The most recent prevalence estimates of type 2 diabetes in youth, as reported by SEARCH, indicate that youth-onset type 2 diabetes is more prevalent among minority racial and ethnicity groups. Among youth with diabetes, the proportion of type 2 diabetes among non-Hispanic whites is 5.5%, while the proportion of type 2 diabetes among non-Hispanic blacks is 37.6%. For American Indian/Alaskan Natives, the proportion of type 2 diabetes is 80.0%. The proportion of type 2 diabetes in Asian or Pacific Islander and Hispanic youth is 34.2 and 35.2%, respectively [5•]. Additionally, among youth < 20 years of age, prevalence increases with age. Overall, based on standardization of SEARCH estimates to the U.S. census population, there were an estimated 20,262 youth with type 2 diabetes in 2009 (Table 1) and a prevalence of 0.24 case subjects/1000 (95% CI: 0.23, 0.26) [5•].

Recent (2012) estimates of youth-onset type 2 diabetes incidence from SEARCH indicate that American Indians and non-Hispanic blacks experience the highest incidence of type 2 diabetes (46.5/100,000/year in American Indians and 32.6/100,000/year in non-Hispanic blacks), relative to non-Hispanic whites (3.9/100,000/year), Hispanics (18.2/100,000/year), and Asian or Pacific Islanders (12.2/100,000/year). Incidence in girls is substantially higher than in boys (16.2/100,000/year in girls versus 9.0/100,000/year in boys) (Table 2) [7••].

Of concern, the incidence of type 2 diabetes has increased considerably over the previous decade, with racial and ethnic minorities driving this increase. SEARCH data indicate an overall 4.8% (95% CI: 3.2, 6.4) annual increase (adjusted for age and sex)in incidence. Annual increases were estimated to be highest among non-Hispanic blacks (6.3%; 95% CI: 4.0, 8.8), Asian/Pacific Islanders (8.5%; 95% CI: 2.0, 15.4), and American Indians (8.9%; 95% CI: 5.0, 13.1) in contrast to an annual increase of just 0.6% (95% CI: − 2.0, 3.4) among non-Hispanic whites and 3.1% (95% CI: 0.8, 5.4%) among Hispanics. The annual increase in incidence among girls was estimated to be nearly twice that of boys (6.2% [95% CI: 4.2, 8.2] versus 3.7% [95% CI: 1.6, 5.8]) [7••].

It has been suggested that the increase in incidence is due to increased surveillance of disease. In a recently conducted study in SEARCH of self-reported modes of case presentation, 65% of youth reported diagnosis as a result of symptoms and 30% reported diagnosis during a routine check-up. The proportion of those reporting diagnosis due to symptoms has decreased overtime, from 72.1% in 2002–2004 to 59.1% in 2008–2010 [8]. This suggests that some proportion of increased disease incidence may be a result of increased disease surveillance, although this is unlikely the main explanation for the increase.

SEARCH projections on type 2 diabetes in youth indicate an increasing and high burden of disease [9•]. By 2050, at current incidence rates, the number of youth with type 2 diabetes may double, primarily due to shifts in the population distribution of racial minorities. Of concern, if the incidence of type 2 diabetes continues to increase, as suggested by SEARCH data, the number of youth with type 2 diabetes may increase more than fourfold [9•].

While it has been well-documented that obesity is a significant determinant for the development of type 2 diabetes, less is known as to the factors that may contribute to the obesogenic environment that ultimately leads to type 2 diabetes in youth. Ina recent sub-study from the SEARCH case-control ancillary study, type 2 diabetes cases (n = 91) and non-diabetic controls (n = 293) from the same catchment areas as the identified cases were compared to evaluate the contribution of neighborhood-level factors. Adjusted for age, sex, race/ethnicity, study site, breastfeeding, maternal diabetes, parental education, and parental income, this study indicated an increased risk of type 2 diabetes in less densely populated residential areas (< 500 residents/sq. mile) versus densely populated areas (1000+ residents/sq. mile) (aOR 3.22, 95% CI: 1.40, 7.41). Small and large towns, as opposed to urban areas, were similarly associated with increased risk (aOR 3.04; 95% CI: 1.25, 7.41). No other associations were observed with adjustment across factors, including housing values, food desert status, proportion of households receiving social security, median household income, and proportion of residents with at least a high school education [11].

Studies conducted in adult populations have suggested that inorganic arsenic (iAs) exposure may increase risk for developing type 2 diabetes [12, 13]. Exposure to arsenic is believed to be increasing, due to increased consumption of rice-based diets that confer increased risk for exposure [14]. In a case-control sub-study, plasma levels of arsenic were evaluated in relation to both type 1 and type 2 diabetes. While associations were observed for type 1 diabetes, no association was observed for type 2 diabetes [15]. One challenge in estimating the effect of arsenic on disease development is estimating exposure, and chronic sources of exposure may be more relevant than recent, high levels of exposure. Additional investigations are needed to establish the relationship, if any, between arsenic and type 2 diabetes [16, 17].

Several reports (recently summarized in Dabelea D. et al., Diabetes in America) have convincingly shown that exposure to maternal diabetes in utero is a significant risk factor for obesity, impaired glucose tolerance, and type 2 diabetes later in life [18•]. Of note, work by the SEARCH case-control study provided novel evidence that intrauterine exposure to maternal diabetes and obesity are each important determinants of type 2 diabetes in 10–19-year-old multi/ethnic youth. In this study, exposure to maternal gestational diabetes mellitus (OR 5.7; 95% CI: 2.4, 13.4) and exposure to maternal pre-pregnancy obesity (OR 2.8; 95% CI: 1.5, 5.2) were independently associated with type 2 diabetes in the offspring. Combined exposure to maternal diabetes and obesity in utero accounted for 47% of the type 2 diabetes risk in this population [19].

In observational studies, breastfeeding is protective against later development of obesity and type 2 diabetes [18•]. In the SEARCH case-control study, the prevalence of breastfeeding (any duration) was lower among youth with type 2 diabetes than among controls and, thus, breastfeeding was associated with significantly lower odds of type 2 diabetes (OR 0.26; 95% CI: 0.15, 0.46) [10•]. Thus, for offspring of pregnancies that carry a high risk for future obesity, early infant diet may represent an opportunity to mitigate risk.

A challenge in many chronic diseases with youth onset is the continuation of disease management through the transition from pediatric to adult care providers [20]. Indicators of disease management through this transition, as evidenced by glycemic control (HbA1c ≥ 75 mmol/mol [9.0%]), were examined in SEARCH in 182 young adults with type 2 diabetes who were initially receiving care through a pediatric provider, who reached age 18–25 while enrolled in SEARCH, and who had at least one follow-up in SEARCH after reaching age 18. In the participants included in analyses, 57% reported transferring to an adult care provider, 15% reported no care, and 28% reported still receiving care from their pediatric provider. Lack of insurance was associated with having no designated health-care provider. Adjusting for disease duration, age at diagnosis, sex, race/ethnicity, and HbA1c at baseline, provider type at follow-up was strongly associated with poor glycemic control, with transition to an adult care provider associated with a 350% increase in odds of poor glycemic control at the follow-up study visit as compared to having continued care with a pediatric care provider (aOR 4.5; 95% CI: 1.8, 11.2). Similarly, no care was associated with increased risk of poor glycemic control (aOR 4.6; 95% CI: 1.4, 14.6) [21].

Psychosocial factors are well-known to be associated with increased risk of poor disease management in type 1 diabetes, but less is known about type 2 diabetes [22]. Symptoms of depression and health-related quality of life markers are collected at SEARCH study visits using the Center for Epidemiologic Studies Depression (CES-D) scale [23] and the Pediatric Quality of Life Inventory (PedsQL) generic and diabetes modules [24]. Using data collected from these assessments and routinely collected data on glycemic control, SEARCH evaluated the association between psychosocial factors early in disease development in relation to glycemic control over time. This study identified lower quality of life scores and more indications of depressive symptoms across time points in participants with type 2 diabetes, as compared to those with type 1 diabetes, and an association between declining diabetes-specific quality of life scores and HbA1c [25]. A recent study of risk factors for health-related quality of life suggested a positive association between female gender and BMI and lower health-related quality of life in type 2 diabetes [26].

At the time that cases are registered in the SEARCH registry, core data elements are abstracted from each registered case’s medical record, including presence of diabetic ketoacidosis (DKA) at diagnosis. DKA is indicated when, in the presence of hypoglycemia, blood bicarbonate levels are < 15 mmol/L, and/or pH is < 7.25 (venous) or < 7.30 (capillary), and/or DKA is indicated in the medical record [28]. Among those with type 2 diabetes, there was a decrease in the proportion of participants with DKA at diagnosis from 11.7% (95% CI: 8.2, 15.2%) in 2002–2003 to 5.7% (95% CI: 4.1, 7.4%) in 2008–2010. DKA at diagnosis was more prevalent among younger age groups, males, and in minority race/ethnicity groups [29].