The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.
Type II is considered a milder form of diabetes because of its slow onset (sometimes developing over the course of several years) and because it usually can be controlled with diet and oral medication. The consequences of uncontrolled and untreated Type II diabetes, however, are the just as serious as those for Type I. This form is also called noninsulin-dependent diabetes, a term that is somewhat misleading. Many people with Type II diabetes can control the condition with diet and oral medications, however, insulin injections are sometimes necessary if treatment with diet and oral medication is not working.
The causes of diabetes mellitus are unclear, however, there seem to be both hereditary (genetic factors passed on in families) and environmental factors involved. Research has shown that some people who develop diabetes have common genetic markers. In Type I diabetes, the immune system, the body's defense system against infection, is believed to be triggered by a virus or another microorganism that destroys cells in the pancreas that produce insulin. In Type II diabetes, age, obesity, and family history of diabetes play a role.
FIGURE 19-1 ■. This figure shows the hyperbolic relationship of insulin resistance and beta cell function. On the y-axis is beta cell function as reflected in the first-phase insulin response during intravenous (IV) glucose infusion; on the x-axis is insulin sensitivity and its mirror image resistance. In a subject with normal glucose tolerance (NGT) and beta-cell reserve, an increase in insulin resistance results in increased insulin release and normal glucose tolerance. In an individual for whom the capacity to increase insulin release is compromised, increasing insulin resistance with partial or no beta-cell compensation results in progression from normal glucose tolerance, to impaired glucose tolerance (IGT), and finally to diabetes (T2D). Differences between these categories are small at high insulin sensitivity, which may be maintained by weight reduction, exercise, and certain drugs. At a critical degree of insulin resistance, due to obesity or other listed factors, only a further small increment in resistance requires a large increase in insulin output. Those that can increase insulin secretion to this extent retain normal glucose tolerance; those who cannot achieve this degree of insulin secretion (e.g., due to a mild defect in genes regulating insulin synthesis, insulin secretion, insulin action, or an ongoing immune destruction of beta cells) now unmask varying degrees of carbohydrate intolerance. The product of insulin sensitivity (the reciprocal of insulin resistance) and acute insulin response (a measurement beta-cell function) has been called the “disposition index.” This index remains constant in an individual with normal beta cell compensation in response to changes in insulin resistance. IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2D, type 2 diabetes.
The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue. Many people, however, have no symptoms during the first few years and are diagnosed on routine testing. A small number of people with type 2 diabetes mellitus can develop a hyperosmolar hyperglycemic state (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure).
Recognizing the symptoms of Type 1 diabetes is critical. Although Type 1 develops gradually, as the body’s insulin production decreases, blood glucose levels can become dangerously high once insulin production is outpaced. Symptoms may develop rapidly and can be mistaken for other illnesses such as the flu and a delayed diagnosis can have serious consequences.
Ketoacidosis, a condition due to starvation or uncontrolled diabetes, is common in Type I diabetes. Ketones are acid compounds that form in the blood when the body breaks down fats and proteins. Symptoms include abdominal pain, vomiting, rapid breathing, extreme lethargy, and drowsiness. Patients with ketoacidosis will also have a sweet breath odor. Left untreated, this condition can lead to coma and death.
Our bodies break down the foods we eat into glucose and other nutrients we need, which are then absorbed into the bloodstream from the gastrointestinal tract. The glucose level in the blood rises after a meal and triggers the pancreas to make the hormone insulin and release it into the bloodstream. But in people with diabetes, the body either can't make or can't respond to insulin properly.
The patient, physician, nurse, and dietician must carefully evaluate the patient's life style, nutritional needs, and ability to comply with the proposed dietary prescription. There are a variety of meal planning systems that can be used by the patient with diabetes; each has benefits and drawbacks that need to be evaluated in order to maximize compliance. Two of the most frequently used ones are the exchange system (see accompanying table) and the carbohydrate counting system.
The above tips are important for you. But it's also crucial to allow yourself time to cope with the diagnosis and commit to making lifestyle changes that will benefit you forever. The good news is the diabetes is a manageable disease; the tough part is that you must think about it daily. Consider finding support—someone that you can talk to about your struggles—be that a friend, another person with diabetes, or a loved one. This may seem trivial, but it truly can help you take control of diabetes so that it doesn't control you. Some next steps that may help you to get on the right track at this early stage in your journey:
There is no single gene that “causes” type 1 diabetes. Instead, there are a large number of inherited factors that may increase an individual’s likelihood of developing diabetes. This is known as multifactorial inheritance. The genes implicated in the development of type 1 diabetes mellitus control the human leukocyte antigen (HLA) system. This system is involved in the complex process of identifying cells which are a normal part of the body, and distinguishing them from foreign cells, such as those of bacteria or viruses. In an autoimmune disease such as diabetes mellitus, this system makes a mistake in identifying the normal ‘self’ cells as ‘foreign’, and attacks the body.
Diabetes is a metabolic disorder that occurs when your blood sugar (glucose), is too high (hyperglycemia). Glucose is what the body uses for energy, and the pancreas produces a hormone called insulin that helps convert the glucose from the food you eat into energy. When the body does not produce enough insulin - or does not produce any at all - the glucose does not reach your cells to be used for energy. This results in diabetes.
^ Jump up to: a b c d GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". The Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise. Intensive lifestyle measures may reduce the risk by over half. The benefit of exercise occurs regardless of the person's initial weight or subsequent weight loss. High levels of physical activity reduce the risk of diabetes by about 28%. Evidence for the benefit of dietary changes alone, however, is limited, with some evidence for a diet high in green leafy vegetables and some for limiting the intake of sugary drinks. In those with impaired glucose tolerance, diet and exercise either alone or in combination with metformin or acarbose may decrease the risk of developing diabetes. Lifestyle interventions are more effective than metformin. A 2017 review found that, long term, lifestyle changes decreased the risk by 28%, while medication does not reduce risk after withdrawal. While low vitamin D levels are associated with an increased risk of diabetes, correcting the levels by supplementing vitamin D3 does not improve that risk.
Say that two people have the same genetic mutation. One of them eats well, watches their cholesterol, and stays physically fit, and the other is overweight (BMI greater than 25) and inactive. The person who is overweight and inactive is much more likely to develop type 2 diabetes because certain lifestyle choices greatly influence how well your body uses insulin.
The diabetic patient should learn to recognize symptoms of low blood sugar (such as confusion, sweats, and palpitations) and high blood sugar (such as, polyuria and polydipsia). When either condition results in hospitalization, vital signs, weight, fluid intake, urine output, and caloric intake are accurately documented. Serum glucose and urine ketone levels are evaluated. Chronic management of DM is also based on periodic measurement of glycosylated hemoglobin levels (HbA1c). Elevated levels of HbA1c suggest poor long-term glucose control. The effects of diabetes on other body systems (such as cerebrovascular, coronary artery, and peripheral vascular) should be regularly assessed. Patients should be evaluated regularly for retinal disease and visual impairment and peripheral and autonomic nervous system abnormalities, e.g., loss of sensation in the feet. The patient is observed for signs and symptoms of diabetic neuropathy, e.g., numbness or pain in the hands and feet, decreased vibratory sense, footdrop, and neurogenic bladder. The urine is checked for microalbumin or overt protein losses, an early indication of nephropathy. The combination of peripheral neuropathy and peripheral arterial disease results in changes in the skin and microvasculature that lead to ulcer formation on the feet and lower legs with poor healing. Approx. 45,000 lower-extremity diabetic amputations are performed in the U.S. each year. Many amputees have a second amputation within five years. Most of these amputations are preventable with regular foot care and examinations. Diabetic patients and their providers should look for changes in sensation to touch and vibration, the integrity of pulses, capillary refill, and the skin. All injuries, cuts, and blisters should be treated promptly. The patient should avoid constricting hose, slippers, shoes, and bed linens or walking barefoot. The patient with ulcerated or insensitive feet is referred to a podiatrist for continuing foot care and is warned that decreased sensation can mask injuries.
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.
2. Home glucose monitoring using either a visually read test or a digital readout of the glucose concentration in a drop of blood. Patients can usually learn to use the necessary equipment and perform finger sticks. They keep a daily record of findings and are taught to adjust insulin dosage accordingly. More recent glucose monitoring devices can draw blood from other locations on the body, such as the forearm.
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Q. My 7yr has Diabetes. She been Diabetic for about 5 weeks and we can't get numbers at a good spot. she aether way to low (30- 60 scary when she gets like this) and to high (300 - 400) We been looking at what she eating calling the physician. he been play with here shots but nothing working. Its when she at school is were the nuber are mostly going up an down. we been trying to work with the school but she the only one in the hole school that has Diabetes. what to do ?
The classic symptoms of diabetes such as polyuria, polydypsia and polyphagia occur commonly in type 1 diabetes, which has a rapid development of severe hyperglycaemia and also in type 2 diabetes with very high levels of hyperglycaemia. Severe weight loss is common only in type 1 diabetes or if type 2 diabetes remains undetected for a long period. Unexplained weight loss, fatigue and restlessness and body pain are also common signs of undetected diabetes. Symptoms that are mild or have gradual development could also remain unnoticed.
The body’s immune system is responsible for fighting off foreign invaders, like harmful viruses and bacteria. In people with type 1 diabetes, the immune system mistakes the body’s own healthy cells for foreign invaders. The immune system attacks and destroys the insulin-producing beta cells in the pancreas. After these beta cells are destroyed, the body is unable to produce insulin.
A 2018 study suggested that three types should be abandoned as too simplistic. It classified diabetes into five subgroups, with what is typically described as type 1 and autoimmune late-onset diabetes categorized as one group, whereas type 2 encompasses four categories. This is hoped to improve diabetes treatment by tailoring it more specifically to the subgroups.
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Which came first: the diabetes or the PCOS? For many women, a diagnosis of polycystic ovary syndrome means a diabetes diagnosis isn’t far behind. PCOS and diabetes are both associated with insulin resistance, meaning there are similar hormonal issues at play in both diseases. Fortunately, managing your PCOS and losing weight may help reduce your risk of becoming diabetic over time.
A random blood sugar of greater than 11.1 mmol/l (200 mg/dl) in association with typical symptoms or a glycated hemoglobin (HbA1c) of ≥ 48 mmol/mol (≥ 6.5 DCCT %) is another method of diagnosing diabetes. In 2009 an International Expert Committee that included representatives of the American Diabetes Association (ADA), the International Diabetes Federation (IDF), and the European Association for the Study of Diabetes (EASD) recommended that a threshold of ≥ 48 mmol/mol (≥ 6.5 DCCT %) should be used to diagnose diabetes. This recommendation was adopted by the American Diabetes Association in 2010. Positive tests should be repeated unless the person presents with typical symptoms and blood sugars >11.1 mmol/l (>200 mg/dl).
There is an overall lack of public awareness of the signs and symptoms of type 1 diabetes. Making yourself aware of the signs and symptoms of type 1 diabetes is a great way to be proactive about your health and the health of your family members. If you notice any of these signs or symptoms, it’s possible that you have (or your child has) type 1 diabetes. A doctor can make that diagnosis by checking blood glucose levels.
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.
Hypoglycemia. Hypoglycemia or “insulin shock” is a common concern in DM management. It typically develops when a diabetic patient takes his or her normal dose of insulin without eating normally. As a result, the administered insulin can push the blood sugar to potentially dangerously low levels. Initially the patient may experience, sweating, nervousness, hunger and weakness. If the hypoglycemic patient is not promptly given sugar (sugar, cola, cake icing), he or she may lose consciousness and even lapse into coma. Questions and Answers about Diabetes and Your Mouth Q: If I have diabetes, will I develop the oral complications that were mentioned? A: It depends. There is a two-way relationship between your oral health and how well your blood sugar is controlled (glycemic control). Poor control of your blood sugar increases your risk of developing the multitude of complications associated with diabetes, including oral complications. Conversely, poor oral health interferes with proper glucose stabilization. Indeed, recent research has shown that diabetic patients who improve their oral health experience a modest improvement in their blood sugar levels. In essence, “Healthy mouths mean healthy bodies.” Q: What are the complications of diabetes therapy that can impact my oral health? A: One of the most worrisome urgent complications associated with diabetes management is the previously described hypoglycemia or insulin shock. In addition, many of the medications prescribed to treat diabetes and its complications, such as hypertension and heart disease, may induce adverse side effects affecting the mouth. Common side effects include dry mouth, taste aberrations, and mouth sores. Q: I have type-2 diabetes. Are my dental problems different than those experienced by people with type-1 diabetes? A: No. All patients with diabetes are at increased risk for the development of dental disease. What is different is that type-2 disease tends to progress more slowly than type-1 disease. Thus, most type-2 diabetes patients are diagnosed later in life, a time in which they are likely to already have existing dental problems. Remember, there is no dental disease unique to diabetes. Uncontrolled or poorly controlled diabetes simply compromises your body’s ability to control the existing disease.
To treat diabetic retinopathy, a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels. Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% retinopathy after 15 years of the disease. Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes.
The prognosis for a person with this health condition is estimated to be a life expectancy of 10 years less than a person without diabetes. However, good blood sugar control and taking steps to prevent complications is shortening this gap and people with the condition are living longer than ever before. It can be reversed with diligent attention to changing lifestyle behaviors.
The most common cause of acquired blindness in many developed nations, diabetic retinopathy is rare in the prepubertal child or within 5 years of onset of diabetes. The prevalence and severity of retinopathy increase with age and are greatest in patients whose diabetic control is poor.  Prevalence rates seem to be declining, yet an estimated 80% of people with type 1 diabetes mellitus develop retinopathy. 
Diabetes Mellitus Diabetes Mellitus Complications Diabetes Mellitus Control in Hospital Diabetes Mellitus Glucose Management Diabetes Resources Diabetes Sick Day Management Diabetic Ketoacidosis Diabetic Ketoacidosis Management in Adults Diabetic Ketoacidosis Management in Children Diabetic Ketoacidosis Related Cerebral Edema Hyperosmolar Hyperglycemic State Metabolic Syndrome Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus Type 2 Diabetes Mellitus in Children
A chronic metabolic disorder marked by hyperglycemia. DM results either from failure of the pancreas to produce insulin (type 1 DM) or from insulin resistance, with inadequate insulin secretion to sustain normal metabolism (type 2 DM). Either type of DM may damage blood vessels, nerves, kidneys, the retina, and the developing fetus and the placenta during pregnancy. Type 1 or insulin-dependent DM has a prevalence of just 0.3 to 0.4%. Type 2 DM (formerly called adult-onset DM) has a prevalence in the general population of 6.6%. In some populations (such as older persons, Native Americans, African Americans, Pacific Islanders, Mexican Americans), it is present in nearly 20% of adults. Type 2 DM primarily affects obese middle-aged people with sedentary lifestyles, whereas type 1 DM usually occurs in children, most of whom are active and thin, although extremely obese children are now being diagnosed with type 2 diabetes as well. See: table; dawn phenomenon; insulin; insulin pump; insulin resistance; diabetic polyneuropathy; Somogyi phenomenon
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.
Treatment of high blood pressure and high cholesterol levels, which can contribute to circulation problems, can help prevent some of the complications of diabetes as well. A low dose of aspirin taken daily is recommended in people with risk factors for heart disease. All people with diabetes who are between 40 and 75 years are given a statin (a drug to decrease cholesterol levels) regardless of cholesterol levels. Younger people with an elevated risk of heart disease should also take a statin .
Certain genetic markers have been shown to increase the risk of developing Type 1 diabetes. Type 2 diabetes is strongly familial, but it is only recently that some genes have been consistently associated with increased risk for Type 2 diabetes in certain populations. Both types of diabetes are complex diseases caused by mutations in more than one gene, as well as by environmental factors.
We give you special kudos for managing your condition, as it is not always easy. If you've had diabetes for a long time, it's normal to burn out sometimes. You may get tired of your day to day tasks, such as counting carbohydrates or measuring your blood sugar. Lean on a loved one or a friend for support, or consider talking to someone else who has diabetes who can provide, perhaps, an even more understanding ear or ideas that can help you.
Insulin is the hormone responsible for reducing blood sugar. In order for insulin to work, our tissues have to be sensitive to its action; otherwise, tissues become resistant and insulin struggles to clear out sugar from the blood. As insulin resistance sets in, the first organ to stop responding to insulin is the liver, followed by the muscles and eventually fat. How does insulin resistance begin? The root of the problem is our diet.
Most cases of diabetes involve many genes, with each being a small contributor to an increased probability of becoming a type 2 diabetic. If one identical twin has diabetes, the chance of the other developing diabetes within his lifetime is greater than 90%, while the rate for nonidentical siblings is 25–50%. As of 2011, more than 36 genes had been found that contribute to the risk of type 2 diabetes. All of these genes together still only account for 10% of the total heritable component of the disease. The TCF7L2 allele, for example, increases the risk of developing diabetes by 1.5 times and is the greatest risk of the common genetic variants. Most of the genes linked to diabetes are involved in beta cell functions.
Weight loss surgery in those with obesity and type two diabetes is often an effective measure. Many are able to maintain normal blood sugar levels with little or no medications following surgery and long-term mortality is decreased. There is, however, a short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.
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.