|Written by Jeffrey R. Waggoner, MD|
The human body evolved in an environment where food was scarce and the daily activities of survival required a great expenditure of physical energy. Americans and western Europeans now live in environments where food is abundant and survival usually does not require "any" physical exercise.
When there is a mismatch between evolution and environment, species typically become extinct. The present epidemic of diabetes is a reflection of an evolutionary mismatch, and while it does not pose an immediate threat to human survival, it extracts an enormous toll in suffering and financial loss.
Types of diabetes
There are 2 basic types of Diabetes Mellitus, type 1 and type 2.
Type 1 diabetes can occur at any age. In children, it usually appears with an abrupt onset. The distinguishing characteristic of Type 1 diabetes is that if left untreated, it causes ketosis and eventually ketoacidosis. It must be treated with insulin—thus it is also called "insulin dependent diabetes."(1)
Type 1 diabetes is caused by a progressive autoimmune destruction of the beta cells. It most commonly affects children, appearing in an acute fashion. Recently, the ability to detect antibodies has identified another population of adult patients who have latent autoimmune diabetes of the adult (LADA). All type 1 diabetics are dependent on exogenous insulin.
The genetic predisposition to Type 1 diabetes is demonstrated by studies in identical twins. These studies show that when one twin develops Type 1 diabetes, islet cell and insulin antibodies are present in the second, initially nondiabetic twin for years before the development of overt diabetes. (1)
Formerly, Type 2 diabetes was called adult onset diabetes. Now, because of the great increase in childhood obesity, Type 2 diabetes is being seen in younger and younger age groups. Type 2 diabetes is caused by peripheral insulin resistance with an insulin-secretory abnormality that varies in severity. Both abnormalities must be present, i.e. all obese patients have a degree of insulin resistance but only those who cannot increase beta-cell production of insulin will develop diabetes. 90% of patients with Type 2 diabetes are obese.
As patients progress from normal glucose tolerance to abnormal glucose tolerance, the first glucose levels that become elevated are postprandial. As hepatic gluconeogenesis declines, fasting hyperglycemia also increases. Type 2 diabetics will usually retain some ability to synthesize insulin—as opposed to type 1 diabetics. Thus even though severe type 2 diabetics may be using insulin as an adjunct or instead of oral hypoglycemic agents, its withdrawal will not produce ketoacidosis. It is also true that most type 2 diabetics will return to normal with weight loss. (2)
There is a subset of Type 2 diabetes called maturity onset diabetes of the young (MODY). This affects many generations of the same family. It has an onset in patients younger than 25 years. There are several types of MODY, and some of the responsible genes may be detected by using commercially available assays.
Gestational diabetes (GDM) is present in approximately 4% of all U.S. pregnancies. If untreated, it can have profound intranatal complications including macrosomia, hypoglycemia, hypocalcemia, and hyperbilirubinemia. It is defined as any degree of glucose intolerance with first recognition of pregnancy. (2)
In general, the complications of diabetes fall into the categories of hypoglycemia and hyperglycemia; increased risk of infections; microvascular complications, e.g., retinopathy and nephropathy; direct neuropathic complications; and macrovascular disease e.g., coronary artery disease, and stroke. In adults between the age of 20 and 74, diabetes is the leading cause of blindness. It is also the most common cause of non-traumatic lower-extremity amputation. It is also the leading cause of end-stage renal disease (ESRD). (2)
When encountering a patient with new onset diabetes or a new patient whose diabetes is not well defined, an initial workup should always consist of a fingerstick glucose and urine for ketones. It is important to distinguish between type 1 and Type 2 diabetes since the former will always require exogenous insulin and be eventually unresponsive to oral hypoglycemics.
Early on, characterizing the nature of a patient’s diabetes is furthered by looking for islet-cell autoantibodies. However, within 6 months levels of these autoantibodies fall. Antibodies to islet-glutamate decarboxylase (GAD) are present early on and remain so. (3)
National guidelines for treatment
National guidelines have been outlined for a program of overall diabetic treatment. These guidelines have been broken down into the categories of screening and diagnosis, staged treatment, targeting and monitored glucose control, followup, surveillance of complications, patient education, and assessment of psycho-social issues.
Approaching the disease within the context of these categories is helpful because even though there is significant variation in specific concerns for individual patients, every patient requires attention to each of the categories. For example, the psycho-social concerns of a young, active insulin-dependent child are almost antithetical to those of an over-weight elderly type 2 diabetic, but both patients need their concerns addressed in an open, aggressive fashion. (4)
4. Type 2 diabetes practice guidelines. National Guideline Clearinghouse.
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