How does type 2 diabetes progress over time? Type 2 diabetes is a progressive disease, meaning that the body’s ability to regulate blood sugar gets worse over time, despite careful management. Over time, the body’s cells become increasingly less responsive to insulin (increased insulin resistance) and beta cells in the pancreas produce less and less insulin (called beta-cell burnout). In fact, when people are diagnosed with type 2 diabetes, they usually have already lost up to 50% or more of their beta cell function. As type 2 diabetes progresses, people typically need to add one or more different types of medications. The good news is that there are many more choices available for treatments, and a number of these medications don’t cause as much hypoglycemia, hunger and/or weight gain (e.g., metformin, pioglitazone, DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, and better insulin). Diligent management early on can help preserve remaining beta cell function and sometimes slow progression of the disease, although the need to use more and different types of medications does not mean that you have failed.

"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used.[39] Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, frequently with ketosis, and sometimes with serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease).[39] These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.[40]
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.

Hemoglobin A1c or HbA1c is a protein on the surface of red blood cells. The HbA1c test is used to monitor blood sugar levels in people with type 1 and type 2 diabetes over time. Normal HbA1c levels are 6% or less. HbA1c levels can be affected by insulin use, fasting, glucose intake (oral or IV), or a combination of these and other factors. High hemoglobin A1c levels in the blood increases the risk of microvascular complications, for example, diabetic neuropathy, eye, and kidney disease.


Don’t be alarmed: This is not diabetic retinopathy, where the blood vessels in the back of the eye are getting destroyed, says Dr. Cypess. In the early stages of diabetes, the eye lens is not focusing well because glucose builds up in the eye, which temporarily changes its shape. “You’re not going blind from diabetes,” Dr. Cypess says he assures patients. “In about six to eight weeks after your blood sugars are stabilized, you’re not going to feel it anymore; the eye will adjust.” Here are more surprising facts you never knew about diabetes.
Type 2 (formerly called 'adult-onset' or 'non insulin-dependent') diabetes results when the body doesn’t produce enough insulin and/or is unable to use insulin properly (this is also referred to as ‘insulin resistance’). This form of diabetes usually occurs in people who are over 40 years of age, overweight, and have a family history of diabetes, although today it is increasingly found in younger people.
Persons with diabetes are prone to infection, delayed healing, and vascular disease. The ease with which poorly controlled diabetic persons develop an infection is thought to be due in part to decreased chemotaxis of leukocytes, abnormal phagocyte function, and diminished blood supply because of atherosclerotic changes in the blood vessels. An impaired blood supply means a deficit in the protective defensive cells transported in the blood. Excessive glucose allows organisms to grow out of control.
Autonomic changes involving cardiovascular control (eg, heart rate, postural responses) have been described in as many as 40% of children with diabetes. Cardiovascular control changes become more likely with increasing duration and worsening control. [18] In a study by 253 patients with type 1 diabetes (mean age at baseline 14.4 y), Cho et al reported that the prevalence of cardiac autonomic dysfunction increases in association with higher body mass index and central adiposity. [19]
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]
Higher levels of sugar in the urine and the vagina can become a breeding ground for the bacteria and yeast that cause these infections. Recurrent infections are particularly worrisome. “Usually when you keep getting infections, doctors will check for diabetes if you don’t already have it,” says Cypress. “Even women who go to the emergency room for urinary tract infections are often checked.” Don’t miss these other silent diabetes complications you need to know about.
Despite our efforts, patients are still likely to suffer myocardial infarction. The Diabetes mellitus, Insulin Glucose infusion in Acute Myocardial Infarction (DIGAMI) study236,237 reported on treating subjects with acute myocardial infarction and either diabetes or raised random plasma glucose (i.e., not necessarily diabetic) with either an intensive insulin infusion and then a four-times daily insulin regimen or conventional treatment. Over a mean follow-up of 3.4 years, there was a 33% death rate in the treatment group compared with a 44% death rate in the control group, an absolute reduction in mortality of 11%. The effect was greatest among the subgroup without previous insulin treatment and at a low cardiovascular risk. Evidence is continuing to accumulate that the diabetic person should have a glucose/insulin infusion after a myocardial infarction.
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.
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.

So what determines where fat is stored, and thus a person's propensity for insulin resistance and type 2 diabetes? Well, just having more fat in the body increases the risk that some of it will get misplaced. But exercise may also have a role in fat placement. Exercise is known to reduce insulin resistance; one way it may do this is by burning fat out of the muscle. Because of this, getting enough exercise may stave off type 2 in some cases. Genes may also help orchestrate the distribution of fat in the body, which illustrates how lifestyle and genetics interact.


Diabetes may have symptoms in some people, and no symptoms in others. Generally, people with Type 1 diabetes have increased thirst (polydipsia), frequent urination (polyuria), and increased hunger (polyphagia). Symptoms may develop over weeks to months.  Untreated, this condition may cause a person to lose consciousness and become very ill (diabetic ketoacidosis).
Brittle diabetics are a subgroup of Type I where patients have frequent and rapid swings of blood sugar levels between hyperglycemia (a condition where there is too much glucose or sugar in the blood) and hypoglycemia (a condition where there are abnormally low levels of glucose or sugar in the blood). These patients may require several injections of different types of insulin during the day to keep the blood sugar level within a fairly normal range.
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.
By simultaneously considering insulin secretion and insulin action in any given individual, it becomes possible to account for the natural history of diabetes in that person (e.g., remission in a patient with T1 diabetes or ketoacidosis in a person with T2DM). Thus, diabetes mellitus may be the result of absolute insulin deficiency, or of absolute insulin resistance, or a combination of milder defects in both insulin secretion and insulin action.1 Collectively, the syndromes of diabetes mellitus are the most common endocrine/metabolic disorders of childhood and adolescence. The application of molecular biologic tools continues to provide remarkable insights into the etiology, pathophysiology, and genetics of the various forms of diabetes mellitus that result from deficient secretion of insulin or its action at the cellular level.
Family or personal history. Your risk increases if you have prediabetes — a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes. You're also at greater risk if you had gestational diabetes during a previous pregnancy, if you delivered a very large baby or if you had an unexplained stillbirth.
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