istics include region and location of residence, marital status, and living arrangements. However, people with NIDDM have fewer years of schooling, are less likely to be employed, and have lower family incomes than the general adult population. Rates of NIDDM in the United States tend to be higher in rural areas and among people with relatively low socioeconomic status.
Genetic, environmental, and lifestyle factors can place a person at increased risk for developing NIDDM. Rates of NIDDM among adults of Hispanic origin, blacks, and Asian-Americans appear to be higher than among whites. The rates of diagnosed NIDDM among some Native Americans (e.g., Pima Indians) are among the highest in the world. It is likely, however, that this high frequency reflects a genetic origin. The most important risk factors for NIDDM are increasing age, higher blood glucose concentration, family history of diabetes, and adiposity. Central distribution of body fat (i.e., high waist-to-hip ratio) is also strongly associated with a higher risk of NIDDM (see Chapters 5 and 21).
Advanced maternal age and the presence of islet cell or insulin antibodies are associated with increased IDDM risk. The incidence of IDDM is similar in males and females, but is 1.5 times higher in whites than in blacks. Although incidence rates vary widely internationally, the risk for siblings of IDDM cases is 7 to 18 times higher than the risk in the general population. Siblings with certain HLA genes are at increased risk for developing IDDM (National Diabetes Data Group, 1985).
The only factor that has been consistently related to the prevalence of diabetes mellitus is relative body weight (West, 1978). In several migrant populations (e.g., Japanese who moved to Hawaii and California and Yemenites who migrated to Israel), the prevalence of diabetes has increased along with Westernization of diet and lifestyle (West, 1978). The association of diabetes (presumably NIDDM) with adiposity persists in both inter- and intrapopulation analyses, despite wide variation in intake of individual nutrients.
The prevalence of diabetes among adults is positively associated with higher percentages of total caloric intake as fats and inversely related to the percentage of calories as carbohydrates. Specific carbohydrates, such as sugar or starch, have not been shown to influence the risk of diabetes.
In a study comparing two Micronesian populationsone at high risk and one at low risk of NIDDMKing et al. (1984) found that estimates of fiber intake had no predictive value in estimating risk of subsequent disease. Metabolic studies indicate that soluble forms of dietary fiber (e.g., guar and pectin) may curtail the glycemic response (glucose levels reached in response to ingestion of a particular food) in people with overt diabetes (Jenkins et al., 1976, 1978, 1979; Monnier et al., 1978; Morgan et al., 1979; LSRO, 1987; Poynard et al., 1980), but there are no data on the possible role of dietary fiber in reducing the risk for this disease.
In large population studies, alcohol intake has been correlated with hyperglycemia. There is no ready explanation for this, except for alcoholics who develop insulin deficiency as a result of chronic pancreatitis. It was suspected that ethanol per se impaired glucose tolerance (Gerard et al., 1977). Yki-Järvinen and Nikkilä (1985) reported that insulin resistance results from excessive alcohol intake by otherwise healthy adults in the United States.
Studies in animals indicate that a decrease in glucose tolerance is induced by chromium deficiency and is reversed by the administration of chromium (see Chapter 14). In hyperglycemic humans, chromium supplementation improved glucose tolerance and lowered insulin levels (Anderson, 1986; Riales and Albrink, 1981; Simonoff, 1984), suggesting that chromium deficiency may be a contributing factor to disease onset. However, no population data have been reported implicating chromium deficiency in humans with diabetes, and chromium supplementation does not improve blood glucose or insulin levels in those with the disease (Anderson, 1986; Rabinowitz et al., 1983). Chromium deficiency in people with diabetes could thus be a consequence rather than a cause of the disease (Simonoff, 1984). In summary, other than data on total caloric intake and NIDDM, there is no evidence that dietary composition influences the risk of diabetes mellitus.
There is a long-standing controversy concerning the macronutrient composition of the diet used for management of people with IDDM and NIDDM (Bierman, 1979; Wood and Bierman, 1986), especially with regard to the optimal proportion of carbohydrate-containing foods. The nutritional requirements of people with diabetes are essentially