When there is excess glucose present in the blood, as with type 2 diabetes, the kidneys react by flushing it out of the blood and into the urine. This results in more urine production and the need to urinate more frequently, as well as an increased risk of urinary tract infections (UTIs) in men and women. People with type 2 diabetes are twice as likely to get a UTI as people without the disease, and the risk is higher in women than in men.
Blood travels throughout your body, and when too much glucose (sugar) is present, it disrupts the normal environment that the organ systems of your body function within. In turn, your body starts to exhibit signs that things are not working properly inside—those are the symptoms of diabetes people sometimes experience. If this problem—caused by a variety of factors—is left untreated, it can lead to a number of damaging complications such as heart attacks, strokes, blindness, kidney failure, and blood vessel disease that may require an amputation, nerve damage, and impotence in men.

Regarding age, data shows that for each decade after 40 years of age regardless of weight there is an increase in incidence of diabetes. The prevalence of diabetes in persons 65 years of age and older is around 25%. Type 2 diabetes is also more common in certain ethnic groups. Compared with a 7% prevalence in non-Hispanic Caucasians, the prevalence in Asian Americans is estimated to be 8.0%, in Hispanics 13%, in blacks around 12.3%, and in certain Native American communities 20% to 50%. Finally, diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy (gestational diabetes).
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.
Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance.[13] Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue.[44] In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood.[10] The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.[13]
Janis McWilliams, RN, MSN, CDE, BC-ADM, responds: Yes, in type 1 diabetes in particular, the onset of symptoms like frequent urination and extreme thirst can be very sudden. In type 2 diabetes, the symptoms tend to come about more gradually, and sometimes there are no signs at all. People who have symptoms should contact their health care provider immediately for an accurate diagnosis. Keep in mind that these symptoms could signal other problems, too.
No single environmental trigger has been identified as causing diabetes mellitus, however both infectious agents and dietary factors are thought to be important. Various viruses have been implicated in the development of type I DM. They may act by initiating or modifying the autoimmune process. In particular, the rubella virus and coxsackie viruses have been closely studied. In particular, congenital rubella infection has shown direct relationships with the development of type 1 diabetes mellitus. This is presumably due to the virus (or antibodies against it) damaging the beta cells of the pancreas. Some research has looked at dietary factors that may be associated with type 1 diabetes. In particular, cow’s milk proteins (such as bovine serum albumin) which may have some similarities to pancreatic islet cell markers may be able to trigger the autoimmune process. Other chemicals including nitrosamines have been identified as causes of diabetes mellitus in animal models, but not in humans.
The beta cells may be another place where gene-environment interactions come into play, as suggested by the previously mentioned studies that link beta cell genes with type 2. "Only a fraction of people with insulin resistance go on to develop type 2 diabetes," says Shulman. If beta cells can produce enough insulin to overcome insulin resistance, a factor that may be genetically predetermined, then a person can stay free of diabetes. But if the beta cells don't have good genes propping them up, then diabetes is the more likely outcome in a person with substantial insulin resistance.
The World Health Organization recommends testing those groups at high risk[54] and in 2014 the USPSTF is considering a similar recommendation.[58] High-risk groups in the United States include: those over 45 years old; those with a first degree relative with diabetes; some ethnic groups, including Hispanics, African-Americans, and Native-Americans; a history of gestational diabetes; polycystic ovary syndrome; excess weight; and conditions associated with metabolic syndrome.[23] The American Diabetes Association recommends screening those who have a BMI over 25 (in people of Asian descent screening is recommended for a BMI over 23).[59]

At present, the American Diabetes Association does not recommend general screening of the population for type 1 diabetes, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age; however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Of all the people with diabetes, only approximately 10% have type 1 diabetes and the remaining 90% have type 2 diabetes.

Often people don't experience symptoms of diabetes until their blood sugars are very high. Symptoms of diabetes include: increased thirst, increased urination, increased hunger, extreme fatigues, numbness and tingling in the extremities (hands and feet), cuts and wounds that are slow to heal, and blurred vision. Some people also experience other less common symptoms including weight loss, dry itchy skin, increased yeast infections, erectile dysfunction, and acanthosis nigricans (thick, "velvety" patches found in the folds or creases of skin, such as the neck, that is indicative of insulin resistance).


It is also important to note that currently one third of those who have IGT are in the productive age between 20-39 yr and, therefore, are likely to spend many years at high risk of developing diabetes and/or complications of diabetes1. Some persons with prediabetes experience reactive hypoglycaemia 2-3 hours after a meal. This is a sign of impaired insulin metabolism indicative of impending occurrence of diabetes. Therefore, periodic medical check-up in people with such signs or risk factors for diabetes would reduce the hazards involved in having undiagnosed diabetes. It would help improve the health status of a large number of people who otherwise would be silent sufferers from the metabolic aberrations associated with diabetes.

The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly.
Viral infections may be the most important environmental factor in the development of type 1 diabetes mellitus, [26] probably by initiating or modifying an autoimmune process. Instances have been reported of a direct toxic effect of infection in congenital rubella. One survey suggests enteroviral infection during pregnancy carries an increased risk of type 1 diabetes mellitus in the offspring. Paradoxically, type 1 diabetes mellitus incidence is higher in areas where the overall burden of infectious disease is lower.
Type 1 diabetes occurs when your immune system, the body’s system for fighting infection, attacks and destroys the insulin-producing beta cells of the pancreas. Scientists think type 1 diabetes is caused by genes and environmental factors, such as viruses, that might trigger the disease. Studies such as TrialNet are working to pinpoint causes of type 1 diabetes and possible ways to prevent or slow the disease.

When you have diabetes, your body becomes less efficient at breaking food down into sugar, so you have more sugar sitting in your bloodstream, says Dobbins. “Your body gets rid of it by flushing it out in the urine.” So going to the bathroom a lot could be one of the diabetes symptoms you’re missing. Most patients aren’t necessarily aware of how often they use the bathroom, says Dr. Cypess. “When we ask about it, we often hear, ‘Oh yeah, I guess I’m going more often than I used to,’” he says. But one red flag is whether the need to urinate keeps you up at night. Once or twice might be normal, but if it’s affecting your ability to sleep, that could be a diabetes symptom to pay attention to. Make sure you know these diabetes myths that could sabotage your health.

Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[61]

Diabetes mellitus type 2 (also known as type 2 diabetes) is a long-term metabolic disorder that is characterized by high blood sugar, insulin resistance, and relative lack of insulin.[6] Common symptoms include increased thirst, frequent urination, and unexplained weight loss.[3] Symptoms may also include increased hunger, feeling tired, and sores that do not heal.[3] Often symptoms come on slowly.[6] Long-term complications from high blood sugar include heart disease, strokes, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations.[1] The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon.[4][5]


In general, women live longer than men do because they have a lower risk of heart disease, but when women develop diabetes, their risk for heart disease skyrockets, and death by heart failure is more likely in women than in men. Another study also found that in people with diabetes, heart attacks are more often fatal for women than they are for men. Other examples of how diabetes affects women differently than men are:
Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system.[10] However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also required.[13]
Insulin-dependent diabetes mellitus is believed to result from autoimmune, environmental, and/or genetic factors. Whatever the cause, the end result is destruction of insulin-producing pancreatic beta cells, a dramatic decrease in the secretion of insulin, and hyperglycemia. Non-insulin-dependent diabetes mellitus is presumably heterogeneous in origin. It is associated with older age, obesity, a family history of diabetes, and ethnicity (genetic components). The vast majority of those with non-insulin-dependent diabetes are overweight Kahn (2003). This form of the disorder has a much slower rate of progression than insulin-dependent diabetes. Over time the ability to respond to insulin decreases, resulting in increased levels of blood glucose. The pancreatic secretion of insulin increases in an attempt to compensate for the elevated levels of glucose. If the condition is untreated, the pancreatic production of insulin decreases and may even cease.

Diabetes mellitus type 2 is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency.[51] This is in contrast to diabetes mellitus type 1 in which there is an absolute insulin deficiency due to destruction of islet cells in the pancreas and gestational diabetes mellitus that is a new onset of high blood sugars associated with pregnancy.[13] Type 1 and type 2 diabetes can typically be distinguished based on the presenting circumstances.[48] If the diagnosis is in doubt antibody testing may be useful to confirm type 1 diabetes and C-peptide levels may be useful to confirm type 2 diabetes,[52] with C-peptide levels normal or high in type 2 diabetes, but low in type 1 diabetes.[53]
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."
If genetics has taught us anything about diabetes, it's that, for most people, genes aren't the whole story. True, a few rare kinds of diabetes—including those collectively called MODY for maturity-onset diabetes of the young—have been traced to defects in a single gene. But for other types of diabetes, hereditary factors are still not well understood.
Type 2 diabetes mellitus (non–insulin-dependent diabetes mellitus [NIDDM]) is a heterogeneous disorder. Most patients with type 2 diabetes mellitus have insulin resistance, and their beta cells lack the ability to overcome this resistance. [6] Although this form of diabetes was previously uncommon in children, in some countries, 20% or more of new patients with diabetes in childhood and adolescence have type 2 diabetes mellitus, a change associated with increased rates of obesity. Other patients may have inherited disorders of insulin release, leading to maturity onset diabetes of the young (MODY) or congenital diabetes. [7, 8, 9] This topic addresses only type 1 diabetes mellitus. (See Etiology and Epidemiology.)
Jump up ^ Feinman, RD; Pogozelski, WK; Astrup, A; Bernstein, RK; Fine, EJ; Westman, EC; Accurso, A; Frassetto, L; Gower, BA; McFarlane, SI; Nielsen, JV; Krarup, T; Saslow, L; Roth, KS; Vernon, MC; Volek, JS; Wilshire, GB; Dahlqvist, A; Sundberg, R; Childers, A; Morrison, K; Manninen, AH; Dashti, HM; Wood, RJ; Wortman, J; Worm, N (January 2015). "Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base". Nutrition. Burbank, Los Angeles County, Calif. 31 (1): 1–13. doi:10.1016/j.nut.2014.06.011. PMID 25287761.
Your body is like a car—it needs fuel to function. Its primary source of fuel is glucose (sugar), which is gained from foods that contain carbohydrates that get broken down. Insulin, a hormone produced by the pancreas, takes sugar from your blood to your cells to use for energy. However, when you have diabetes, either your pancreas isn't making enough insulin or the insulin that your body is making isn't being used the way it's supposed to be, typically because the cells become resistant to it.
Insulin-dependent diabetes mellitus is believed to result from autoimmune, environmental, and/or genetic factors. Whatever the cause, the end result is destruction of insulin-producing pancreatic beta cells, a dramatic decrease in the secretion of insulin, and hyperglycemia. Non-insulin-dependent diabetes mellitus is presumably heterogeneous in origin. It is associated with older age, obesity, a family history of diabetes, and ethnicity (genetic components). The vast majority of those with non-insulin-dependent diabetes are overweight Kahn (2003). This form of the disorder has a much slower rate of progression than insulin-dependent diabetes. Over time the ability to respond to insulin decreases, resulting in increased levels of blood glucose. The pancreatic secretion of insulin increases in an attempt to compensate for the elevated levels of glucose. If the condition is untreated, the pancreatic production of insulin decreases and may even cease.

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.
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%.
When there is excess glucose present in the blood, as with type 2 diabetes, the kidneys react by flushing it out of the blood and into the urine. This results in more urine production and the need to urinate more frequently, as well as an increased risk of urinary tract infections (UTIs) in men and women. People with type 2 diabetes are twice as likely to get a UTI as people without the disease, and the risk is higher in women than in men.
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