IMPORTANCE Despite concern about an “epidemic,” there are limited data on trends in prevalence of either type 1 or type 2 diabetes across US race and ethnic groups. OBJECTIVE To estimate changes in the prevalence of type 1 and type 2 diabetes in US youth, by sex, age, and race/ethnicity between 2001 and 2009. DESIGN, SETTING, AND PARTICIPANTS Case patients were ascertained in 4 geographic areas and 1 managed health care plan. The study population was determined by the 2001 and 2009 bridged-race intercensal population estimates for geographic sites and membership counts for the health plan. MAIN OUTCOMES AND MEASURES Prevalence (per 1000) of physician-diagnosed type 1 diabetes in youth aged 0 through 19 years and type 2 diabetes in youth aged 10 through 19 years. RESULTS In 2001, 4958 of 3.3 million youth were diagnosed with type 1 diabetes for a prevalence of 1.48 per 1000 (95% CI, 1.44–1.52). In 2009, 6666 of 3.4 million youth were diagnosed with type 1 diabetes for a prevalence of 1.93 per 1000 (95% CI, 1.88–1.97). In 2009, the highest prevalence of type 1 diabetes was 2.55 per 1000 among white youth (95% CI, 2.48–2.62) and the lowest was 0.35 per 1000 in American Indian youth (95% CI, 0.26–0.47) and type 1 diabetes increased between 2001 and 2009 in all sex, age, and race/ethnic subgroups except for those with the lowest prevalence (age 0–4 years and American Indians). Adjusted for completeness of ascertainment, there was a 21.1% (95% CI, 15.6%–27.0%) increase in type 1 diabetes over 8 years. In 2001, 588 of 1.7 million youth were diagnosed with type 2 diabetes for a prevalence of 0.34 per 1000 (95% CI, 0.31–0.37). In 2009, 819 of 1.8 million were diagnosed with type 2 diabetes for a prevalence of 0.46 per 1000 (95% CI, 0.43–0.49). In 2009, the prevalence of type 2 diabetes was 1.20 per 1000 among American Indian youth (95% CI, 0.96–1.51); 1.06 per 1000 among black youth (95% CI, 0.93–1.22); 0.79 per 1000 among Hispanic youth (95% CI, 0.70–0.88); and 0.17 per 1000 among white youth (95% CI, 0.15–0.20). Significant increases occurred between 2001 and 2009 in both sexes, all age-groups, and in white, Hispanic, and black youth, with no significant changes for Asian Pacific Islanders and American Indians. Adjusted for completeness of ascertainment, there was a 30.5% (95% CI, 17.3%–45.1%) overall increase in type 2 diabetes. CONCLUSIONS AND RELEVANCE Between 2001 and 2009 in 5 areas of the United States, the prevalence of both type 1 and type 2 diabetes among children and adolescents increased. Further studies are required to determine the causes of these increases.

No abstract

Aims/hypothesis To evaluate whether exposure to maternal gestational diabetes (GDM) is associated with adiposity and fat distribution in a multiethnic population of children. Methods Retrospective cohort study of 82 children exposed to maternal GDM and 379 unexposed youths 6-13 years of age with measured BMI, waist circumference, skinfold thickness, and visceral and subcutaneous abdominal fat. Results Exposure to maternal GDM was associated with higher BMI (p=0.02), larger waist circumference (p=0.004), more subcutaneous abdominal fat (p=0.01) and increased subscapular to triceps skinfold thickness ratio (p=0.01) in models adjusted for age, sex, race/ethnicity and Tanner stage. Adjustment for socioeconomic factors, birthweight and gestational age, maternal smoking during pregnancy and current diet and physical activity did not influence associations; however, adjustment for maternal pre-pregnancy BMI attenuated all associations. Conclusions/interpretation Exposure to maternal GDM is associated with increased overall and abdominal adiposity, and a more central fat distribution pattern in 6-to 13-yearold youths from a multi-ethnic population, providing further support for the fetal overnutrition hypothesis.

Background and Objective Poor maternal diet in pregnancy can influence fetal growth and development. We tested the hypothesis that poor maternal diet quality during pregnancy would increase neonatal adiposity (percent fat mass, %FM) at birth by increasing the fat mass (FM) component of neonatal body composition. Methods Our analysis was conducted using a pre-birth observational cohort of 1,079 mother-offspring pairs. Pregnancy diet was assessed via repeated Automated Self-Administered 24-hour dietary recalls, from which Healthy Eating Index-2010 (HEI-2010) scores were calculated for each mother. HEI-2010 was dichotomized into scores ≤ 57 and scores > 57, with low scores representing poorer diet quality. Neonatal %FM was assessed within 72 hours after birth with air displacement plethysmography. Using univariate and multivariate linear models, we analyzed the relationship between maternal diet quality and neonatal %FM, FM, and fat-free mass (FFM) while adjusting for pre-pregnancy body mass index (BMI), physical activity, maternal age, smoking, energy intake, preeclampsia, hypertension, infant sex, and gestational age. Results Total HEI-2010 score ranged between 18.2 and 89.5 (mean: 54.2, SD: 13.6). An HEI-2010 score ≤ 57 was significantly associated with higher neonatal %FM (β = 0.58, 95% CI 0.07, 1.1, p<0.05) and FM (β=20.74; 95% CI 1.49, 40.0; p<0.05) but no difference in FFM. Conclusions Poor diet quality during pregnancy increases neonatal adiposity independent of maternal pre-pregnancy BMI and total caloric intake. This further implicates maternal diet as a potentially important exposure for fetal adiposity.

OBJECTIVETo establish minimal clinically important difference (MCID) scores representing the smallest detectable change in quality of life (QOL), using the Pediatric Quality of Life Inventory (PedsQL) Generic Core and Diabetes Module among youth with diabetes and their parents, and to identify demographic and clinical correlates of QOL change over 1 year.RESEARCH DESIGN AND METHODSParticipants in the SEARCH for Diabetes in Youth Study aged >5 years and parents of youth aged <18 years completed PedsQL surveys at their initial and 12-month study visits. MCIDs for each PedsQL module were calculated using one standard error of measurement. Demographic and clinical characteristics associated with QOL change were identified through multiple linear and logistic regression analyses.RESULTSThe sample comprised 5,004 youth (mean age, 12.5 ± 4.7 years; mean diabetes duration, 3.4 ± 3.7 years). Of 100 possible points, PedsQL total score MCIDs for youth with type 1 and type 2 diabetes, respectively, were Generic Core, 4.88, 6.27 (parent) and 4.72, 5.41 (youth); Diabetes Module, 4.54, 6.06 (parent) and 5.27, 5.96 (youth). Among 1,402 youth with a follow-up visit, lower baseline QOL, male sex, private insurance, having type 1 diabetes, longer diabetes duration, and better glycemic control predicted improvements in youth- and parent-reported PedsQL total scores over 1 year. Clinically meaningful (≥1 MCID) improvements in total score for at least one PedsQL module were predicted by private insurance, lower BMI, and lower A1C at baseline.CONCLUSIONSThese diabetes-specific reference points to interpret clinically meaningful change in PedsQL scores can be used in clinical care and research for youth with type 1 and type 2 diabetes.

Aims/hypothesis-Recent studies have provided evidence that intrauterine exposure to maternal diabetes has lifelong effects on adult offspring, including increased risks of obesity, type 2 diabetes and cardiovascular disease. The aim of this study was to assess the relationship between exposure to maternal diabetes in utero and cardiovascular risk factors in healthy children and to investigate whether these associations are independent of maternal prepregnancy BMI and offspring attained BMI.Methods-Data were from a retrospective cohort of children aged 6-13 years born during 1994-2002. Multiple linear regression was used to examine the associations between exposure and cardiovascular risk factors with adjustment for demographic factors and pubertal stage and additionally for maternal prepregnancy BMI and offspring attained BMI.Results-Ninety-nine offspring of diabetic pregnancies had significantly increased E-selectin, vascular adhesion molecule 1 (VCAM1), leptin, waist circumference, BMI and systolic blood pressure and decreased adiponectin levels compared with 422 offspring of non-diabetic pregnancies after adjustment for age, sex and race/ethnicity (p<0.05 for each risk factor). Additional adjustment for maternal prepregnancy BMI substantially attenuated group differences in the risk factors except for E-selectin, VCAM1 and waist circumference, which remained significantly higher in exposed children.Conclusions/interpretation-Compared with unexposed children, healthy offspring exposed to maternal diabetes in utero have a worse cardiovascular risk profile. In particular, offspring have substantially increased levels of circulating cellular adhesion molecules, which are biomarkers of adverse endothelium perturbation and may be related to the earliest preclinical stages of atherosclerosis and diabetes.

Objective-To examine associations between exposure to maternal diabetes in utero and body mass index (BMI) growth trajectories from birth through 13 years of age among a diverse cohort of youth.Study design-Mixed linear effects models were constructed to assess differences in BMI and BMI growth velocity from birth through 13 years of age for 95 subjects exposed to diabetes in utero and 409 unexposed subjects enrolled in a retrospective cohort study.Results-The overall BMI growth trajectory (adjusted for sex and race/ethnicity) was not significantly different for exposed and unexposed subjects from birth through 26 months of age (p=0.48). However, the overall growth trajectory from 27 months of age through 13 years differed by exposure status (p=0.008), adjusted for sex and race/ethnicity. The difference was primarily due to a significantly higher BMI growth velocity among exposed youth between 10-13 years, increasing by 4.56 kg/m 2 compared to 3.51 kg/m 2 in the unexposed (p=0.005). Control for demographic variables, socioeconomic factors and maternal pre-pregnancy BMI did not alter the observed associations.Conclusions-Exposure to maternal diabetes in utero accelerates BMI growth in late childhood thus increasing long-term obesity risk. KeywordsGestational diabetes; fetal overnutrition; fetal exposure to diabetes; childhood obesity; childhood BMI; growth trajectoryThe rapid increases in childhood obesity observed worldwide herald an alarming forecast for future burden of hypertension, diabetes and cardiovascular disease (1-3). Significant research has suggested the existence of critical periods for the development of childhood obesity. Fetal life, the time period of greatest developmental plasticity, has been suggested to be one such important period (4). Indeed, several pregnancy factors have been associated with greater obesity in the offspring, including maternal pre-pregnancy BMI (5,6), gestational weight gain (7,8), and gestational diabetes (9-12).Corresponding Author: Dana Dabelea, MD, PhD, Associate Professor, Department of Epidemiology, Colorado School of Public Health, University of Colorado Denver, Tel: 303-724-4414, Dana.Dabelea@ucdenver.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The possibility that intrauterine exposure to maternal diabetes could place offspring at increased risk for obesity and related metabolic consequences later in life has generated considerable interest. Maternal diabetes is a recognized risk factor for excess fetal growth, macrosomia and increased fetal adiposity (13,14). However, less is known about the pattern of po...

This paper resulted from a conference entitled “Lactation and Milk: Defining and refining the critical questions” held at the University of Colorado School of Medicine from January 18–20, 2012. The mission of the conference was to identify unresolved questions and set future goals for research into human milk composition, mammary development and lactation. We first outline the unanswered questions regarding the composition of human milk (Section I) and the mechanisms by which milk components affect neonatal development, growth and health and recommend models for future research. Emerging questions about how milk components affect cognitive development and behavioral phenotype of the offspring are presented in Section II. In Section III we outline the important unanswered questions about regulation of mammary gland development, the heritability of defects, the effects of maternal nutrition, disease, metabolic status, and therapeutic drugs upon the subsequent lactation. Questions surrounding breastfeeding practice are also highlighted. In Section IV we describe the specific nutritional challenges faced by three different populations, namely preterm infants, infants born to obese mothers who may or may not have gestational diabetes, and infants born to undernourished mothers. The recognition that multidisciplinary training is critical to advancing the field led us to formulate specific training recommendations in Section V. Our recommendations for research emphasis are summarized in Section VI. In sum, we present a roadmap for multidisciplinary research into all aspects of human lactation, milk and its role in infant nutrition for the next decade and beyond.