The prevalence of diagnosed diabetes among American adults has increased by 40 percent in 10 years and rose from 4.9 percent in 1990 to 6.9 percent in 1999 (Narayon and colleagues, 2003). More worryingly, it is estimated that this incidence will increase another 165 percent by 2050. To put this into perspective, the lifetime risk of diabetes in individuals born in 2000 is 33 percent for males and 39 percent for females! This increase primarily is due to type 2 diabetes, which is also referred to as diabesity. As discussed in Chapter 43, this term reflects the strong relationship of diabetes with the current epidemic of obesity in the United States and other countries (Gale, 2003; Mokdad and associates, 2003).


The increasing prevalence of type 2 diabetes in general, and in younger people in particular, has led to an increasing number of pregnancies with this complication (Ferrara and co-workers, 2004). Many women found to have gestational diabetes are likely to have type 2 diabetes that has previously gone undiagnosed (Feig and Palda, 2002). Indeed, the incidence of diabetes complicating pregnancy has increased approximately 40 percent between 1989 and 2004 (Getahun and colleagues, 2008). In Los Angeles County, Baraban and co-workers (2008) reported that the age-adjusted prevalence tripled from 14.5 cases per 1000 women in 1991 to 47.9 cases per 1000 in 2003.


There is keen interest in events that precede diabetes, and this includes the mini-environment of the uterus, where it is believed that early imprinting can have effects later in life (Saudek, 2002). For example, in utero exposure to maternal hyperglycemia leads to fetal hyperinsulinemia, causing an increase in fetal fat cells, which leads to obesity and insulin resistance in childhood (Feig and Palda, 2002). This in turn leads to impaired glucose tolerance and diabetes in adulthood. Thus, a cycle of fetal exposure to diabetes leading to childhood obesity and glucose intolerance is set in motion. This sequence has been reported in Pima Indians as well as a heterogeneous Chicago population (Silverman and colleagues, 1995).


Diabetes is now classified based on the pathogenic processes involved (Powers, 2008). Absolute insulin deficiency characterizes type 1 diabetes, whereas defective insulin secretion or insulin resistance characterizes type 2 diabetes (Table 52-1). The terms insulin-dependent diabetes mellitus (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) are no longer used. Age is also no longer used in classification, because pancreatic β-cell destruction can begin at any age. Most commonly, its onset is before age 30, but in 5 to 10 percent of affected individuals, onset is after age 30 years. Type 2 diabetes, although most typical with increasing age, also develops in obese adolescents.

Table Graphic Jump Location
Table 52-1. Etiological Classification of Diabetes Mellitus 

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