Types of Diabetes: Detailed Descriptions
After the discovery of insulin in 1921, people who were diagnosed with diabetes were successfully treated with insulin, though there was very little of it to go around, at first. The first such person to receive an injection of insulin was a 14 year old child named Leonard Thompson of Toronto, Canada, who had developed diabetes three years earlier. At the time he received the injection, he weighed 65 pounds and was near death. His symptoms reversed and he lived until 1935 when he died of pneumonia.
In the 1920s, the pharmaceutical company, Eli Lilly and Company, collaborated with Dr. Banting and Charles Best to isolate and purify insulin to treat diabetes. In 1923, Lilly produced what was called at that time, "Isletin."
Over time, it became apparent that two different types of diabetes existed: "Juvenile Diabetes" which characteristically presented itself in younger people (under the age of approximately 24 years) and required the injection of insulin several times each day, and "Adult-Onset Diabetes," – a form of diabetes in which the victim was typically over the age of 40 and did not require exogenous insulin injections to survive. In 1959, this distinction was made official.
Eventually, Juvenile Diabetes became known as Insulin-Dependent Diabetes Mellitus or IDDM, for obvious reasons, and Adult-Onset Diabetes became known as Non-Insulin Dependent Diabetes or NIDDM. In time, it was found that people with NIDDM often benefited from the use of exogenous insulin. Consequently, the name "non-insulin dependent" became a misnomer.
In 1997, the decision was made by the American Diabetes Association to simplify and clarify, and to identify the two main types of diabetes as just Type 1 and Type 2. Current classifications of diabetes include four clinical classes as identified below: DMT1, DMT2, Other Specific Types of Diabetes -- due to other causes, e.g. genetic defects in beta-cell function or insulin action, diseases of the exocrine pancreas (e.g. cystic fibrosis), and drug- or chemical-induced (such as in the treatment of AIDS or after organ transplantation) – and, Gestational Diabetes Mellitus (GDM) – diabetes diagnosed during pregnancy that is not overt diabetes) (American Diabetes Association, 2011).
Type 1 Diabetes (DMT1)
Type 1 diabetes most often affects persons under the age of 24 (but this is certainly not the "magic age"). Of those with diabetes, only about 10% have DMT1. In this case, there is an absolute lack of insulin activity, either because the beta cells in the pancreas simply do not produce it or because, once they do, the body inactivates it in some fashion. Whatever the case, the critical point is that there is no effective insulin activity in the body. It is characterized by rapid onset of symptoms, especially thirst, frequency of urination, and lassitude. (See Appendix A: Pathophysiology of Diabetic Ketoacidosis.) Treatment consists of balancing exogenous insulin administered by injections (or continuous subcutaneous insulin infusions, also called CSII or the insulin pump), nutrition/eating patterns, exercise, and self-monitoring of blood glucose.
Type 2 Diabetes (DMT2)
In contrast, Type 2 diabetes (DMT2) is by far the more common type of diabetes, comprising approximately 90% of all cases. The underlying problem in DMT2 is insulin resistance which creates a relative lack of insulin for the body's metabolic needs.
Until the past 15-20 years, DMT2 was a disease of older people (Adult-Onset Diabetes), the incidence of DMT2 among children is growing exponentially in this country. More information on that will be offered later in the self-study, but suffice it to say that there is an explanation for this phenomenon when one recognizes the growing incidence of obesity among the nation's children.
For reasons that are not clearly understood, the cells in the body of an individual with DMT2 become more and more resistant to the body's own insulin, thereby interfering with the transport of sugar across cell membranes to be used by the cells of the body. Initially, the body responds by producing more insulin to maintain normoglycemia. But, the pancreatic cells that produce insulin – the beta cells of the pancreas – can do only so much for so long and eventually they cannot keep up with the demand. Consequently, insulin resistance combined with diminished secretion of insulin results in subjective and objective symptoms of DMT2. The excess sugar collects in the blood and creates the objective and subjective indicators of diabetes: hyperglycemia, polydipsia, polyuria, and fatigue. Blood sugar rises significantly when the transportation of sugar into the cell is impaired.
Another defect complicating the above pathology is the fact that DMT2 is associated with elevations in glucagon secretion from the liver, leading particularly to postprandial (after meal) blood glucose elevations. In Type 2 diabetes, the body is not forced to resort to abnormal pathways to meet its metabolic needs -- there is sufficient insulin for this. Consequently, the signs and symptoms of undiagnosed DMT2 are not as noticeable as they are in undiagnosed DMT1.
Early in the metabolic derangement characteristic of the DMT2, excess insulin is secreted to compensate for the reduced insulin activity. Glucose levels can be maintained in the normal range for some time in this hyperinsulinemic state. However, associations have been discovered between hyperinsulinemia and the development of obesity, hypertension, dyslipidemia, and atherosclerosis (a cluster of metabolic disorders previously referred to as Syndrome X but now called the metabolic syndrome) all of which are known to be related to cardiovascular disease (Fonseca, 2007; Li et al., 2006).
Type 2 diabetes characteristically does not produce ketones in the blood or urine. This is because the body does not have to resort to fat metabolism to meet its energy needs. Essentially, the problem is a result of a relative lack of insulin: excessive demands for insulin perhaps due to resistance to insulin by target tissues and/or defective secretion of insulin. Hyperglycemia and glucosuria are typical laboratory findings as well as polydipsia, polyuria, fatigue, and infections or wounds that do not heal. Acidosis, ketonemia, and ketonuria are typically not present. (Both may be present, however, in the individual with DMT2 who has an infection). Since symptoms are usually less severe, professional intervention may not be sought early. Consequently, damage may occur (retinal, renal, neurological, cardiovascular, cerebrovascular) before the condition is diagnosed.
When compensatory hyperinsulinemia fails to maintain normal glucose levels, pathophysiologic changes result in further compounding the hyperglycemia -- overproduction of glucose by the liver, increased insulin resistance, and dysfunction of pancreatic beta cells. This is the body's attempt to correct a perceived problem, but is, in fact, highly maladaptive.
Initially, attempts to control the blood glucose in the individual diagnosed with DMT2 will be made through nutritional instruction, exercise, and an oral agent, metformin (unless contraindicated). Some regimens include both oral agents and insulin. Insulin injections are nearly always necessary when the individual with DMT2 experiences pregnancy, unusual stress, infections, develops an allergy to oral hypoglycemic agents, and in all conditions which increase the metabolic demands on the body that result in loss of control of the blood glucose. A key to success requires frequent blood glucose determinations (and documentation) by the patient, as well as frequent re-evaluations with the patient's health care provider to determine the extent to which glycemic control is being obtained.
A caution is in order with regard to aggressive use of insulin in persons with DMT2. As stated above, evidence suggests an association between hyperinsulinemia (higher than normal levels of insulin in the blood) and cardiovascular disease (Fonseca, 2007; Li et al., 2006). On the other hand, the use of exogenous insulin in conjunction with oral agents that reduce resistance to insulin could lessen this problem by actually reducing the amount of insulin secreted. In fact, many persons with DMT2 are controlled in precisely this manner. (Note: The presence of ketoacidosis strongly suggests the underlying problem is type 1 diabetes, not type 2 diabetes.) When improvement in glycemic control is achieved with insulin, it would then be appropriate to introduce oral agents and discontinue the use of insulin.
[This self-study is updated periodically, but is not updated every year. Throughout the self-study, references are made to the American Diabetes Association's standards of medical care. These are reviewed and published each year on the American Diabetes Association's (ADA) web page at http://www.diabetes.org. To see the most current standards, go to http://www.diabetes.org, click on "Research & Practice”, and then click on "Clinical Practice Guidelines”. It is in this way that you can remain current on the ADA's clinical practice recommendations.]
Think about what characteristics of DMT1 and DMT2 described above you would use to complete the chart.
|Comparison of DMT1 and DMT2|
Previous names for the condition:
Typical age at onset:
Gestational Diabetes Mellitus (GDM)
GDM refers to diabetes that is diagnosed during pregnancy (typically during the last trimester). Since even mild glucose intolerance is associated with a greater than expected incidence of perinatal mortality and morbidity of the neonate, it is important that the condition is promptly diagnosed and effectively managed. Management includes specific dietary modifications alone or, in some cases, dietary modifications plus insulin. Following delivery, glucose metabolism may change to normal, remain as impaired glucose tolerance, or become overt diabetes. It is highly likely that a woman who has GDM will develop DMT2 at some time in her future.
The American Diabetes Association recommends screening for GDM at the first prenatal visit in patients who have risk factors for diabetes, and then, if warranted, arranging for testing using standard diagnostic criteria (2014). Screening for GDM is performed at 24-28 weeks gestation in those not known to have had diabetes in the past. Among women who have had GDM, the recommendation is to screen them for diabetes every three years for the rest of their lives.
Other Conditions of Glucose Intolerance or Pre-Diabetes as defined by the American Diabetes Association:
- Impaired Fasting Glucose (IFG) – Diagnosed by results of a fasting blood glucose of 100 mg/dL to 125 mg/dL
- Impaired Glucose Tolerance (IGT) – Diagnosed by results at 2 hours in the standardized oral glucose tolerance test of 140 mg/dL to 199 mg/dL (American Diabetes Association, 2014, p. S16)
Either of the above has been identified as a risk factor for the future development of diabetes and for cardiovascular disease.