The notion is understandable. Blood sugar levels are high in diabetes, so a common idea has held that eating sugar somehow triggers the disease process. However, the major diabetes organizations take a different view. The American Diabetes Association1 and Diabetes UK2 have labelled this notion a “myth,” as has the Joslin Diabetes Center,3 which wrote, “Diabetes is not caused by eating too much sugar.” These and other organizations have worked to educate people about the causes of diabetes and the role that foods play in the disease process.


Because type 2 diabetes is linked to high levels of sugar in the blood, it may seem logical to assume that eating too much sugar is the cause of the disease. But of course, it’s not that simple. “This has been around for years, this idea that eating too much sugar causes diabetes — but the truth is, type 2 diabetes is a multifactorial disease with many different types of causes,” says Lynn Grieger, RDN, CDE, a nutrition coach in Prescott, Arizona, and a medical reviewer for Everyday Health. “Type 2 diabetes is really complex.”
What are symptoms of type 2 diabetes in children? Type 2 diabetes is becoming increasingly common in children, and this is linked to a rise in obesity. However, the condition can be difficult to detect in children because it develops gradually. Symptoms, treatment, and prevention of type 2 diabetes are similar in children and adults. Learn more here. Read now
Type 2 diabetes (T2D) is more common than type 1 diabetes with about 90 to 95 percent of people with diabetes having T2D. According to the Centers for Disease Control and Prevention’s report, 30.3 million Americans, or 9.4% of the US population have diabetes.1 More alarming, an estimated 84 million more American adults have prediabetes, which if not treated, will advance to diabetes within five years.1
Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.

Screening for undiagnosed T2DM is recommended at the first prenatal visit in women with above risk factors, using standard diagnostic method criteria. Screening for gestational diabetes (GDM) at 24-28 wk of gestation is recommended in women who do not have previous history of diabetes, as GDM remains asymptomatic11. A history of GDM carries a high risk for developing diabetes.
Type 2 diabetes typically starts with insulin resistance. That is, the cells of the body resist insulin’s efforts to escort glucose into the cells. What causes insulin resistance? It appears to be caused by an accumulation of microscopic fat particles within muscle and liver cells.4 This fat comes mainly from the diet—chicken fat, beef fat, cheese fat, fish fat, and even vegetable fat. To try to overcome insulin resistance, the pancreas produces extra insulin. When the pancreas can no longer keep up, blood sugar rises. The combination of insulin resistance and pancreatic cell failure leads to type 2 diabetes.
Diabetes is one of the first diseases described[21] with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine."[110] The first described cases are believed to be of type 1 diabetes.[110] Indian physicians around the same time identified the disease and classified it as madhumeha or honey urine noting that the urine would attract ants.[110] The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius Of Memphis.[110] The disease was rare during the time of the Roman empire with Galen commenting that he had only seen two cases during his career.[110]
Diabetes mellitus is linked with an increased risk of heart attacks, strokes, poor blood circulation to the legs and damage to the eyes, feet and kidneys. Early diagnosis and strict control of blood sugar, blood pressure and cholesterol levels can help to prevent or delay these complications associated with diabetes. Maintaining a healthy lifestyle (regular exercise, eating healthily and maintaining a healthy weight) is important in reducing the risk of developing type 2 diabetes.
A second oral agent of another class or insulin may be added if metformin is not sufficient after three months.[76] Other classes of medications include: sulfonylureas, thiazolidinediones, dipeptidyl peptidase-4 inhibitors, SGLT2 inhibitors, and glucagon-like peptide-1 analogs.[76] As of 2015 there was no significant difference between these agents.[76] A 2018 review found that SGLT2 inhibitors may be better than glucagon-like peptide-1 analogs or dipeptidyl peptidase-4 inhibitors.[92]
Scientists have done studies of twins to help estimate how important genes are in determining one's risk of developing diabetes. Identical twins have identical genes and thus the same genetic risk for a disease. Research has found that if one identical twin has type 1 diabetes, the chance that the other twin will get the disease is roughly 40 or 50 percent. For type 2 diabetes, that risk goes up to about 80 or 90 percent. This might suggest that genes play a bigger role in type 2 than in type 1, but that isn't necessarily so. Type 2 is far more common in the general population than type 1, which means that regardless of genetics both twins are more likely to develop type 2 diabetes.
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.
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.

There are many complications of diabetes. Knowing and understanding the signs of these complications is important. If caught early, some of these complications can be treated and prevented from getting worse. The best way to prevent complications of diabetes is to keep your blood sugars in good control. High glucose levels produce changes in the blood vessels themselves, as well as in blood cells (primarily erythrocytes) that impair blood flow to various organs.


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.
Elevated homocysteine levels in the blood called hyperhomocysteinemia, is a sign that the body isn't producing enough of the amino acid homocysteine. is a rare and serious condition that may be inherited (genetic). People with homocystinuria die at an early age. Symptoms of hyperhomocysteinemia include developmental delays, osteoporosis, blood clots, heart attack, heart disease, stroke, and visual abnormalities.
Get Educated: The American Diabetes Association advises that all persons with diabetes receive diabetes self-management education (DSME) at diagnosis and thereafter. A certified diabetes educator or other qualified health professional can give you the tools you need to understand and take care of your diabetes. In addition, these individuals are trained to create a customized plan that works for you. Diabetes self-management education is a patient-centered approach that enables patients to get involved in their care.
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.

Infections. Poorly controlled diabetes can lead to a variety of tissue infections. The most commonly encountered is a yeast infection (Candida) and the presence of dry mouth further increases one’s risk (see PATIENT INFORMATION SHEET – Oral Yeast Infections). Typically, affected areas appear redder than the surrounding tissue and commonly affected sites include the tongue, palate, cheeks, gums, or corners of the mouth (see Right). There is conflicting data regarding cavity risk in the diabetic patient, but those who have dry mouth are clearly at increased risk for developing cavities.


Assemble a Medical Team: Whether you've had diabetes for a long time or you've just been diagnosed, there are certain doctors that are important to see. It is extremely important to have a good primary care physician. This type of doctor will help coordinate appointments for other physicians if they think that you need it. Some primary physicians treat diabetes themselves, whereas others will recommend that you visit an endocrinologist for diabetes treatment. An endocrinologist is a person who specializes in diseases of the endocrine system, diabetes being one of them.
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.
Endocrinology A chronic condition which affects ±10% of the general population, characterized by ↑ serum glucose and a relative or absolute ↓ in pancreatic insulin production, or ↓ tissue responsiveness to insulin; if not properly controlled, the excess glucose damages blood vessels of the eyes, kidneys, nerves, heart Types Insulin dependent–type I and non-insulin dependent–type II diabetes Symptoms type 1 DM is associated with ↑ urine output, thirst, fatigue, and weight loss (despite an ↑ appetite), N&V; type 2 DM is associated with, in addition, non-healing ulcers, oral and bladder infections, blurred vision, paresthesias in the hands and feet, and itching Cardiovascular MI, stoke Eyes Retinal damage, blindness Legs/feet Nonhealing ulcers, cuts leading to gangrene and amputation Kidneys HTN, renal failure Neurology Paresthesias, neuropathy Diagnosis Serum glucose above cut-off points after meals or when fasting; once therapy is begun, serum levels of glycosylated Hb are measured periodically to assess adequacy of glucose control Management Therapy reflects type of DM; metformin and triglitazone have equal and additive effects on glycemic control Prognosis A function of stringency of glucose control and presence of complications. See ABCD Trial, Brittle diabetes, Bronze diabetes, Chemical diabetes, Gestational diabetes, Insulin-dependent diabetes, Metformin, MODY diabetes, Nephrogenic diabetes insipidus, Non-insulin-dependent diabetes mellitus, Pseudodiabetes, Secondary diabetes, Starvation diabetes, Troglitazone.

While there is a strong genetic component to developing this form of diabetes, there are other risk factors - the most significant of which is obesity. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes, and this holds true in children as well as adults. It is estimated that the chance to develop diabetes doubles for every 20% increase over desirable body weight.
DKA usually follows increasing hyperglycemia and symptoms of osmotic diuresis. Users of insulin pumps, by virtue of absent reservoirs of subcutaneous insulin, may present with ketosis and more normal blood glucose levels. They are more likely to present with nausea, vomiting, and abdominal pain, symptoms similar to food poisoning. DKA may manifest as respiratory distress.

It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.


Although the signs of diabetes can begin to show early, sometimes it takes a person a while to recognize the symptoms. This often makes it seem like signs and symptoms of diabetes appear suddenly. That’s why it’s important to pay attention to your body, rather than simply brushing them off. To that end, here are some type 1 and type 2 diabetes symptoms that you may want to watch out for:

Watch for thirst or a very dry mouth, frequent urination, vomiting, shortness of breath, fatigue and fruity-smelling breath. You can check your urine for excess ketones with an over-the-counter ketones test kit. If you have excess ketones in your urine, consult your doctor right away or seek emergency care. This condition is more common in people with type 1 diabetes but can sometimes occur in people with type 2 diabetes.
The blood glucose levels may jump after people eat foods they did not realize were high in carbohydrates. Emotional stress, an infection, and many drugs tend to increase blood glucose levels. Blood glucose levels increase in many people in the early morning hours because of the normal release of hormones (growth hormone and cortisol), a reaction called the dawn phenomenon. Blood glucose may shoot too high if the body releases certain hormones in response to low blood glucose levels (Somogyi effect). Exercise may cause the levels of glucose in the blood to fall low.
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Signs and symptoms of this life-threatening condition include a blood sugar reading higher than 600 mg/dL (33.3 mmol/L), dry mouth, extreme thirst, fever greater than 101 F (38 C), drowsiness, confusion, vision loss, hallucinations and dark urine. Your blood sugar monitor may not be able to give you an exact reading at such high levels and may instead just read "high."
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.

Originally described in approximately 30% of patients with type 1 diabetes mellitus, limited joint mobility occurs in 50% of patients older than age 10 years who have had diabetes for longer than 5 years. The condition restricts joint extension, making it difficult to press the hands flat against each other. The skin of patients with severe joint involvement has a thickened and waxy appearance.


Jump up ^ Pignone M, Alberts MJ, Colwell JA, Cushman M, Inzucchi SE, Mukherjee D, Rosenson RS, Williams CD, Wilson PW, Kirkman MS (June 2010). "Aspirin for primary prevention of cardiovascular events in people with diabetes: a position statement of the American Diabetes Association, a scientific statement of the American Heart Association, and an expert consensus document of the American College of Cardiology Foundation". Diabetes Care. 33 (6): 1395–402. doi:10.2337/dc10-0555. PMC 2875463. PMID 20508233.
This information is not designed to replace a physician's independent judgment about the appropriateness or risks of a procedure for a given patient. Always consult your doctor about your medical conditions. Vertical Health & EndocrineWeb do not provide medical advice, diagnosis or treatment. Use of this website is conditional upon your acceptance of our user agreement.
DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance
Jump up ^ McBrien, K; Rabi, DM; Campbell, N; Barnieh, L; Clement, F; Hemmelgarn, BR; Tonelli, M; Leiter, LA; Klarenbach, SW; Manns, BJ (6 August 2012). "Intensive and Standard Blood Pressure Targets in Patients With Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis". Archives of Internal Medicine. 172 (17): 1–8. doi:10.1001/archinternmed.2012.3147. PMID 22868819.
Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.
Weight fluctuations also fall under the umbrella of possible diabetes signs and symptoms. When you lose sugar through frequent urination, you also lose calories. At the same time, diabetes may keep the sugar from your food from reaching your cells — leading to constant hunger. The combined effect is potentially rapid weight loss, especially if you have type 1 diabetes.
Information on mortality rates for type 1 diabetes mellitus is difficult to ascertain without complete national registers of childhood diabetes, although age-specific mortality is probably double that of the general population. [35, 36] Children aged 1-4 years are particularly at risk and may die due to DKA at the time of diagnosis. Adolescents are also a high-risk group. Most deaths result from delayed diagnosis or neglected treatment and subsequent cerebral edema during treatment for DKA, although untreated hypoglycemia also causes some deaths. Unexplained death during sleep may also occur and appears more likely to affect young males. [37]
The good news is that if you have diabetes, you have a great amount of control in managing your disease. Although it can be difficult to manage a disease on a daily basis, the resources and support for people with diabetes is endless. It's important for you to receive as much education as possible so that you can take advantage of all the good information that is out there (and weed out the bad).
If you have type 2 diabetes and your body mass index (BMI) is greater than 35, you may be a candidate for weight-loss surgery (bariatric surgery). Blood sugar levels return to normal in 55 to 95 percent of people with diabetes, depending on the procedure performed. Surgeries that bypass a portion of the small intestine have more of an effect on blood sugar levels than do other weight-loss surgeries.
Is it your fault for getting type 2 diabetes? No – type 2 diabetes is not a personal failing. It develops through a combination of factors that are still being uncovered and better understood. Lifestyle (food, exercise, stress, sleep) certainly plays a major role, but genetics play a significant role as well. Type 2 diabetes is often described in the media as a result of being overweight, but the relationship is not that simple. Many overweight individuals never get type 2, and some people with type 2 were never overweight, (although obesity is probably an underlying cause of insulin resistance). To make matters worse, when someone gains weight (for whatever reason), the body makes it extremely difficult to lose the new weight and keep it off. If it were just a matter of choice or a bit of willpower, we would probably all be skinny. At its core, type 2 involves two physiological issues: resistance to the insulin made by the person’s beta cells and too little insulin production relative to the amount one needs.
All children with type 1 diabetes mellitus require insulin therapy. Most require 2 or more injections of insulin daily, with doses adjusted on the basis of self-monitoring of blood glucose levels. Insulin replacement is accomplished by giving a basal insulin and a preprandial (premeal) insulin. The basal insulin is either long-acting (glargine or detemir) or intermediate-acting (NPH). The preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-acting (regular).
Diabetes is a condition in which the body cannot properly store and use fuel for energy. The body's main fuel is a form of sugar called glucose, which comes from food (after it has been broken down). Glucose enters the blood and is used by cells for energy. To use glucose, the body needs a hormone called insulin that's made by the pancreas. Insulin is important because it allows glucose to leave the blood and enter the body's cells.
Doctors and people with diabetes have observed that infections seem more common if you have diabetes. Research in this area, however, has not proved whether this is entirely true, nor why. It may be that high levels of blood sugar impair your body's natural healing process and your ability to fight infections. For women, bladder and vaginal infections are especially common.
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin.[38] It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were found in children.[citation needed]
All types of diabetes mellitus have something in common. Normally, your body breaks down the sugars and carbohydrates you eat into a special sugar called glucose. Glucose fuels the cells in your body. But the cells need insulin, a hormone, in your bloodstream in order to take in the glucose and use it for energy. With diabetes mellitus, either your body doesn't make enough insulin, it can't use the insulin it does produce, or a combination of both.
Merck & Co., Inc., Kenilworth, NJ, USA is a global healthcare leader working to help the world be well. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Merck Manual was first published in 1899 as a service to the community. The legacy of this great resource continues as the Merck Manual in the US and Canada and the MSD Manual outside of North America. Learn more about our commitment to Global Medical Knowledge.
Patients with type 1 diabetes require life-long treatment with exogenous (artificial) insulin to regulate their blood sugar levels. This insulin may be given through the use of a hypodermic needle (seen right), or other methods such as the use of an insulin pump. Over time, many patients suffer chronic complications: vascular, neurological and organ-specific (such as kidney and eye disease). The frequency and severity of these complications is related to duration that the patient has suffered the disease for, and by how well their blood sugar levels have been controlled. If blood sugar levels, blood pressure and lipids are tightly controlled, many complications of diabetes may be prevented. Some patients may develop the major emergency complication of diabetes, known as ketoacidosis (extremely high blood glucose levels accompanied with extremely low insulin levels), which has a mortality rate of 5-10%.
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.
Jump up ^ Seida, Jennifer C.; Mitri, Joanna; Colmers, Isabelle N.; Majumdar, Sumit R.; Davidson, Mayer B.; Edwards, Alun L.; Hanley, David A.; Pittas, Anastassios G.; Tjosvold, Lisa; Johnson, Jeffrey A. (Oct 2014). "Effect of Vitamin D3 Supplementation on Improving Glucose Homeostasis and Preventing Diabetes: A Systematic Review and Meta-Analysis". The Journal of Clinical Endocrinology & Metabolism. 99 (10): 3551–60. doi:10.1210/jc.2014-2136. PMC 4483466. PMID 25062463.
While it's conceivable that scientists will isolate a single factor as causing type 1 and type 2, the much more likely outcome is that there is more than one cause. Each person seems to take a unique path in developing diabetes. Someday, doctors may be able to assess an individual's genetic risk for diabetes, allowing him or her to dodge the particular environmental factors that would trigger the disease. And perhaps if the baffling question of why a person gets diabetes can be put to rest, the answer will also offer a cure for the disease.
Commonly, diabetic patients’ random blood glucose measurement will be greater than 200 mg/dL. Additionally, diabetic patients’ urinalysis will be positive for greater than 30 mg/g of microalbumin on at least two of three consecutive sampling dates. Type 2 diabetics who have had diabetes mellitus for more than 2 years will usually have a fasting C-peptide level greater than 1.0 ng/dL. Patients with type 1 diabetes will have islet cell and anti-insulin autoantibodies present in their blood within 6 months of diagnosis. These antibodies, though, usually fade after 6 months.
Scientists have done studies of twins to help estimate how important genes are in determining one's risk of developing diabetes. Identical twins have identical genes and thus the same genetic risk for a disease. Research has found that if one identical twin has type 1 diabetes, the chance that the other twin will get the disease is roughly 40 or 50 percent. For type 2 diabetes, that risk goes up to about 80 or 90 percent. This might suggest that genes play a bigger role in type 2 than in type 1, but that isn't necessarily so. Type 2 is far more common in the general population than type 1, which means that regardless of genetics both twins are more likely to develop type 2 diabetes.
Type 1 diabetes in pediatric patients has been linked to changes in cognition and brain structure, with a study by Siller et al finding lower volume in the left temporal-parietal-occipital cortex in young patients with type 1 diabetes than in controls. The study also indicated that in pediatric patients, higher severity of type 1 diabetes presentation correlates with greater structural differences in the brain at about 3 months following diagnosis. The investigators found that among study patients with type 1 diabetes, an association existed between the presence of diabetic ketoacidosis at presentation and reduced radial, axial, and mean diffusivity in the major white matter tracts on magnetic resonance imaging (MRI). In those with higher glycated hemoglobin (HbA1c) levels, hippocampal, thalamic, and cerebellar white matter volumes were lower, as was right posterior parietal cortical thickness, while right occipital cortical thickness was greater. Patients in the study were aged 7-17 years. [43]
Long-term complications arise from the damaging effects of prolonged hyperglycemia and other metabolic consequences of insulin deficiency on various tissues. Although long-term complications are rare in childhood, maintaining good control of diabetes is important to prevent complications from developing in later life. [39] The likelihood of developing complications appears to depend on the interaction of factors such as metabolic control, genetic susceptibility, lifestyle (eg, smoking, diet, exercise), pubertal status, and gender. [40, 41] Long-term complications include the following:
1. Monitoring of blood glucose status. In the past, urine testing was an integral part of the management of diabetes, but it has largely been replaced in recent years by self monitoring of blood glucose. Reasons for this are that blood testing is more accurate, glucose in the urine shows up only after the blood sugar level is high, and individual renal thresholds vary greatly and can change when certain medications are taken. As a person grows older and the kidney is less able to eliminate sugar in the urine, the renal threshold rises and less sugar is spilled into the urine. The position statement of the American Diabetes Association on Tests of Glycemia in Diabetes notes that urine testing still plays a role in monitoring in type 1 and gestational diabetes, and in pregnancy with pre-existing diabetes, as a way to test for ketones. All people with diabetes should test for ketones during times of acute illness or stress and when blood glucose levels are consistently elevated.
It is important to record blood glucose readings taken at different times of the day – after fasting (before breakfast) as well as 2 hours after a meal. This allows your doctor to see a snapshot of how your blood glucose levels vary during the day and to recommend treatments accordingly. Most blood glucose meters now have "memory" that stores a number of blood glucose tests along with the time and date they were taken. Some even allow for graphs and charts of the results to be created and sent to your phone.
DM is a strong independent predictor of short- and long-term recurrent ischemic events, including mortality, in acute coronary syndrome (ACS),6,7 including unstable angina and non-ST-elevation MI (NSTEMI),8 ST-elevation MI (STEMI) treated medically,9 and ACS undergoing percutaneous coronary intervention (PCI).10,11 Furthermore, the concomitant presence of cardiovascular risk factors and comorbidities that negatively affect the outcomes of ACS is higher in DM patients.12
The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation of diabetes with other diseases, and he discussed differential diagnosis from the snakebite which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.[110]
Beta cells are vulnerable to more than just bad genes, which may explain the associations between type 2 diabetes and environmental factors that aren't related to how much fat a body has or where it is stored. Beta cells carry vitamin D receptors on their surface, and people with vitamin D deficiency are at increased risk for type 2. Plus, several studies have shown that people with higher levels of toxic substances in their blood—such as from the PCBs found in fish fat—are at increased risk of type 2 diabetes, though a cause-and-effect relationship hasn't been proved. (Toxic substances and vitamin D have also been implicated in type 1 diabetes, but the disease mechanism may be unrelated to what's going on in type 2.)
Insulin is essential to process carbohydrates, fat, and protein. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and by stimulating the conversion of glucose to glycogen (glycogenesis) as a carbohydrate store. Insulin also inhibits the release of stored glucose from liver glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides, free fatty acids, and ketones. It also stimulates fat storage. Additionally, insulin inhibits the breakdown of protein and fat for glucose production (gluconeogenesis) in the liver and kidneys.
Scientists have done studies of twins to help estimate how important genes are in determining one's risk of developing diabetes. Identical twins have identical genes and thus the same genetic risk for a disease. Research has found that if one identical twin has type 1 diabetes, the chance that the other twin will get the disease is roughly 40 or 50 percent. For type 2 diabetes, that risk goes up to about 80 or 90 percent. This might suggest that genes play a bigger role in type 2 than in type 1, but that isn't necessarily so. Type 2 is far more common in the general population than type 1, which means that regardless of genetics both twins are more likely to develop type 2 diabetes.

Diagnosis. The most common diagnostic tests for diabetes are chemical analyses of the blood such as the fasting plasma glucose. Capillary blood glucose monitoring can be used for screening large segments of the population. Portable equipment is available and only one drop of blood from the fingertip or earlobe is necessary. Capillary blood glucose levels have largely replaced analysis of the urine for glucose. Testing for urinary glucose can be problematic as the patient may have a high renal threshold, which would lead to a negative reading for urinary glucose when in fact the blood glucose level was high.

The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.[123]
Since cardiovascular disease is a serious complication associated with diabetes, some have recommended blood pressure levels below 130/80 mmHg.[89] However, evidence supports less than or equal to somewhere between 140/90 mmHg to 160/100 mmHg; the only additional benefit found for blood pressure targets beneath this range was an isolated decrease in stroke risk, and this was accompanied by an increased risk of other serious adverse events.[90][91] A 2016 review found potential harm to treating lower than 140 mmHg.[92] Among medications that lower blood pressure, angiotensin converting enzyme inhibitors (ACEIs) improve outcomes in those with DM while the similar medications angiotensin receptor blockers (ARBs) do not.[93] Aspirin is also recommended for people with cardiovascular problems, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes.[94]
Periodontal Disease. Periodontal disease is a commonly observed dental problem for patients with diabetes. It is similar to the periodontal disease encountered among nondiabetic patients. However, as a consequence of the impaired immunity and healing associated with diabetes, it may be more severe and progress more rapidly (see Right). The potential for these changes points to the need for periodic professional evaluation and treatment.
Type 2 diabetes is usually associated with being overweight (BMI greater than 25), and is harder to control when food choices are not adjusted, and you get no physical activity. And while it’s true that too much body fat and physical inactivity (being sedentary) does increase the likelihood of developing type 2, even people who are fit and trim can develop this type of diabetes.2,3
It's not as clear what the rest of the type 1 genes are up to, but researchers are eager to find out. "Even though something accounts for a small part [of the genetic risk], it could have a significant impact," says Stephen Rich, PhD, director of the Center for Public Health Genomics at the University of Virginia School of Medicine. Understanding these genes' role may clue researchers in to less obvious biological pathways involved in type 1 diabetes, and to possible prevention strategies.
In the exchange system, foods are divided into six food groups (starch, meat, vegetable, fruit, milk, and fat) and the patient is taught to select items from each food group as ordered. Items in each group may be exchanged for each other in specified portions. The patient should avoid concentrated sweets and should increase fiber in the diet. Special dietetic foods are not necessary. Patient teaching should emphasize that a diabetic diet is a healthy diet that all members of the family can follow.
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.
×