Approximately 7.8 million diagnosed cases of diabetes were reported in the United States in 1993. Insulin dependent diabetes mellitus (IDDM) comprised about 7% of all diagnosed cases of diabetes mellitus while the remaining 90% to 95% of cases may be considered noninsulin dependent diabetes mellitus (NIDDM). An estimated 625,000 new cases of diabetes are diagnosed annually in the United States. The prevalence of NIDDM is two to three times greater among Mexican Americans than in non-Hispanic Whites.[2-6]
In 1996, an estimated 890,000 Texans had diagnosed diabetes while another estimated 890,000 had undiagnosed diabetes. Almost 9% of both Hispanic and African American Texans have been diagnosed with diabetes as compared to 5% of White Texans. Between 1989 and 1994, almost 22,000 Texans older than age 40 died from complications of diabetes. In 1992, Texas spent more than $4 billion on the costs of diabetes and related problems.[9,10]
NIDDM, a chronic progressive disorder, may take years to develop, presumably starting with genetic susceptibility in most cases. The simplest evidence supporting NIDDM's genetic component is that this disorder occurs more frequently in certain ethnic groups and in certain families. The ethnic and familial clustering likely results from shared genes and shared behavioral and environmental risk factors. Studies of populations that derive from ethnic groups with different genetic risks of developing NIDDM provide indirect evidence for a genetic component of NIDDM. Hispanics in the southwestern United States share genes of Native Americans and of non-Hispanic Whites. The risk of NIDDM in this Hispanic population has been shown to be intermediate between the very high NIDDM prevalence in the Native American population and the relatively low NIDDM prevalence in the non-Hispanic White population.[1,12]
Presence of NIDDM in a family member constitutes an established risk factor for NIDDM. Individuals with at least one diabetic parent have a much higher incidence of NIDDM than those of similar body habitus who do not have a diabetic parent. Several studies of twins suggest that NIDDM is highly concordant among monozygous and less concordant among dizygous twins, indicating that genetic factors play a major role in the etiology of NIDDM. However, since the concordance in monozygous twins is much less than 100%, a role for nongenetic factors in NIDDM development is evident.
Obesity is the dominating risk factor that appears to facilitate transition from a genetic predisposition for NIDDM to onset of the disease. Central obesity has been shown to be the major predictor of NIDDM, associated initially with insulin resistance and impaired glucose tolerance, and subsequently with loss of insulin secretory capacity.[15,16] The major nutritional risk factor for NIDDM is excess dietary fat intake, which predicted the risk for NIDDM development in individuals with impaired glucose tolerance in the San Luis Valley Diabetes Study.[17,18] In addition, nondiabetic individuals who developed diabetes in the San Antonio Heart Study consumed more saturated fat and cholesterol and less polyunsaturated fat than those who remained nondiabetic.
Physical inactivity also has been associated with increased onset of NIDDM, whereas regular physical training and exercise increase insulin sensitivity. Behavioral interventions to modify the risk factors for NIDDM by restricting dietary fat, together with increased physical activity, decrease hyperglycemia significantly. A six-year study of 47-49-year-old males with early stage NIDDM demonstrated that it is possible to prevent or postpone NIDDM onset in at risk individuals by changing diet and exercise habits.
Mexican Americans in south Texas have a three- to five-fold increase in NIDDM prevalence, greater adiposity, and a less favorable distribution of …