According to the National Center for Health Statistics (2013), the number of adults diagnosed with diabetes in the United States has tripled from 6.9 million in 1991 to 20.9 million in 2011. Astoundingly, the Centers for Disease Control and Prevention (2010) have estimated that the number of Americans with diabetes will range from 1 in 3 to 1 in 5 by 2050. Reasons for this rise include an aging population more likely to develop type 2 diabetes, increases in minority groups at particular risk for type 2 diabetes, and dramatic increases in obesity—also referred to as diabesity. This term reflects the strong relationship of diabetes with the current obesity epidemic in the United States and underlines the critical need for diet and lifestyle interventions to change the trajectory of both.
There is keen interest in events that precede diabetes, and this includes the uterine environment, where early imprinting is believed to 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. This leads to obesity and insulin resistance in childhood (Feig, 2002). This in turn leads to impaired glucose tolerance and diabetes in adulthood. This cycle of fetal exposure to diabetes leading to childhood obesity and glucose intolerance has been reported in Pima Indians and a heterogeneous Chicago population (Silverman, 1995).
In nonpregnant individuals, the type of diabetes is based on its presumed etiopathogenesis and its pathophysiological manifestations. Absolute insulin deficiency characterizes type 1 diabetes. In contrast, defective insulin secretion, insulin resistance, or increased glucose production characterizes type 2 diabetes (Table 57-1). Both types are generally preceded by a period of abnormal glucose homeostasis. The terms insulin-dependent diabetes mellitus (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) are now obsolete. Pancreatic β-cell destruction can begin at any age, but type 1 diabetes is clinically apparent most often before age 30. Type 2 diabetes usually develops with advancing age but is increasingly identified in younger obese adolescents.
TABLE 57-1Etiological Classification of Diabetes Mellitus |Favorite Table|Download (.pdf) TABLE 57-1 Etiological Classification of Diabetes Mellitus
|Type 1: β-Cell destruction, usually absolute insulin |
| deficiency |
| Immune-mediated |
| Idiopathic |
|Type 2: Ranges from predominantly insulin resistance to predominantly an insulin secretory defect with insulin resistance |
|Other types |
| Genetic mutations of β-cell function—MODY 1–6, others |
| Genetic defects in insulin action |
| Genetic syndromes—Down, Klinefelter, Turner |
| Diseases of the exocrine pancreas—pancreatitis, cystic fibrosis |
| Endocrinopathies—Cushing syndrome, pheochromocytoma, others |
| Drug or chemical induced—glucocorticosteroids, thiazides, β-adrenergic agonists, others |
| Infections—congenital rubella, cytomegalovirus, coxsackievirus |
|Gestational diabetes |
Classification During Pregnancy
Diabetes is the most common medical complication of pregnancy. Women can be separated into those who were ...