Recent figures from the Centers for Disease Control and Prevention (CDC)¹ show a disturbing increase in the number of Americans with diabetes mellitus (DM). The CDC reported that 7.8 percent, or 23.6 million Americans, have DM, including 5.7 million who are undiagnosed. Several national programs have been implemented to buck this alarming trend. Many initiatives focus on DM screening and monitoring in nontraditional health care settings, including offices of oral health care professionals. In some geographic areas, such as New York City, long-term glucose control measurements—glycosylated hemoglobin (HbA_1c) values—need to be reported to the New York Department of Health and Mental Hygiene.² This is an unprecedented attempt to track this epidemic. Epidemiologic studies enable assessment of the severity of the problem and may give us some insight on how to prevent the development of a disease. However, such studies cannot determine the "true" cause of the disease, which is essential for optimizing prevention efforts.

Traditionally, DM has been viewed as a glucocentric disease—focusing on glucose metabolism as the determining factor for disease development. This has generated prevention methods and treatment modalities directed at decreasing sugar intake, lessening absorption and slowing glucose metabolism, as well as attempting to lower plasma glucose levels directly.

Another theory related to the pathogenesis of DM—alluded to more than 50 years ago³—has recently attracted renewed interest.⁴ This new concept shifts the emphasis for DM type 2 (DM 2) from a glucose-oriented approach to a lipocentric concept—lipid overload causing some type of lipid toxicity. Numerous studies have suggested that one of the most important fundamental underlying causes of the development of DM 2 is the effect of abnormal lipid metabolism on the ability of insulin to exert its influence on the body’s capability to use glucose.

For instance, it has been shown that free fatty acids (FFAs) can inhibit insulin-mediated suppression of glycogenolysis and gluconeogenesis processes in the liver, as well as uptake of glucose into myocytes in muscles.⁵ Also, FFAs have been shown to amass in the pancreas, resulting in beta cell destruction and an ultimate decrease in insulin secretion.⁶ The clinical significance of using this theoretical approach to DM 2 pathogenesis, and subsequent treatment, was demonstrated in a recent study of patients undergoing gastric banding accompanied by weight loss.⁷ The majority of patients achieved remission of their DM.

Most patients affected by DM exhibit signs and symptoms of cardiovascular disease, which is the No. 1 cause of death in these patients. To prevent the development and subsequent dire consequences of DM 2, reducing hyperglycemia has become the mainstay of DM therapy. As insulin resistance has been blamed for many complications associated with DM 2, overcoming this resistance seems to be a rational treatment approach to the disease. This has been attempted by giving patients numerous daily injections of insulin to achieve more constant normal plasma glucose levels.

However, this approach has resulted in excessive harmful side effects. These effects include an increase in deaths from multiple causes—fatal myocardial infarctions and cerebrovascular accidents, possibly due to increased lipid deposits and atherosclerosis.⁸ Thus, perhaps it would be beneficial initially to try to prevent the development of hyperglycemia by focusing on reducing caloric intake to reduce FFA and lipid production.

There is ample evidence that we are in the midst of a DM epidemic resulting in the development of diseases associated with a high degree of morbidity and mortality. Although treatment of DM and associated diseases has become more effective, we need to take a step backward and identify patients at risk. Only then can we institute effective preventive measures.

To do this, it is important to recognize the etiology and pathogenesis of these diseases. Although hyperglycemia may have an independent role in the development of atherosclerosis,⁹ new evidence is constantly challenging established concepts. As with many other diseases, it is not clear if known pathogenic processes can be applied to all people who have DM. Both in medicine and dentistry, we traditionally define diseases on the basis of clinical presentations rather than on pathogenesis. This practice thwarts attempts at effective prevention and more targeted interventions.

We traditionally define diseases on the basis of clinical presentations rather than on pathogenesis. This practice thwarts attempts at effective prevention.

Many oral health care providers are willing to take on the task of DM prevention. It would be worthwhile to augment these efforts not only by providing patients with glucose monitoring, but also by engaging patients in a dialogue about healthy behaviors. To do this effectively, we need to have a good understanding of underlying disease processes, yet recognize that traditional methods and approaches constantly need to be refined and redefined to be in tune with new and emerging information.

In closing, I will note that with this issue of JADA is packaged a Special Supplement on DM, made possible through an educational grant from the Colgate-Palmolive Co., New York City. It is our intent that this Special Supplement will provide oral health care providers with updated and relevant information and encourage them to take an active role in the care of patients with DM.