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 fromautoimmune destruction of insulin- producing beta cells of the pancreas. [2] 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. [3] 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. [4] Untreated, type 1 diabetes is ultimately fatal, but the disease can be controlled with supplemental insulin. Insulin is most commonly administered by injection at periodic intervals several times per day, though other options, such as insulin pumps, exist. Transplantation, both of the entire pancreas and pancreatic islet cells, is a possible cure in some cases. Type 1 diabetes can be distinguished from type 2 by autoantibody testing - glutamic acid decarboxylase autoantibodies (GADA), islet cell autoantibodies (ICA), insulinoma-associated (IA-2) autoantibodies, and zinc transporter autoantibodies (ZnT8) are present in individuals with type 1 diabetes, but not type 2. The C-peptide assay, which measures endogenous insulin production, can also be used. Treatment must be continued indefinitely and does not usually impair normal daily activities. Patients are usually trained to manage their disease independently, but for some individuals this can be a challenge. Complications may arise from both low blood sugar and high blood sugar, both due to the non-physiological 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 cause long-term damage to organs Signs and symptoms[edit ]
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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
fromautoimmune destruction of insulin-producing beta cells of the pancreas.[2] 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.[3]
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.[4]
Untreated, type 1 diabetes is ultimately fatal, but the disease can be controlled with supplemental
insulin. Insulin is most commonly administered by injection at periodic intervals several times per
day, though other options, such as insulin pumps, exist. Transplantation, both of the entire
pancreas and pancreatic islet cells, is a possible cure in some cases.
Type 1 diabetes can be distinguished from type 2 by autoantibody testing - glutamic acid
Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by
demonstrating any one of the following:[17]
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.)[18]
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 withmacrosomia 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.[19] 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.[20]
Autoantibodies[edit]
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), autoantibodies targeting the phosphatase-related IA-2 molecule, and zinc
transporter autoantibodies (ZnT8).[6] 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%.[6] 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.[6] Islet cell autoantibodies are
detected by conventional immunofluorescence, while the rest are measured with
specific radiobinding assays.[6]
Prevention[edit]
Type 1 diabetes is not currently preventable.[21] Some researchers believe it might be prevented at
the latent autoimmune stage, before it starts destroying beta cells.[7]
Immunosuppressive drugs[edit]
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.[7]
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.[7] 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.[7] The duration of the effect is still unknown,
however.[7] In 2011, Phase III studies with otelixizumab and teplizumab both failed to show clinical
efficacy, potentially due to an insufficient dosing schedule.[22][23]
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.[7]
Diet[edit]
Some research has suggested breastfeeding decreases the risk in later life;[24][25] various other
nutritional risk factors are being studied, but no firm evidence has been found.[26] 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.[27]
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 the niacinamide version, 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 niacinamide.[28]
Type 1 diabetes is also referred to as "sugar diabetes" due to the fact that a diet consisting of large
amounts of sugar can be fatal. Diets consisting of large quantities of fat (i.e. butter and oil) also put
the patient at a higher risk of cardiovascular disease.
Management[edit]
Further information: Diabetes management
Insulin therapy[edit]
Main article: Insulin therapy
Type 1 is treated with insulin replacement therapy—either via subcutaneous injection or insulin
pump, 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.[29] 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.[30]
Continuous glucose monitors can alert patients to the presence of dangerously high or low blood
sugar levels, but technical issues have limited the effect these devices have had on clinical
practice[citation needed].
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).[31] 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[edit]
Main article: 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.[32]
Islet cell transplantation[edit]
Main article: 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 involvingimmunosuppressants, 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 transplantation.[33] 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[edit]
Stem Cell Educator Therapy induces immune balance by using cord blood-derived multipotent stem
cells[34] 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.[35] 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[36] 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 reversesautoimmunity, induces tolerance and
promotes regeneration of islet beta cells[37] 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[edit]
Depression[edit]
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)[38] Women with type 1 diabetes are more likely to be depressed than
men with type 1 diabetes,[38] and an increased incidence of depression has also been associated
with youth with type 1 diabetes.[39] According to the Canadian Diabetes Association, 15% of people
living with diabetes have major depression.[40] Psychological distress is also reported in the parents
of youth with type 1 diabetes.[41] 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.[42]
Eating disorders[edit]
Recent research has found that eating disorders are more common in females with type 1
diabetes[43] (prevalence = 10.15%) than in females without it (prevalence = 4.5%), as were sub-
threshold eating disorders (13.8% vs. 7.6%)[44]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[edit]
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.[45] Type 1 diabetics may also neglect physical
activity due to reduced perceived position effects as well as increased perceived negative aspects of
that activity.[46]
Complications[edit]
Further information: Complications of diabetes mellitus
Complications of poorly managed type 1 diabetes mellitus may include cardiovascular
disease, diabetic neuropathy, and diabetic retinopathy, among others. However, cardiovascular
disease[47] as well as neuropathy[48] may have an autoimmune basis, as well.
Driving[edit]
Studies conducted in the United States[49] and Europe[50] 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.[51][52] This disruption in brain functioning, neuroglycopenia, can impair driving
ability.[51][53] 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.[54] 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[55] and are relatively
slower at processing information.[56] 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 80 mg/dl. Instead, these drivers are advised
to treat hypoglycemia and delay driving until their BG is above 90 mg/dl.[54] 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.[57][58]
[59] An internet-version of this training has also been shown to have significant beneficial results.[60] Additional NIH funded research to develop internet interventions specifically to help improve
driving safety in drivers with type 1 diabetes is currently underway.[61]
Epidemiology[edit]
Type 1 diabetes causes an estimated 5–10% of all diabetes cases[62] or 11–22 million worldwide.[21] 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.[63] The incidence of type 1 diabetes has been increasing by about
3% per year.[63]
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.[4][64]
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
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.[65]
Economics[edit]
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 person with diabetes).[66]
Research[edit]
Funding for research into type 1 diabetes originates from government, industry (e.g., pharmaceutical
companies), and charitable organizations. Government funding in the United States 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,[67] Diabetes Australia, the Canadian Diabetes
Association.
Types of research[edit]
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 online.[68][69]
Generally the research can be divided into the following categories:
Before people get type 1 diabetes[edit]
Research here relates to prevention of type 1 diabetes in those deemed at risk.
After people get type 1 diabetes[edit]
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[edit]
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.[70] 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[71] – 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.[72]
Specific Areas of Research[edit]
GAD65 vaccine[edit]
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.[7] Patients treated with the substance showed higher levels of regulatory cytokines, thought to
protect the beta cells.[73] Phase III trials are under way in the USA[74] and in Europe.[75][76][77] Two
prevention studies, where the vaccine is given to persons who have not yet developed diabetes are
underway.[78][79][80]
T helper cell shift[edit]
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.[81] This phenomenon is commonly known as acquired immune tolerance.
Labile diabetes[edit]
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".[82] 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.[83] 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.[84] 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.[85] 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.[86]
Because labile 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:[87]
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.[87] 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.[88]
Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic
condition in which the pancreas produces little or no insulin, a hormone needed to allow sugar
(glucose) to enter cells to produce energy. The far more common type 2 diabetes occurs when the
body becomes resistant to the effects of insulin or doesn't make enough insulin.
Various factors may contribute to type 1 diabetes, including genetics and exposure to certain
viruses. Although type 1 diabetes typically appears during childhood or adolescence, it also can
develop in adults.
Despite active research, type 1 diabetes has no cure, although it can be managed. With proper
treatment, people who have type 1 diabetes can expect to live longer, healthier lives than they did in
the past.
SymptomsBy Mayo Clinic staff
Controlling Your Diabetes
Type 1 diabetes signs and symptoms can come on quickly and may include:
Increased thirst and frequent urination
Extreme hunger
Weight loss
Fatigue
Blurred vision
When to see a doctor
Consult your doctor if you notice any type 1 diabetes signs and symptoms.