Kelly West Lecture: Primary Prevention of Type II Diabetes Mellitus

Abstract

A useful paradigm for developing a public health strategy for combating chronic diseases consists of three phases: observational epidemiological studies, first cross-sectional and then prospective; intervention trials; and, finally, public health action. Although the field of cardiovascular epidemiology is well advanced into the third phase, i.e., public health action, the field of diabetes epidemiology is at least a generation behind and has only recently entered the phase of prospective observational studies. Part of the reason for this lag may be that, unlike cardiovascular disease, non-insulin-dependent (type II) diabetes has not been traditionally viewed as an epidemic, thereby detracting from a sense of urgency about the disease. Although this perspective may be appropriate for white populations, data from around the world make it increasingly apparent that type II diabetes has indeed reached epidemic proportions in non-white populations. Prospective studies are needed to firmly establish risk factors on which public health actions can be confidently based. Although anthropometric and metabolic risk factors such as obesity, body fat distribution, and circulating glucose and insulin concentrations are becoming well established as risk factors for type II diabetes, much less is known about behavioral risk factors. These latter risk factors are especially important because they are often amenable to public health action. There are preliminary data suggesting that decreased physical activity and increased fat consumption may be behavioral risk factors for diabetes. Decreased total energy intake, reflecting either low levels of physical activity or an intrinsically low metabolic rate, perhaps genetic in origin, may also be a diabetes risk factor. Unlike the field of cardiovascular epidemiology, in which there is already a critical mass of intervention trials on primary prevention, such trials are essentially nonexistent in the field of diabetes epidemiology; they are urgently needed. Although the notion of a single gene causing diabetes is clearly simplistic, there is a reasonable expectation that genetic markers can be identified that would be useful in screening for genetic susceptibles, at least in selected predisposed populations. Such markers could then be used to identify target populations for primary-prevention trials and public health action. Although primary-prevention trials should not be deferred until genetic markers are available, these two research paths may someday converge and genetic markers may come to play an important role in screening individuals as part of a comprehensive public health strategy. Numerous trial designs should be considered for testing hypotheses about the primary prevention of type II diabetes. These include single risk factor, multiple risk factor, and factorial designs.(ABSTRACT TRUNCATED AT 400 WORDS)

Glycemia and Cardiovascular Risk

“…With variable numbers of people with diabetes included in these populations, glucose levels could have been merely a proxy for the presence of diabetic subjects, whose cardiovascular risk was increased for reasons unrelated to glycemia per se. The second development was the recognition that glucose concentrations in many populations followed a bimodal distribution and, thus, that the cutpoint between euglycemia and diabetes was not purely arbitrary (2). These findings reinforced the notion that glycemic level as a cardiovascular risk factor in the normal population and glycemic level as a cardiovascular risk factor in diabetic subjects constituted two separate questions.…”

Use of glycated hemoglobin (HbA1C) and impaired glucose tolerance in the screening of undiagnosed diabetes in the Malaysian population

“…Type 2 DM results from the interaction between genetic predisposition, behavioral and environmental risk factors (3). Although the genetic basis of type 2 DM has yet to be identified there is strong evidence that such modifiable risk factors as obesity and physical inactivity are the main non genetic determinants of the disease (4,5,6). Prevention of diabetes is a worthy cause especially as diabetes is linked to contemporary lifestyle (7).…”

Obesity and upper body fat distribution in Mexican American children from families with a diabetic proband

“…Since then, many studies have been conducted seeking associations of the occurrence of NIDDM with fatness patterns on the upper part of the body, both cross-sectionally (Feldman et al, 1969; Kissebah et al, 1982; Szathmary and Holt, 1983; Mueller et al, 1984) and prospectively (Stern, 1991). Most studies, however, have Concentrated on samples of adults because the prevalence of NIDDM is very low in children or adolescents.…”