Diabetes is the third most prevalent severe chronic disease of childhood and a leading cause of retinopathy, nephropathy, neuropathy, and coronary and peripheral vascular disease later in life. Diabetes diagnosed in youth, defined as age <18 years, and young adults is not always easy to classify into one of the main etiologic “types”, i.e., type 1 or type 2. This is especially true since obesity, classically associated with type 2 diabetes, is now more common among youth with type 1 diabetes. Data suggest that youth with diabetes autoantibodies and obesity are metabolically similar to thin type 1 diabetic youth and do not have “type 1.5” or “double diabetes.” The prevalence of diabetes in U.S. youth in 2009 was 2.2 per 1,000 overall; the prevalence of type 1 diabetes was 1.93 per 1,000 and that of type 2 diabetes was 0.24 per 1,000. Non-Hispanic white youth had the highest prevalence of type 1 diabetes, followed by non-Hispanic black youth. Type 2 diabetes was found to occur in all racial/ethnic groups, but the proportion of type 1 to type 2 diabetes varied greatly by race/ethnicity, with type 2 diabetes representing only 5.5% of cases of diabetes in non-Hispanic white youth, but 80% of diabetes in American Indian youth. Between 2001 and 2009, a 31% increase in prevalence of type 2 diabetes and a 21% increase in prevalence of type 1 diabetes were observed.
Risk factors for type 1 diabetes include genetics, especially the HLA region, and environmental factors, such as viruses and early life diet, though few nongenetic factors are well established. Type 2 diabetes risk factors include genetics, which explains only a small percentage of risk, intrauterine exposure to maternal obesity and diabetes, and high gestational weight gain, as well as postnatal obesity with rapid catch-up growth from low birth weight. Breastfeeding appears to reduce the risk of type 2 diabetes in youth.
The major complications of youth-onset diabetes were once thought to develop only after achieving adult age. Newer data suggest that with sensitive techniques, diabetic retinopathy, neuropathy, and elevated urine albumin concentrations can be detected after 3–5 years of diabetes duration. In addition, increased arterial stiffness, reduced heart rate variability (as a sign of cardiac autonomic neuropathy), and carotid artery wall thickening can also be detected and are associated with higher levels of glycemia. These subclinical and clinical outcomes appear to be more common among youth with type 2 than type 1 diabetes at the same duration. Cardiovascular disease risk factors (e.g., lipids, blood pressure, inflammatory and oxidative stress markers) are also elevated after short durations, especially in youth with type 2 diabetes or those with poor glycemic control. Mortality among youth with diabetes is elevated compared to nondiabetic controls by 30%–200%. Those with type 1 diabetes diagnosed before age 20 years have a life expectancy that is 15–27 years shorter than that of nondiabetic persons, although substantial improvements in life expectancy have been noted among those diagnosed after 1965. No life expectancy studies are available among youth with type 2 diabetes.
The earlier onset of both type 1 and type 2 diabetes results in a longer duration of diabetes at any adult age than in prior years. Thus, women with youth-onset diabetes are now more likely to have diabetes during their pregnancies, which results in increased offspring risk for both obesity and diabetes. In addition, complications development is duration dependent, so persons with youth-onset diabetes now face chronic kidney disease and dialysis, myocardial infarction, and stroke at younger ages than persons who develop diabetes as adults, resulting in greater life-years lost and higher health care costs. Since type 2 diabetes and many of the risk factors for complications in both types of diabetes cluster in youth who are economically disadvantaged, significant efforts to improve care will be required.