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|Diabetes type 1|
|Classification and external resources|
A blue circle symbol for diabetes.
Diabetes mellitus type 1 (also known as type 1 diabetes, or T1DM; formerly insulin dependent diabetes or juvenile diabetes) is a form of diabetes mellitus that results from autoimmune destruction of insulin-producing beta cells of the pancreas. The subsequent lack of insulin leads to increased blood and urine glucose. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.
Incidence varies from 8 to 17 per 100,000 in Northern Europe and the U.S. with a high of about 35 per 100,000 in Scandinavia to a low of 1 per 100,000 in Japan and China.
Eventually, type 1 diabetes is fatal unless treated with insulin. Injection is the most common method of administering insulin, although another method is insulin pumps. Other alternatives are Pancreatic transplants that have been used, as well as pancreatic islet cell transplantation. Transplantation is experimental yet growing.
Most people who develop type 1 are otherwise healthy. Although the cause of type 1 diabetes is still not fully understood, it is believed to be of immunological origin.
Type 1 treatment must be continued indefinitely in all cases. Treatment should not significantly impair normal activities but can be done adequately if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken. However, treatment remains quite burdensome for many people. Complications may be associated with both low blood sugar and high blood sugar, both largely due to the nonphysiological manner in which insulin is replaced. Low blood sugar may lead to seizures or episodes of unconsciousness, and requires emergency treatment. High blood sugar may lead to increased fatigue and can also result in long-term damage to organs.
Signs and symptoms 
The classical symptoms of type 1 diabetes include: polyuria (frequent urination), polydipsia (increased thirst), Xerostomia (dry mouth), polyphagia (increased hunger), fatigue, and weight loss. Type 1 diabetics are often first diagnosed when they present with diabetic ketoacidosis. These symptoms could be xeroderma (dry skin), rapid deep breathing, drowsiness, abdominal pain, and vomiting.
Type 1 diabetes is a polygenic disease, meaning many different genes contribute to its onset. Depending on locus or combination of loci, it can be dominant, recessive, or somewhere in between. The strongest gene, IDDM1, is located in the MHC Class II region on chromosome 6, at staining region 6p21. Certain variants of this gene increase the risk for decreased histocompatibility characteristic of type 1. Such variants include DRB1 0401, DRB1 0402, DRB1 0405, DQA 0301, DQB1 0302 and DQB1 0201, which are common in North Americans of European ancestry and in Europeans. Some variants also appear to be protective.
The risk of a child developing type 1 diabetes is about 10% if the father has it, about 10% if a sibling has it, about 4% if the mother has type 1 diabetes and was aged 25 or younger when the child was born, and about 1% if the mother was over 25 years old when the child was born.
Environmental factors can influence expression of type 1. For identical twins, when one twin had type 1 diabetes, the other twin only had it 30%–50% of the time. Despite having exactly the same genome, one twin had the disease, where the other did not; this suggests environmental factors, in addition to genetic factors, can influence disease prevalence. Other indications of environmental influence include the presence of a 10-fold difference in occurrence among Caucasians living in different areas of Europe, and a tendency to acquire the incidence of the disease of the destination country for people who migrate.
One theory, discussed by DeLisa Fairweather and Noel R. Rose, among others, proposes that type 1 diabetes is a virus-triggered autoimmune response in which the immune system attacks virus-infected cells along with the beta cells in the pancreas. The Coxsackie virus family or rubella is implicated, although the evidence is inconclusive. In type 1, pancreatic beta cells in the islets of Langerhans are destroyed, decreasing endogenous insulin production. This distinguishes type 1's origin from type 2. The type of diabetes a patient has is determined only by the cause—fundamentally by whether the patient is insulin resistant (type 2) or insulin deficient without insulin resistance (type 1).
This vulnerability is not shared by everyone, for not everyone infected by the suspected virus develops type 1 diabetes. This has suggested presence of a genetic vulnerability and there is indeed an observed inherited tendency to develop type 1. It has been traced to particular HLA genotypes, though the connection between them and the triggering of an autoimmune reaction is still poorly understood.
Some researchers believe the autoimmune response is influenced by antibodies against cow's milk proteins. No connection has been established between autoantibodies, antibodies to cow's milk proteins, and type 1 diabetes. A subtype of type 1 (identifiable by the presence of antibodies against beta cells) typically develops slowly, so is often confused with type 2. In addition, a small proportion of type 2 cases manifest a genetic form of the disease called maturity onset diabetes of the young.
Vitamin D in doses of 2000 IU per day given during the first year of a child's life has been connected in one study in northern Finland (where intrinsic production of Vitamin D is low due to low natural light levels) with an 80% reduction in the risk of getting type 1 diabetes later in life. The causal connection, if any, is obscure.
Chemicals and drugs 
Some chemicals and drugs preferentially destroy pancreatic cells. Pyrinuron (Vacor, N-3-pyridylmethyl-N'-p-nitrophenyl urea), a rodenticide introduced in the United States in 1976, selectively destroys pancreatic beta cells, resulting in type 1 diabetes after accidental or intentional ingestion. Vacor was withdrawn from the U.S. market in 1979, but is still used in some countries. Zanosar is the trade name for streptozotocin, an antibiotic and antineoplastic agent used in chemotherapy for pancreatic cancer; it also kills beta cells, resulting in loss of insulin production. Other pancreatic problems, including trauma, pancreatitis or tumors (either malignant or benign), can also lead to loss of insulin production.
The pathophysiology in diabetes type 1 is basically a destruction of beta cells in the pancreas, regardless of which risk factors or causative entities have been present.
Individual risk factors can have separate pathophysiological processes to, in turn, cause this beta cell destruction. Still, a process that appears to be common to most risk factors is an autoimmune response towards beta cells, involving an expansion of autoreactive CD4+ T helper cells and CD8+ T cells, autoantibody-producing B cells and activation of the innate immune system.
|Condition||2 hour glucose||Fasting glucose||HbA1c|
|Normal||<7.8 (<140)||<6.1 (<110)||<6.0|
|Impaired fasting glycaemia||<7.8 (<140)||≥ 6.1(≥110) & <7.0(<126)||6.0–6.4|
|Impaired glucose tolerance||≥7.8 (≥140)||<7.0 (<126)||6.0–6.4|
|Diabetes mellitus||≥11.1 (≥200)||≥7.0 (≥126)||≥6.5|
Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:
- Fasting plasma glucose level at or above 7.0 mmol/L (126 mg/dL).
- Plasma glucose at or above 11.1 mmol/L (200 mg/dL) two hours after a 75 g oral glucose load as in a glucose tolerance test.
- Symptoms of hyperglycemia and casual plasma glucose at or above 11.1 mmol/L (200 mg/dL).
- Glycated hemoglobin (hemoglobin A1C) at or above 6.5. (This criterion was recommended by the American Diabetes Association in 2010, although it has yet to be adopted by the WHO.)
About a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis (a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids) by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening, detection of hyperglycemia during other medical investigations, and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that may be caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.
A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/L) is considered diagnostic for diabetes mellitus.
Patients with fasting glucose levels from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) are considered to have impaired fasting glucose. Patients with plasma glucose at or above 140 mg/dL (7.8 mmol/L), but not over 200 mg/dL (11.1 mmol/L), two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus and cardiovascular disease.
The appearance of diabetes-related autoantibodies has been shown to be able to predict the appearance of diabetes type 1 before any hyperglycemia arises, the main ones being islet cell autoantibodies, insulin autoantibodies, autoantibodies targeting the 65-kDa isoform of glutamic acid decarboxylase (GAD) and autoantibodies targeting the phosphatase-related IA-2 molecule. By definition, the diagnosis of diabetes type 1 can be made first at the appearance of clinical symptoms and/or signs, but the emergence of autoantibodies may itself be termed "latent autoimmune diabetes". Not everyone with autoantibodies progresses to diabetes type 1, but the risk increases with the number of antibody types, with three to four antibody types giving a risk of progressing to diabetes type 1 of 60%–100%. The time interval from emergence of autoantibodies to frank diabetes type 1 can be a few months in infants and young children, but in some people it may take years – in some cases more than 10 years. Islet cell autoantibodies are detected by conventional immunofluorescence, while the rest are measured with specific radiobinding assays.
Immunosuppressive drugs 
Cyclosporine A, an immunosuppressive agent, has apparently halted destruction of beta cells (on the basis of reduced insulin usage), but its nephrotoxicity and other side effects make it highly inappropriate for long-term use.
Anti-CD3 antibodies, including teplizumab and otelixizumab, had suggested evidence of preserving insulin production (as evidenced by sustained C-peptide production) in newly diagnosed type 1 diabetes patients. A probable mechanism of this effect was believed to be preservation of regulatory T cells that suppress activation of the immune system and thereby maintain immune system homeostasis and tolerance to self-antigens. The duration of the effect is still unknown, however. In 2011, Phase III studies with otelixizumab and teplizumab both failed to show clinical efficacy, potentially due to an insufficient dosing schedule.
An anti-CD20 antibody, rituximab, inhibits B cells and has been shown to provoke C-peptide responses three months after diagnosis of type 1 diabetes, but long-term effects of this have not been reported.
Some research has suggested breastfeeding decreases the risk in later life; various other nutritional risk factors are being studied, but no firm evidence has been found. Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes, though the causal relationship is obscure.
Children with antibodies to beta cell proteins (i.e. at early stages of an immune reaction to them) but no overt diabetes, and treated with vitamin B3 (niacin), had less than half the diabetes onset incidence in a seven-year time span than did the general population, and an even lower incidence relative to those with antibodies as above, but who received no vitamin B3.
Insulin therapy 
Type 1 is treated with insulin replacement therapy—either via subcutaneous injection or insulin pump, from companies such as medtronics, along with attention to dietary management, typically including carbohydrate tracking, and careful monitoring of blood glucose levels using glucose meters. Today, the most common insulins are biosynthetic products produced using genetic recombination techniques; formerly, cattle or pig insulins were used, and even sometimes insulin from fish. Major global suppliers include Eli Lilly and Company, Novo Nordisk, and Sanofi-Aventis. A more recent trend, from several suppliers, is insulin analogs which are slightly modified insulins with different onset or duration of action times.
Untreated type 1 diabetes commonly leads to coma, often from diabetic ketoacidosis, which is fatal if untreated. Ketoacidosis causes cerebral edema (accumulation of liquid in the brain). This complication is very life-threatening; it makes ketoacidosis the most common cause of death in pediatric diabetes.
Continuous glucose monitors have been developed and marketed which can alert patients to the presence of dangerously high or low blood sugar levels, but technical limitations have limited the impact these devices have had on clinical practice so far.
Treatment of diabetes focuses on lowering blood sugar or glucose (BG) to the near normal range, approximately 80–140 mg/dl (4.4–7.8 mmol/L). The ultimate goal of normalizing BG is to avoid long-term complications that affect the nervous system (e.g. peripheral neuropathy leading to pain and/or loss of feeling in the extremities), and the cardiovascular system (e.g. heart attacks, vision loss). People with type 1 diabetes always need to use insulin, but treatment can lead to low BG (hypoglycemia), i.e. BG less than 70 mg/dl (3.9 mmol/l). Hypoglycemia is a very common occurrence in people with diabetes, usually the result of a mismatch in the balance among insulin, food and physical activity, although the nonphysiological method of delivery also plays a role.
Pancreas transplantation 
In more extreme cases, a pancreas transplant can restore proper glucose regulation. However, the surgery and accompanying immunosuppression required is considered by many physicians to be more dangerous than continued insulin replacement therapy, so is generally only used with or some time after a kidney transplant. One reason for this is that introducing a new kidney requires taking immunosuppressive drugs such as cyclosporine. Nevertheless this allows the introduction of a new, functioning pancreas to a patient with diabetes without any additional immunosuppressive therapy. However, pancreas transplants alone can be wise in patients with extremely labile type 1 diabetes mellitus.
Islet cell transplantation 
Experimental replacement of beta cells (by transplant or from stem cells) is being investigated in several research programs. Islet cell transplantation is less invasive than a pancreas transplant, which is currently the most commonly used approach in humans.
In one variant of this procedure, islet cells are injected into the patient's liver, where they take up residence and begin to produce insulin. The liver is expected to be the most reasonable choice because it is more accessible than the pancreas, and islet cells seem to produce insulin well in that environment. The patient's body, however, will treat the new cells just as it would any other introduction of foreign tissue, unless a method is developed to produce them from the patient's own stem cells or an identical twin is available who can donate stem cells. The immune system will attack the cells as it would a bacterial infection or a skin graft. Thus, patients now also need to undergo treatment involving immunosuppressants, which reduce immune system activity.
Recent studies have shown islet cell transplants have progressed to the point where 58% of the patients in one study were insulin-independent one year after transplantion. Scientists in New Zealand with Living Cell Technologies are currently in human trials with Diabecell, placing pig islets within a protective capsule derived of seaweed which enables insulin to flow out and nutrients to flow in, while protecting the islets from immune system attack via white blood cells.
Stem Cell Educator Therapy 
Stem Cell Educator Therapy induces immune balance by using cord blood-derived multipotent stem cells with embryonic and hematopoietic characteristics. A closed-loop system that circulates a patient's blood through a blood cell separator, briefly co-cultures the patient's lymphocytes with adherent cord blood stem cells in vitro, and returns the educated lymphocytes (but not the cord blood stem cells) to the patient's circulation. Through the Stem Cell Education process the patient's lymphocytes are modified by the Autoimmune Regulator AIRE that activates certain genes due to contact with the cord blood stem cells.
The clinical trial (NCT01350219) reveals that a single treatment with the Stem Cell Educator provides lasting reversal of autoimmunity that allows improvement of metabolic control in subjects with long-standing type 1 diabetes. The on-going phase II clinical study about Stem Cell Educator Therapy has proved 100% effectiveness in type 1 diabetics, even in patients who lost the ability to produce their own insulin (C-peptide < 0,01 µg/l before treatment).
After treatment, the increased expression of co-stimulating molecules (specifically, CD28 and ICOS), increases in the number of CD4+CD25+Foxp3+ Tregs, and restoration of Th1/Th2/Th3 cytokine balance indicate this therapy reverses autoimmunity, induces tolerance and promotes regeneration of islet beta cells without showing any adverse effects so far.
Successful immune modulation by cord blood stem cells and the resulting clinical improvement in patient status may have important implications for other autoimmune diseases but does not raise any safety or ethical issues.
Psychological effects 
Depression and depressive symptoms are generally more common in people living with Type 1 Diabetes. One review article suggested that the prevalence rate of depression is more than three times higher in diabetics than non-diabetics; an average prevalence of 12% was found (range of 5.8–43.4% in studies reviewed) Women with Type 1 Diabetes are more likely to be depressed than men with Type 1 Diabetes, and an increased incidence of depression has also been associated with youth with Type 1 Diabetes. According to the Canadian Diabetes Association, 15% of people living with Diabetes have major depression. Psychological distress is also reported in the parents of youth with Type 1 Diabetes. Recent evidence has suggested that reduced pre-frontal cortical thickness is associated with depression in people with Type 1 Diabetes. These neurological changes may be caused by long-term reduced glycemic control and may increase risk of depression.
Eating Disorders 
Recent research has found that eating disorders are more common in females with Type 1 Diabetes (prevalence = 10.15%) than in females without it (prevalence = 4.5%), as were sub-threshold eating disorders (13.8% vs. 7.6%) Some participants (11.0%) in the same study reported manipulating insulin dosages to promote weight loss. Higher blood-sugar levels are associated with polyuria and reduced appetite, which can result in weight loss. Similarly, mean hemoglobin A1c levels were higher in participant with a DSM-IV disorder (9.4%) than those without (8.6%). This behavior was reported by 42% of participant who had a DSM-IV disorder.
The disorder of omission of insulin for weight control has been named diabulimia, a portmanteau of diabetes and bulimia, although it is not currently recognized as a formal diagnosis in the medical community.
Social Cognition and Self-Care 
Results from recent research suggest that people with Type 1 Diabetes may neglect precise self-care due to social fear related to fear of hypoglycemia. Type 1 Diabetics may also neglect physical activity due to reduced perceived position effects as well as increased perceived negative aspects of that activity.
Complications of poorly managed type 1 diabetes mellitus may include cardiovascular disease, diabetic neuropathy, and diabetic retinopathy, among others. However, cardiovascular disease as well as neuropathy may have an autoimmune basis, as well.
Studies conducted in the United States and Europe showed that drivers with type 1 diabetes had twice as many collisions as their nondiabetic spouses, demonstrating the increased risk of driving collisions in the type 1 diabetes population. Diabetes can compromise driving safety in several ways. First, long-term complications of diabetes can interfere with the safe operation of a vehicle. For example, diabetic retinopathy (loss of peripheral vision or visual acuity), or peripheral neuropathy (loss of feeling in the feet) can impair a driver’s ability to read street signs, control the speed of the vehicle, apply appropriate pressure to the brakes, etc.
Second, hypoglycemia can affect a person’s thinking processes, coordination, and state of consciousness. This disruption in brain functioning, neuroglycopenia, can impair driving ability. A study involving people with type 1 diabetes found that individuals reporting two or more hypoglycemia-related driving mishaps differ physiologically and behaviorally from their counterparts who report no such mishaps. For example, during hypoglycemia, drivers who had two or more mishaps reported fewer warning symptoms, their driving was more impaired, and their body released less epinephrine (a hormone that helps raise BG). Additionally, individuals with a history of hypoglycemia-related driving mishaps appear to use sugar at a faster rate and are relatively slower at processing information. These findings indicate that although anyone with type 1 diabetes may be at some risk of experiencing disruptive hypoglycemia while driving, there is a subgroup of type 1 drivers who are more vulnerable to such events.
Given the above research findings, drivers with type 1 diabetes and a history of driving mishaps are recommended to never drive when their BG is less than 70 mg/dl. Instead, these drivers are advised to treat hypoglycemia and delay driving until their BG is above 90 mg/dl. Such drivers should also learn as much as possible about what causes their hypoglycemia, and use this information to avoid future hypoglycemia while driving.
Studies funded by the National Institutes of Health (NIH) have demonstrated that face-to-face training programs designed to help individuals with type 1 diabetes better anticipate, detect, and prevent extreme BG can reduce the occurrence of future hypoglycemia-related driving mishaps. An internet-version of this training has also been shown to have significant beneficial results. Additional NIH funded research to develop internet interventions specifically to help improve driving safety in drivers with type 1 diabetes is currently underway.
Type 1 diabetes causes an estimated 5–10% of all diabetes cases or 11–22 million worldwide. In 2006 it affected 440,000 children under 14 years of age and was the primary cause of diabetes in those less than 10 years of age. The incidence of type 1 diabetes has been increasing by about 3% per year.
Rates vary widely by country. In Finland, the incidence is a high of 35 per 100,000 per year, in Japan and China a low of 1 to 3 per 100,000 per year, and in Northern Europe and the U.S., an intermediate of 8 to 17 per 100,000 per year.
Type 1 diabetes was previously known as juvenile diabetes to distinguish it from type 2 diabetes, which generally has a later onset; however, the majority of new-onset type 1 diabetes is seen in adults. Studies using antibody testing (glutamic acid decarboxylase antibodies, islet cell antibodies, and insulinoma-associated autoantibodies) to distinguish between type 1 and type 2 diabetes demonstrate that most new-onset type 1 diabetes is seen in adults. Adult-onset type 1 autoimmune diabetes is two to three times more common than classic childhood-onset autoimmune diabetes.
In the US in 2008, about one million people were diagnosed with type 1 diabetes. The disease was estimated to cause $10.5 billion in annual medical costs ($875 per month per diabetic) and an additional $4.4 billion in indirect costs ($366 per month per diabetic).
Funding for research into type 1 diabetes can originate from either government, industry (for example pharmaceutical companies) or charity based sources. Government funding in the US is distributed via the National Institute of Health, and in the UK via the National Institute for Health Research or the Medical Research Council. The Juvenile Diabetes Research Foundation, originally founded by parents of children with type 1 diabetes, is the world’s largest provider of charity based funding for type 1 diabetes research. Other charities include The American Diabetes Association, Diabetes UK, Diabetes Research and Wellness Foundation , Diabetes Australia , The Canadian Diabetes Association
Types of research 
A significant amount of research is being undertaken in type 1 diabetes, and these will be outlined in the links that fund the research mentioned above. Clinical trials in type 1 diabetes that are currently ongoing can also be found through searching online on www.clinicaltrials.gov, or www.controlled-trials.com.
Generally the research can be divided into the following categories
Before people get type 1 diabetes 
Research here relates to prevention of type 1 diabetes in those deemed at risk.
After people get type 1 diabetes 
Research here relates to therapies aimed at cure (islet transplant, pancreas transplant and stem cells), the artificial pancreas, prevention of diabetic complications, new insulins and other drugs for treating type 1 diabetes.
At the time people are diagnosed type 1 diabetes 
People generally have some residual insulin producing beta cells present at the time they are diagnosed with type 1 diabetes. The exact number of cells is difficult to know but current estimates suggest that this can be anywhere between 10-25%. These cells are not sufficient to cope with the body’s insulin requirements (which is why the blood sugar levels are high), and the person will need immediate insulin treatment. However preserving these cells has been shown to have long lasting health benefits including reducing the rates of hypoglycaemia and risks of complications. There is therefore a significant amount of research now being undertaken in patients newly diagnosed with type 1 diabetes to see if residual beta cells can be preserved. This research includes:
- using drugs to suppress the autoimmune response against the remaining beta cells. Many of these trials are coordinated via TRIALNET – an international group of researchers with an interest in preventing type 1 diabetes. These drugs can work either through suppressing the whole immune response (e.g. anti CD3, anti CD20, CTLA4-Ig, anti-IL1 beta), or whether more specific ‘antigen specific’ drugs can be found that just suppress the immune response against the islet. The latter will clearly be better because it has less risk of side effects, but is harder to achieve.
- adopting a healthier lifestyle to preserve beta cells. Research has already shown that exercise is very effective at preserving beta cells in people with type 2 diabetes. Therefore research is now being conducted to see if exercise can have the same benefit in type 1 diabetes ()
Specific Areas of Research 
GAD65 vaccine 
Injections with a vaccine containing GAD65, an autoantigen involved in type 1 diabetes, has in clinical trials delayed the destruction of beta cells when treated within six months of diagnosis. Patients treated with the substance showed higher levels of regulatory cytokines, thought to protect the beta cells. Phase III trials are under way in the USA and in Europe. Two prevention studies, where the vaccine is given to persons who have not yet developed diabetes are underway.
T helper cell shift 
If a biochemical mechanism can be found to prevent the immune system from attacking beta cells, it may be administered to prevent commencement of diabetes type 1. Several groups are trying to achieve this by causing the activation state of the immune system to change from type 1 T helper cell (Th1) state ("attack" by killer T Cells) to Th2 state (development of new antibodies). This Th1-Th2 shift occurs via a change in the type of cytokine signaling molecules being released by T-cells. Instead of proinflammatory cytokines, the T-cells begin to release cytokines that inhibit inflammation. This phenomenon is commonly known as "acquired immune tolerance".
Brittle diabetes 
Insulin-dependent diabetes characterized by dramatic and recurrent swings in glucose levels, often occurring for no apparent reason, is sometimes known as brittle diabetes, unstable diabetes or labile diabetes, although some experts say the "brittle diabetes" concept "has no biologic basis and should not be used". The results of such swings can be irregular and unpredictable hyperglycemias, frequently involving ketosis, and sometimes serious hypoglycemias. Brittle diabetes occurs no more frequently than in 1% to 2% of diabetics. An insulin pump may be recommended for brittle diabetes to reduce the number of hypoglycemic episodes and better control the morning rise of blood sugar due to the dawn phenomenon. In a small study, 10 of 20 brittle diabetic patients aged 18–23 years who could be traced had died within 22 years, and the remainder, though suffering high rates of complications, were no longer brittle. These results were similar to those of an earlier study by the same authors which found a 19% mortality in 26 patients after 10.5 years.
Because brittle diabetes is defined as "episodes of hypoglycemia or hyperglycemia that, whatever their cause, constantly disrupt a patient's life", it can have many causes, some of which include:
- errors in diabetes management, which can include too much insulin being given.
- interactions with other medical conditions.
- psychological problems.
- biological factors that interfere with how insulin is processed within the body.
One of these biological factors is the production of insulin autoantibodies. High antibody titers can cause episodes of hyperglycemia by neutralizing the insulin, cause clinical insulin resistance requiring doses of over 200 IU/day. However, antibodies may also fail to buffer the release of the injected insulin into the bloodstream after subcutaneous injection, resulting in episodes of hypoglycemia. In some cases, changing the type of insulin administered can resolve this problem. There have been a number of reports that insulin autoantibodies can act as a "sink" for insulin and affect the time to peak, half-life, distribution space, and metabolic clearance, though in most patients these effects are small.
See also 
- "Diabetes Blue Circle Symbol". International Diabetes Federation. 17 March 2006.
- "Type 1 Diabetes Mellitus". Retrieved 2008-08-04.
- Cooke DW, Plotnick L (November 2008). "Type 1 diabetes mellitus in pediatrics". Pediatr Rev 29 (11): 374–84; quiz 385. doi:10.1542/pir.29-11-374. PMID 18977856.
- Kasper, Dennis L; Braunwald, Eugene; Fauci, Anthony; et al. (2005). Harrison's Principles of Internal Medicine (16th ed.). New York: McGraw-Hill. ISBN 0-07-139140-1.
- "One Step Closer to a Cure—Interview; Patrick Perry, Saturday Evening Post". Retrieved 2008-11-02.
- BMI & Diabetes (Report). Drexel U. http://www.idea.library.drexel.edu/bitstream/1860/2806/1/Markowitz_Jessica.pdf. Retrieved 25 November 2009.
- "webmd Symptoms Type I Diabetes".
- Knip, M.; Veijola, R.; Virtanen, S. M.; Hyoty, H.; Vaarala, O.; Akerblom, H. K. (2005). "Environmental Triggers and Determinants of Type 1 Diabetes". Diabetes 54: S125–S136. doi:10.2337/diabetes.54.suppl_2.S125. PMID 16306330.
- Bluestone, J. A.; Herold, K.; Eisenbarth, G. (2010). "Genetics, pathogenesis and clinical interventions in type 1 diabetes". Nature 464 (7293): 1293–1300. Bibcode:2010Natur.464.1293B. doi:10.1038/nature08933. PMID 20432533.
- Genetics & Diabetes, Diabetes Information. Dr. Warram. Joslin Diabetes Center and Joslin Clinic
- "OMIM Entry – %222100 – DIABETES MELLITUS, INSULIN-DEPENDENT; IDDM". Ncbi.nlm.nih.gov. Retrieved 29 November 2011.
- "Nature Immunology 3", 338 – 340 (2002), doi:10.1038/ni0402-338
- "Donner", "Horst"; "Harald Rau, Paul G. Walfish, Jens Braun, Thorsten Siegmund, Reinhard Finke, Jürgen Herwig, Klaus H. Usadel and Klaus Badenhoop" ("2007"). "CTLA4 Alanine-17 Confers Genetic Susceptibility to Graves’ Disease and to type 1 Diabetes Mellitus". "The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 1 143–146". "The Journal of Clinical Endocrinology & Metabolism". Retrieved 2008-02-06.
- "content.nejm.org". content.nejm.org. Retrieved 29 November 2011.
- Hana Malcova, Zdenek Sumnik, Pavel Drevinek, Jitrenka Venhacova, Jan Lebl, Ondrej Cinek (7 October 2005). "Absence of breast-feeding is associated with the risk of type 1 diabetes: a case–control study in a population with rapidly increasing incidence". European Journal of Pediatrics 165 (Volume 165, Number 2 / February, 2006): 114–119. doi:10.1007/s00431-005-0008-9. ISSN 0340-6199. PMID 16211397. (print) (online).
- Chatzigeorgiou A, Harokopos V, Mylona-Karagianni C, Tsouvalas E, Aidinis V, Kamper EF (September 2010). "The pattern of inflammatory/anti-inflammatory cytokines and chemokines in type 1 diabetic patients over time". Ann. Med. 42 (6): 426–38. doi:10.3109/07853890.2010.495951. PMID 20568978.
- Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: report of a WHO/IDF consultation. Geneva: World Health Organization. 2006. p. 21. ISBN 978-92-4-159493-6.
- Vijan, S (March 2010). "Type 2 diabetes". Annals of Internal Medicine 152 (5): ITC31-15. doi:10.1059/0003-4819-152-5-201003020-01003. PMID 20194231.
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