuse of this system may lead to dysfunction.

"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used.[39] Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, frequently with ketosis, and sometimes with serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease).[39] These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.[40]
Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with type 1 associated with youth and type 2 with being overweight.[108] The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus, which is also associated with frequent urination.[108] Effective treatment was not developed until the early part of the 20th century, when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922.[108] This was followed by the development of the long-acting insulin NPH in the 1940s.[108]

Diabetes mellitus (DM), commonly referred to as diabetes, is a group of metabolic disorders in which there are high blood sugar levels over a prolonged period.[10] Symptoms of high blood sugar include frequent urination, increased thirst, and increased hunger.[2] If left untreated, diabetes can cause many complications.[2] Acute complications can include diabetic ketoacidosis, hyperosmolar hyperglycemic state, or death.[3] Serious long-term complications include cardiovascular disease, stroke, chronic kidney disease, foot ulcers, and damage to the eyes.[2]

Insulin is vital to patients with type 1 diabetes - they cannot live without 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 may result.


People with diabetes either don't make insulin or their body's cells no longer are able to use the insulin, leading to high blood sugars. By definition, diabetes is having a blood glucose level of greater than or equal to126 milligrams per deciliter (mg/dL) after an 8-hour fast (not eating anything), or by having a non-fasting glucose level greater than or equal to 200 mg/dL along with symptoms of diabetes, or a glucose level of greater than or equal to 200 mg/dL on a 2-hour glucose tolerance test, or an A1C greater than or equal to 6.5%. Unless the person is having obvious symptoms of diabetes or is in a diabetic crisis, the diagnosis must be confirmed with a repeat test.


The good news is that prevention plays an important role in warding off these complications. By maintaining tight control of your blood glucose—and getting it as close to normal as possible—you’ll help your body function in the way that it would if you did not have diabetes. Tight control helps you decrease the chances that your body will experience complications from elevated glucose levels.
It’s not uncommon for patients to suddenly feel unsteady and immediately need to reach for carbs, says Marjorie Cypress, a nurse practitioner at an endocrinology clinic in Albuquerque, New Mexico, and 2014 president of health care and education for the American Diabetes Association. “When you have high blood sugar, your body has a problem regulating its glucose,” she explains. “If you’ve eaten something high in carbohydrates, your body shoots out a little too much insulin, and your glucose drops quickly. This makes you feel shaky, and you tend to crave carbs or sugar. This can lead to a vicious cycle.” These are the best foods for someone on a diabetic diet.

Kidney disease: According to the Centers for Disease Control and Prevention (CDC), an estimated 33 percent of people with diabetes have chronic kidney disease. Diabetes can also damage blood vessels in the kidneys, impairing function. The kidneys play a vital role in balancing fluid levels and removing waste from the body. Kidney health is therefore vital for preserving overall health.


Unlike people with type 1 diabetes, people with type 2 diabetes produce insulin; however, the insulin their pancreas secretes is either not enough or the body is unable to recognize the insulin and use it properly (insulin resistance). When there isn't enough insulin or the insulin is not used as it should be, glucose (sugar) can't get into the body's cells and builds up in the bloodstream instead. When glucose builds up in the blood instead of going into cells, it causes damage in multiple areas of the body. Also, since cells aren't getting the glucose they need, they can't function properly.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
Medications used to treat diabetes do so by lowering blood sugar levels. There is broad consensus that when people with diabetes maintain tight glucose control (also called "tight glycemic control") -- keeping the glucose levels in their blood within normal ranges - that they experience fewer complications like kidney problems and eye problems.[84][85] There is however debate as to whether this is cost effective for people later in life.[86]
Nerve damage (neuropathy). Excess sugar can injure the walls of the tiny blood vessels (capillaries) that nourish your nerves, especially in the legs. This can cause tingling, numbness, burning or pain that usually begins at the tips of the toes or fingers and gradually spreads upward. Poorly controlled blood sugar can eventually cause you to lose all sense of feeling in the affected limbs. Damage to the nerves that control digestion can cause problems with nausea, vomiting, diarrhea or constipation. For men, erectile dysfunction may be an issue.
Type 2 diabetes is one of the major degenerative diseases in the Western world today. It happens when your body can’t use insulin properly, or can’t make enough insulin. Insulin is a hormone the assists the body’s cells in utilizing glucose. It also helps the body store extra sugar in fat, liver, and muscle cells. If you don’t have insulin, your body can’t use the sugar in the bloodstream.

The typical symptoms of diabetes mellitus are the three “polys:” polyuria, polydipsia, and polyphagia. Because of insulin deficiency, the assimilation and storage of glucose in muscle adipose tissues, and the liver is greatly diminished. This produces an accumulation of glucose in the blood and creates an increase in its osmolarity. In response to this increased osmotic pressure there is depletion of intracellular water and osmotic diuresis. The water loss creates intense thirst and increased urination. The increased appetite (polyphagia) is not as clearly understood. It may be the result of the body's effort to increase its supply of energy foods even though eating more carbohydrates in the absence of sufficient insulin does not meet the energy needs of the cells.

You are more likely to develop type 2 diabetes if you are not physically active and are overweight or obese. Extra weight sometimes causes insulin resistance and is common in people with type 2 diabetes. The location of body fat also makes a difference. Extra belly fat is linked to insulin resistance, type 2 diabetes, and heart and blood vessel disease. To see if your weight puts you at risk for type 2 diabetes, check out these Body Mass Index (BMI) charts.
Type 2 diabetes is different. A person with type 2 diabetes still produces insulin but the body doesn't respond to it normally. Glucose is less able to enter the cells and do its job of supplying energy (a problem called insulin resistance). This raises the blood sugar level, so the pancreas works hard to make even more insulin. Eventually, this strain can make the pancreas unable to produce enough insulin to keep blood sugar levels normal.
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In general, women live longer than men do because they have a lower risk of heart disease, but when women develop diabetes, their risk for heart disease skyrockets, and death by heart failure is more likely in women than in men. Another study also found that in people with diabetes, heart attacks are more often fatal for women than they are for men. Other examples of how diabetes affects women differently than men are:
Your doctor will check your blood glucose levels, and if you are diagnosed with diabetes, your doctor will guide you on a plan to keep your blood sugar levels normal. If your diabetes is mild, your doctor will likely recommend a diet plan, exercise, and weight loss. Your doctor may prescribe medications that help reduce blood sugar levels. In some women, insulin may be necessary.
The classic presenting symptoms of type 1 diabetes mellitus are discussed below. For some children, the first symptoms of diabetes mellitus are those of diabetic ketoacidosis. This is a serious and life-threatening condition, requiring immediate treatment. Ketoacidosis occurs due to a severe disturbance in the body’s metabolism. Without insulin, glucose cannot be taken up into cells. Instead fats are broken down for energy which can have acid by-products.  

That said, some research does suggest that eating too many sweetened foods can affect type 2 diabetes risk, and with the Centers for Disease Control and Prevention (CDC) estimating that 30.3 million Americans have the disease — and that millions of more individuals are projected to develop it, too — understanding all the risk factors for the disease, including sugar consumption, is essential to help reverse the diabetes epidemic.


If sugars in general are not associated with increased diabetes risk, but sodas are, it suggests the possibility that something other than sugar explains this relationship.16 Sodas are often accompanied by cheeseburgers, chicken nuggets, and other unhealthful foods. That is, soda consumption can be a sign of a diet focusing on fast foods or an overall unhealthful diet and lifestyle. And sugary snack foods (e.g., cookies and snack pastries) are often high in fat; the sugar lures us in to the fat calories hiding inside. Some, but not all, observational trials have sought to control for these confounding variables. 
A metabolic disease in which carbohydrate use is reduced and that of lipid and protein enhanced; it is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma; long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
Using insulin to get blood glucose levels to a healthy level is a good thing, not a bad one. For most people, type 2 diabetes is a progressive disease. When first diagnosed, many people with type 2 diabetes can keep their blood glucose at a healthy level with a combination of meal planning, physical activity, and taking oral medications. But over time, the body gradually produces less and less of its own insulin, and eventually oral medications may not be enough to keep blood glucose levels in a healthy range. 
Viral infections may be the most important environmental factor in the development of type 1 diabetes mellitus, [26] probably by initiating or modifying an autoimmune process. Instances have been reported of a direct toxic effect of infection in congenital rubella. One survey suggests enteroviral infection during pregnancy carries an increased risk of type 1 diabetes mellitus in the offspring. Paradoxically, type 1 diabetes mellitus incidence is higher in areas where the overall burden of infectious disease is lower.
Type 2 (formerly called 'adult-onset' or 'non insulin-dependent') diabetes results when the body doesn’t produce enough insulin and/or is unable to use insulin properly (this is also referred to as ‘insulin resistance’). This form of diabetes usually occurs in people who are over 40 years of age, overweight, and have a family history of diabetes, although today it is increasingly found in younger people.
What is type 2 diabetes and prediabetes? Behind type 2 diabetes is a disease where the body’s cells have trouble responding to insulin – this is called insulin resistance. Insulin is a hormone needed to store the energy found in food into the body’s cells. In prediabetes, insulin resistance starts growing and the beta cells in the pancreas that release insulin will try to make even more insulin to make up for the body’s insensitivity. This can go on for a long time without any symptoms. Over time, though, the beta cells in the pancreas will fatigue and will no longer be able to produce enough insulin – this is called “beta burnout.” Once there is not enough insulin, blood sugars will start to rise above normal. Prediabetes causes people to have higher-than-normal blood sugars (and an increased risk for heart disease and stroke). Left unnoticed or untreated, blood sugars continue to worsen and many people progress to type 2 diabetes. After a while, so many of the beta cells have been damaged that diabetes becomes an irreversible condition. 
People with diabetes can benefit from education about the disease and treatment, good nutrition to achieve a normal body weight, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.[80][81]
Type 2 diabetes usually begins with insulin resistance, a condition in which muscle, liver, and fat cells do not use insulin well. As a result, your body needs more insulin to help glucose enter cells. At first, the pancreas makes more insulin to keep up with the added demand. Over time, the pancreas can’t make enough insulin, and blood glucose levels rise.
Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with type 1 associated with youth and type 2 with being overweight.[108] The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus, which is also associated with frequent urination.[108] Effective treatment was not developed until the early part of the 20th century, when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922.[108] This was followed by the development of the long-acting insulin NPH in the 1940s.[108]
With gestational diabetes, risks to the unborn baby are even greater than risks to the mother. Risks to the baby include abnormal weight gain before birth, breathing problems at birth, and higher obesity and diabetes risk later in life. Risks to the mother include needing a cesarean section due to an overly large baby, as well as damage to heart, kidney, nerves, and eye.
Insulin — the hormone that allows your body to regulate sugar in the blood — is made in your pancreas. Essentially, insulin resistance is a state in which the body’s cells do not use insulin efficiently. As a result, it takes more insulin than normal to transport blood sugar (glucose) into cells, to be used immediately for fuel or stored for later use. A drop in efficiency in getting glucose to cells creates a problem for cell function; glucose is normally the body’s quickest and most readily available source of energy.
There are some interesting developments in blood glucose monitoring including continuous glucose sensors. 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. One version is specifically designed to interface with their insulin pumps. In most cases 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). However, in 2013 the US FDA approved the first artificial pancreas type device, meaning an implanted sensor and pump combination that stops insulin delivery when glucose levels reach a certain low point. All of these devices need to be correlated to fingersticks measurements for a few hours before they can function independently. The devices can then provide readings for 3 to 5 days.
Type 2 diabetes is partly preventable by staying a normal weight, exercising regularly, and eating properly.[1] Treatment involves exercise and dietary changes.[1] If blood sugar levels are not adequately lowered, the medication metformin is typically recommended.[7][14] Many people may eventually also require insulin injections.[9] In those on insulin, routinely checking blood sugar levels is advised; however, this may not be needed in those taking pills.[15] Bariatric surgery often improves diabetes in those who are obese.[8][16]
The typical symptoms of diabetes mellitus are the three “polys:” polyuria, polydipsia, and polyphagia. Because of insulin deficiency, the assimilation and storage of glucose in muscle adipose tissues, and the liver is greatly diminished. This produces an accumulation of glucose in the blood and creates an increase in its osmolarity. In response to this increased osmotic pressure there is depletion of intracellular water and osmotic diuresis. The water loss creates intense thirst and increased urination. The increased appetite (polyphagia) is not as clearly understood. It may be the result of the body's effort to increase its supply of energy foods even though eating more carbohydrates in the absence of sufficient insulin does not meet the energy needs of the cells.
Janis McWilliams, RN, MSN, CDE, BC-ADM, responds: Yes, in type 1 diabetes in particular, the onset of symptoms like frequent urination and extreme thirst can be very sudden. In type 2 diabetes, the symptoms tend to come about more gradually, and sometimes there are no signs at all. People who have symptoms should contact their health care provider immediately for an accurate diagnosis. Keep in mind that these symptoms could signal other problems, too.
When your blood sugar is out of whack, you just don’t feel well, says Cypress, and might become more short-tempered. In fact, high blood sugar can mimic depression-like symptoms. “You feel very tired, you don’t feel like doing anything, you don’t want to go out, you just want to sleep,” Cypress says. She’ll see patients who think they need to be treated for depression, but then experience mood improvement after their blood sugar normalizes.
Diabetes mellitus is a public health problem around the world. In 1980, 108 million adults worldwide had diabetes (4.7% of the global population). By 2014 this had risen to 422 million adults (8.5% of the global population). By 2040, the number is expected to be 642 million adults. In the UK, there is estimated to be between 3 and 4 million people with diabetes. Type 2 diabetes accounts for more than 90% of all patients with diabetes. 
Monitoring your caloric intake may be helpful if you’re overweight, but everyone with type 2 diabetes should track how many carbs they’re taking in. That can be tricky because carbs are in many of the common foods you may already eat, but there are both good and bad sources of carbs. Fruits and vegetables, for example, are good sources, while pretzels and cookies are bad sources. (29)

A 2009 study shows how genetic information may shed light on the environment-gene interactions that lead to type 1. In the study, researchers found that one of the type 1 genes mediates the immune system's response to viruses. This finding supported the longtime hypothesis that a virus may somehow make the immune system attack the insulin-producing cells in the pancreas in people who are genetically susceptible to developing diabetes.
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.
Type I diabetes, sometimes called juvenile diabetes, begins most commonly in childhood or adolescence. In this form of diabetes, the body produces little or no insulin. It is characterized by a sudden onset and occurs more frequently in populations descended from Northern European countries (Finland, Scotland, Scandinavia) than in those from Southern European countries, the Middle East, or Asia. In the United States, approximately three people in 1,000 develop Type I diabetes. This form also is called insulin-dependent diabetes because people who develop this type need to have daily injections of insulin.

Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity.[17] As of 2015 there were approximately 392 million people diagnosed with the disease compared to around 30 million in 1985.[11][18] Typically it begins in middle or older age,[6] although rates of type 2 diabetes are increasing in young people.[19][20] Type 2 diabetes is associated with a ten-year-shorter life expectancy.[10] Diabetes was one of the first diseases described.[21] The importance of insulin in the disease was determined in the 1920s.[22]

Diabetes mellitus occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries,[101] where more than 80% of diabetic deaths occur.[105] The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030.[106] The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet).[101][106] The global prevalence of diabetes might increase by 55% between 2013 and 2035.[101]
George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, American College of Endocrinology

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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