Despite the long-held belief that growth hormone supplementation provides psychosocial benefits to patients with Turner syndrome (TS), this assumption has never been rigorously tested in a randomized control trial. As a sub-study of the Canadian growth-hormone trial, parent-, and patient-completed standardized questionnaires were used to compare 70 girls with TS who received injections (GH group) and 61 similarly followed untreated TS controls (C) on multiple facets of psychosocial functioning. Questionnaires were given (i) at baseline (session 1, mean age = 10.4 y), (ii) before estrogen therapy for puberty induction (session 2, mean age = 13.0 y), (iii) after 1 year of estrogen therapy (session 3, mean age = 14.4 y), and (iv) when growth stopped (session 4, mean age = 16.3 y). Groups were compared for multiple facets of psychosocial function within social, behavioral, self-esteem, and academic domains. Results were also correlated with indices of adult height. We found no global (i.e., across-session) group differences on any scales or subscales of the four domains. In both GH and C groups, age-related improvements were seen for social problems, externalizing behavior problems, and school functioning and age-related declines for social competence and social relations. Both parents and patients claimed GH received less teasing than C but C had more friends than GH. Results from analyses conducted within individual sessions showed that while GH at early sessions claimed to be more popular, more socially engaged, better adapted, and to have higher self-esteem than C, C was reported to be less anxious, depressed, and withdrawn than GH at adult height. The correlation analyses revealed different effects of adult height and height gain on outcome for the two groups. In GH, both height parameters were correlated with multiple parent- and/or self-reported indices from the four psychosocial domains, whereas in C, only adult height and two indices (viz., total self-concept and school functioning), were correlated. The observed modest gains in psychosocial functioning for patients with TS treated with GH highlight the need for alternative approaches to assist them in coping with the challenges of their condition.

AimsTo evaluate the association between neighbourhood-level inequity and glycaemic control in paediatric participants with Type 1 diabetes using the Neighbourhood Equity Index (NEI).MethodsThe NEI was linked to the clinical data of 519 children with diabetes followed at the Hospital for Sick Children (Toronto, Canada). The NEI is a composite measure of inequity developed using the World Health Organization's Urban Health Equity Assessment and Response Tool (HEART), which encompasses 15 weighted indicators evaluating economic, social, environmental and lifestyle factors. The geographic distribution of participants was determined using postal codes, and the relationship between HbA(1c) and NEI was evaluated using regression and spatial analysis techniques.ResultsParticipants' mean HbA(1c) was significantly correlated with NEI (R = -0.24, P < 0.0001). Regression analysis demonstrated that NEI was a strong predictor of mean HbA(1c) (P < 0.0001), accounting for differences in HbA(1c) as large as 1.0% (11 mmol/mol) when controlled for age, sex, diabetes duration, insulin pump therapy and number of annual clinic visits. Geo-mapping using spatial scan testing revealed the presence of two clusters of low-equity neighbourhoods containing 3.22 (P = 0.001) and 2.83 (P = 0.02) times more participants with HbA(1c) 9.5% (80 mmol/mol) than expected.ConclusionsOur findings demonstrated that NEI was a significant predictor of HbA(1c) in our clinic population and a useful tool for investigating spatial trends related to inequities in health, providing evidence that a composite, area-based measure of overall inequity is well suited to the study of glycaemic control in urban paediatric Type 1 diabetes populations.

BackgroundAdolescents with type 1 diabetes (T1D) are at increased risk of early adult-onset cardiovascular disease. This study compared standard echocardiographic parameters in patients screened for the Adolescent Type 1 Diabetes Cardio-Renal Intervention Trial (AdDIT) with healthy controls.MethodsStandard M-mode, B-mode and Doppler echocardiography was performed in all subjects. In subgroup analysis, T1D separated into tertiles according to risk of developing microalbuminuria as per the AdDIT protocol, were compared with the subgroup of healthy controls that underwent the same baseline clinical assessment including glycemic measures and serum lipids. Between groups comparisons were performed using Student’s t-tests, with p-values <0.05 considered significant.ResultsWe studied 188 T1D patients (M:F 93:95; age 14.4±2.1 years; disease duration 7.0 [1.7-15.0] years) and compared to 178 controls (M:F 84:94; age 14.5±1.6 years). Sex, age and height were similar, but T1D were heavier. T1D had increased systolic (114±10 vs. 110±9 mmHg; p=0.0001) and diastolic blood pressures (62±7 vs. 58±7 mmHg; <0.0001), but decreased resting heart rates (65±9 vs. 68±12 beats per minute; p=0.0312). Left ventricular (LV) dimensions along with indexed LV mass were all similar, except for posterior wall thickness which was increased in T1D (0.66±0.11 vs. 0.64±0.11cm; p=0.0258), as has been previously reported. Systolic function indices, ejection fraction (68±5 vs. 66±5 %; p=0.0020) and mean velocity of circumferential shortening (1.18±0.18 vs. 1.14±0.16 circ/sec; p=0.0161), were increased in T1D. Diastolic function indices, mitral valve E, A and E/A were all similar, but deceleration (154±17 vs. 149±20 msec; p=0.0235) and isovolumetric relaxation times (74±17 vs. 76±8 msec; p=0.0070) were increased. In sub-group analysis, we compared 53 high-risk, 71 medium-risk and 64 low-risk T1D vs. 59 controls. As expected all the T1D sub-groups had increased fasting blood glucose and HbA1c, and also HDL cholesterol. Total and LDL cholesterol and triglycerides were similar. Only LV posterior wall thickness remained increased when comparing the T1D subgroups vs. controls (0.67±0.11 high-risk, 0.66±0.11 medium-risk, 0.67±0.13 low-risk vs. 0.62±0.10 cm controls; p=0.0172, p=0.0327, p=0.0182, respectively).ConclusionAdolescent T1D of short to intermediate disease duration, have early suggestion of blood pressure, diastolic dysfunction and left ventricular geometric changes, which may contribute to increased risk of early adult-onset cardiovascular disease. BackgroundAdolescents with type 1 diabetes (T1D) are at increased risk of early adult-onset cardiovascular disease. This study compared standard echocardiographic parameters in patients screened for the Adolescent Type 1 Diabetes Cardio-Renal Intervention Trial (AdDIT) with healthy controls. Adolescents with type 1 diabetes (T1D) are at increased risk of early adult-onset cardiovascular disease. This study compared standard echocardiographic parameters in patients screened for the Adolescent Type 1 Diabetes Cardio-Renal Intervention Trial (AdDIT) with healthy controls. MethodsStandard M-mode, B-mode and Doppler echocardiography was performed in all subjects. In subgroup analysis, T1D separated into tertiles according to risk of developing microalbuminuria as per the AdDIT protocol, were compared with the subgroup of healthy controls that underwent the same baseline clinical assessment including glycemic measures and serum lipids. Between groups comparisons were performed using Student’s t-tests, with p-values <0.05 considered significant. Standard M-mode, B-mode and Doppler echocardiography was performed in all subjects. In subgroup analysis, T1D separated into tertiles according to risk of developing microalbuminuria as per the AdDIT protocol, were compared with the subgroup of healthy controls that underwent the same baseline clinical assessment including glycemic measures and serum lipids. Between groups comparisons were performed using Student’s t-tests, with p-values <0.05 considered significant. ResultsWe studied 188 T1D patients (M:F 93:95; age 14.4±2.1 years; disease duration 7.0 [1.7-15.0] years) and compared to 178 controls (M:F 84:94; age 14.5±1.6 years). Sex, age and height were similar, but T1D were heavier. T1D had increased systolic (114±10 vs. 110±9 mmHg; p=0.0001) and diastolic blood pressures (62±7 vs. 58±7 mmHg; <0.0001), but decreased resting heart rates (65±9 vs. 68±12 beats per minute; p=0.0312). Left ventricular (LV) dimensions along with indexed LV mass were all similar, except for posterior wall thickness which was increased in T1D (0.66±0.11 vs. 0.64±0.11cm; p=0.0258), as has been previously reported. Systolic function indices, ejection fraction (68±5 vs. 66±5 %; p=0.0020) and mean velocity of circumferential shortening (1.18±0.18 vs. 1.14±0.16 circ/sec; p=0.0161), were increased in T1D. Diastolic function indices, mitral valve E, A and E/A were all similar, but deceleration (154±17 vs. 149±20 msec; p=0.0235) and isovolumetric relaxation times (74±17 vs. 76±8 msec; p=0.0070) were increased. In sub-group analysis, we compared 53 high-risk, 71 medium-risk and 64 low-risk T1D vs. 59 controls. As expected all the T1D sub-groups had increased fasting blood glucose and HbA1c, and also HDL cholesterol. Total and LDL cholesterol and triglycerides were similar. Only LV posterior wall thickness remained increased when comparing the T1D subgroups vs. controls (0.67±0.11 high-risk, 0.66±0.11 medium-risk, 0.67±0.13 low-risk vs. 0.62±0.10 cm controls; p=0.0172, p=0.0327, p=0.0182, respectively). We studied 188 T1D patients (M:F 93:95; age 14.4±2.1 years; disease duration 7.0 [1.7-15.0] years) and compared to 178 controls (M:F 84:94; age 14.5±1.6 years). Sex, age and height were similar, but T1D were heavier. T1D had increased systolic (114±10 vs. 110±9 mmHg; p=0.0001) and diastolic blood pressures (62±7 vs. 58±7 mmHg; <0.0001), but decreased resting heart rates (65±9 vs. 68±12 beats per minute; p=0.0312). Left ventricular (LV) dimensions along with indexed LV mass were all similar, except for posterior wall thickness which was increased in T1D (0.66±0.11 vs. 0.64±0.11cm; p=0.0258), as has been previously reported. Systolic function indices, ejection fraction (68±5 vs. 66±5 %; p=0.0020) and mean velocity of circumferential shortening (1.18±0.18 vs. 1.14±0.16 circ/sec; p=0.0161), were increased in T1D. Diastolic function indices, mitral valve E, A and E/A were all similar, but deceleration (154±17 vs. 149±20 msec; p=0.0235) and isovolumetric relaxation times (74±17 vs. 76±8 msec; p=0.0070) were increased. In sub-group analysis, we compared 53 high-risk, 71 medium-risk and 64 low-risk T1D vs. 59 controls. As expected all the T1D sub-groups had increased fasting blood glucose and HbA1c, and also HDL cholesterol. Total and LDL cholesterol and triglycerides were similar. Only LV posterior wall thickness remained increased when comparing the T1D subgroups vs. controls (0.67±0.11 high-risk, 0.66±0.11 medium-risk, 0.67±0.13 low-risk vs. 0.62±0.10 cm controls; p=0.0172, p=0.0327, p=0.0182, respectively). ConclusionAdolescent T1D of short to intermediate disease duration, have early suggestion of blood pressure, diastolic dysfunction and left ventricular geometric changes, which may contribute to increased risk of early adult-onset cardiovascular disease. Adolescent T1D of short to intermediate disease duration, have early suggestion of blood pressure, diastolic dysfunction and left ventricular geometric changes, which may contribute to increased risk of early adult-onset cardiovascular disease.

Preclinical detection of myocardial dysfunction in adolescents with type 1 diabetes (T1D) may help identify individuals at increased risk of adult-onset cardiovascular disease, who would most benefit from early intervention strategies. This study compared echocardiographic assessment of myocardial function in patients screened for the Adolescent Type 1 Diabetes Cardio-Renal Intervention Trial (AdDIT) with healthy controls. Myocardial function assessment included tissue Doppler, strain and strain rate imaging. In subgroup analysis, T1D separated into tertiles according to urinary albumin:creatinine ratio as per the AdDIT protocol, were compared with the subgroup of healthy controls that underwent the same baseline clinical assessment including glycemic measures and serum lipids. Between groups comparisons were performed using Student's t-tests, with p-values <0.05 considered significant. We studied 188 T1D patients (M:F 93:95; age 14.4±2.1 years; disease duration 7.0 [1.7-15.0] years) and compared to 178 controls (M:F 84:94; age 14.5±1.6 years). Sex, age and height were similar. T1D were heavier with increased systolic and diastolic blood pressures, but decreased resting heart rates. Lateral mitral valve annulus myocardial velocities, E' (17.5±2.6 vs. 18.6±2.6 cm/s; p=0.0001), A' (5.4±1.1 vs. 5.9±1.1 cm/s; p<0.0001) and S (10.5±1.8 vs. 11.1±2.0 cm/s; p=0.0017) were decreased and mitral valve E/E' (5.8±1.1 vs. 5.4±1.0; p=0.0002) increased. Global left ventricular (LV) circumferential strain (-20.4±2.3 vs. -19.5±1.7 %; p=0.0002) and longitudinal strain (-19.6±1.7 vs. -18.9±1.9 %; p=0.0003) were different, but systolic and diastolic global longitudinal strain rates were similar. Basal rotation was similar, but apical rotation (6.26±2.97 vs. 5.28±2.45 degrees; p=0.0012) and LV twist (10.35±3.58 vs. 9.33±3.05 degrees; p=0.0065) were increased. In sub-group analysis, we compared 59 controls vs. 53 high-risk, 71 medium-risk and 64 low-risk T1D. As expected all the T1D sub-groups had increased fasting blood glucose and HbA1c, and also HDL cholesterol. Total and LDL cholesterol and triglycerides were similar. Only global LV circumferential strain in the medium-risk tertile remained different when comparing the smaller T1D subgroups vs. controls (-19.4±1.6 vs. -18.8±1.7 %; p=0.0312). Significant changes in myocardial function are evident in adolescent T1D of short to intermediate disease duration, suggesting these may be clinically useful preclinical markers of deterioration in cardiac performance to guide early intervention.

High intraglomerular pressure causes renal inflammation in experimental models of diabetes. Our objective was to determine whether renal hyperfiltration, a surrogate for intraglomerular hypertension, is associated with increased excretion of urinary cytokines/chemokines in patients with type 1 diabetes mellitus.

Diabet. Med. 29, 1297–1302 (2012)AbstractAims Patients with the highest albumin:creatinine ratio within the normal range are at an increased risk for developing microalbuminuria. The mechanistic basis for this is unknown, but may be related to renal inflammation. Our goal was to characterize the urinary excretion of cytokines/chemokines in normoalbuminuric adolescents with Type 1 diabetes to determine whether higher range normoalbuminuria is associated with evidence of renal inflammation.Methods Forty‐two urinary cytokines/chemokines were measured in subjects who were screened for the Adolescent Type 1 Diabetes Cardio‐Renal Intervention Trial. Urinary cytokines/chemokines were compared across low (n = 50), middle (n = 50) or high (n = 50) albumin:creatinine ratio tertile groups.Results At baseline, participants in the upper tertile were younger and had shorter diabetes duration compared with the other groups. Other clinical characteristics were similar. Urinary levels of interleukin 6, interleukin 8, platelet‐derived growth factor‐AA and RANTES differed across albumin:creatinine ratio tertiles, with higher values in patients in the middle and high tertiles compared with the lower tertile (ANCOVA P ≤ 0.01).Conclusions Within the normal albumin:creatinine ratio range, higher urinary albumin excretion is associated with elevated urinary levels of inflammatory markers. Ultimately, this may provide mechanistic insights into disease pathophysiology and stratify the risk of nephropathy in Type 1 diabetes.

Diabet. Med. 28, 10–18 (2011)AbstractAims To review and synthesize the published evidence on the possible association between childhood obesity and the subsequent risk of Type 1 diabetes.Methods The PubMed database was systematically searched for studies using childhood obesity, BMI or %weight‐for‐height as the exposure variable and subsequent Type 1 diabetes as the outcome. Studies were only included if assessment of obesity preceded the diagnosis of Type 1 diabetes.Results Eight case–control studies and one cohort study were included, comprising a total of 2658 cases. Of these nine studies, seven reported a significant association between childhood obesity, BMI or %weight‐for‐height and increased risk for Type 1 diabetes. Meta‐analysis of the four studies that reported childhood obesity as a categorical exposure produced a pooled odds ratio of 2.03 (95% CI 1.46–2.80) for subsequent Type 1 diabetes; however, in those studies, age at obesity assessment varied from age 1 to 12 years. A dose–response relationship was supported by a continuous association between childhood BMI and subsequent Type 1 diabetes in a meta‐analysis of five studies (pooled odds ratio 1.25 (95%CI 1.04–1.51) per 1 sd higher BMI).Conclusion There is overall evidence for an association between childhood obesity, or higher BMI, and increased risk of subsequent Type 1 diabetes. Several theories have been proposed for a causal relationship. Reduction in Type 1 diabetes should be considered as a potential additional benefit of preventing childhood obesity.

Objective. To assess the impact of exercise consultation on physical activity (PA) levels, anthropometric measures, and metabolic markers in obese adolescents. Methods. Obese adolescents (14–18 years) were randomized to either an exercise consultation (intervention group) or to review "Canada's Physical Activity Guide for Youth" (control group). Outcomes, including accelerometry, anthropometrics, blood pressure, stage of exercise behavior change, fasting glucose, insulin, and lipids, were measured at baseline and 3 months later. Results. Thirty adolescents (mean ; ) completed the study. At follow-up, the intervention group had significantly greater PA compared with controls ( ). Similarly, the intervention group weighed an average 2.6 kg less than the control group ( ), with a mean BMI z-score of 2.15 compared to 2.21 for controls ( ). No other differences were noted. Conclusion. Exercise consultation may be a simple approach to increase PA levels, reduce weight, and lower BMI in obese adolescents.

Objective: To evaluate glycaemic targets set by diabetes teams, their perception by adolescents and parents, and their influence on metabolic control.Methods: Clinical data and questionnaires were completed by adolescents, parents/carers and diabetes teams in 21 international centres. HbA1c was measured centrally.Results: A total of 2062 adolescents completed questionnaires (age 14.4 +/- 2.3 yr; diabetes duration 6.1 +/- 3.5 yr). Mean HbA 1c = 8.2 +/- 1.4% with significant differences between centres (F = 12.3; p < 0.001) range from 7.4 to 9.1%. There was a significant correlation between parent (r = 0.20) and adolescent (r = 0.21) reports of their perceived ideal HbA1c and their actual HbA1c result (p < 0.001), and a stronger association between parents' (r = 0.39) and adolescents' (r = 0.4) reports of the HbA1c they would be happy with and their actual HbA1c result. There were significant differences between centres on parent and adolescent reports of ideal and happy with HbA1c (8.1 < F > 17.4;p < 0.001). A lower target HbA1c and greater consistency between members of teams within centres were associated with lower centre HbA1c (F = 16.0; df = 15; p < 0.001).Conclusions: Clear and consistent setting of glycaemic targets by diabetes teams is strongly associated with HbA1c outcome in adolescents. Target setting appears to play a significant role in explaining the differences in metabolic outcomes between centres.

AIMS:To assess the importance of family factors in determining metabolic outcomes in adolescents with Type 1 diabetes in 19 countries.METHODS:Adolescents with Type 1 diabetes aged 11-18 years, from 21 paediatric diabetes care centres, in 19 countries, and their parents were invited to participate. Questionnaires were administered recording demographic data, details of insulin regimens, severe hypoglycaemic events and number of episodes of diabetic ketoacidosis. Adolescents completed the parental involvement scale from the Diabetes Quality of Life for Youth--Short Form (DQOLY-SF) and the Diabetes Family Responsibility Questionnaire (DFRQ). Parents completed the DFRQ and a Parental Burden of Diabetes score. Glycated haemoglobin (HbA(1c)) was analysed centrally on capillary blood.RESULTS:A total of 2062 adolescents completed a questionnaire, with 2036 providing a blood sample; 1994 parents also completed a questionnaire. Family demographic factors that were associated with metabolic outcomes included: parents living together (t = 4.1; P < 0.001), paternal employment status (F = 7.2; d.f. = 3; P < 0.001), parents perceived to be over-involved in diabetes care (r = 0.11; P < 0.001) and adolescent-parent disagreement on responsibility for diabetes care practices (F = 8.46; d.f. = 2; P < 0.001). Although these factors differed between centres, they did not account for centre differences in metabolic outcomes, but were stronger predictors of metabolic control than age, gender or insulin treatment regimen.CONCLUSIONS:Family factors, particularly dynamic and communication factors such as parental over-involvement and adolescent-parent concordance on responsibility for diabetes care appear be important determinants of metabolic outcomes in adolescents with diabetes. However, family dynamic factors do not account for the substantial differences in metabolic outcomes between centres.

AIMS:To determine whether higher than average albumin excretion during early puberty identifies subjects who will subsequently develop microalbuminuria (MA) and clinical proteinuria.METHODS:Longitudinal data from the Oxford Regional Prospective Study of Childhood Diabetes (ORPS; n = 554, median duration of follow-up 10 years; range 3.0-16.7) with assessment of albumin/creatinine ratios in three early morning urine samples collected annually. An albumin excretion phenotype was derived from longitudinal data, for each individual, defining deviation from the mean of regression models, including covariates gender, age, duration of diabetes and age at assessment. Tracking of the phenotypes was confirmed in a second independent cohort from Perth, Australia.RESULTS:The albumin excretion phenotype showed reasonable correlation between age 11-15 years and age 16-18 years in both cohorts, indicative of good 'tracking'. In the ORPS cohort, tertiles of the albumin excretion phenotype at aged 11-15 years were predictive of subsequent risk for the development of MA. All of the subjects developing clinical proteinuria had an albumin excretion phenotype in the upper tertile or an HbA(1c) > 9% at aged 11-15 years.CONCLUSIONS:Identification of adolescents at risk of diabetic nephropathy using an albumin excretion phenotype is feasible. When combined with elevated HbA(1c), it may identify subjects for trial of early intervention with angiotensin-converting enzyme inhibitors/angiotensin-II receptor antagonists and statins to improve long-term prognosis in these subjects where sustained improvement in glycaemic control may be difficult to achieve.

The presence of cystic fibrosis (CF)-related diabetes was evaluated in 19 adolescents with CF by continuous glucose monitoring system (CGMS) and oral glucose tolerance testing. CGMS confirmed diabetic glucose excursions in 7/19 subjects deemed diabetic on oral glucose tolerance testing. CGMS is a useful tool for detecting hyperglycemia in CF.

AIMS:To determine whether children with Type 1 diabetes mellitus (DM) miss more school than their non-DM siblings and peers and to identify factors associated with school absenteeism in children with DM.METHODS:School absenteeism data for the 2000-01 school year were obtained for 78 children with DM, 38 non-DM siblings and 118,269 age-matched peers in Toronto, Ontario. Questionnaires and hospital records were utilized to evaluate child-, family- and diabetes-related factors associated with school absenteeism in children with DM.RESULTS:Children with DM missed only slightly, albeit significantly more school than both their non-DM siblings (mean +/-sd: 10.9 +/- 8.9 vs. 8.1 +/- 8.1 days, P < 0.001) and peers (median: 8.8 vs. 5.5 days, P = 0.0005). A multiple regression analysis indicated that school absenteeism in children with DM was associated with their parents' attitudes towards school attendance (P = 0.002), poorer metabolic control (P = 0.006), shorter disease duration (P = 0.006) and a lack of aggressive behaviour (P = 0.02).CONCLUSIONS:With current management strategies, near normal school attendance is a reasonable goal for all children with DM and should be strongly encouraged by parents, educators and health care professionals.

Objectives To determine incidence, outcomes, and risk factors for pediatric cerebral edema with diabetic ketoacidosis (CEDKA) in Canada.Study design This was a case-control study nested within a population-based active surveillance study of CEDKA in Canada from July 1999 to June 2001. Cases are patients with DKA < 16 years of age with cerebral edema. Two unmatched control subjects per case are patients with DKA without cerebral edema.Results Thirteen cases of CEDKA were identified over the surveillance period for an incidence rate of 0.51%; 23% died and 15% survived with neurologic sequelae. CEDKA was present at initial presentation of DKA in 19% of cases. CEDKA was associated with lower initial bicarbonate (P =.001), higher initial urea (P =.001), and higher glucose at presentation (P = .014). Although there was a trend to association with higher fluid rates and treatment with bicarbonate, these were not independent predictors.Conclusions CEDKA remains a significant problem with a high mortality rate. No association was found between the occurrence of CEDKA and treatment factors. The presence of cerebral edema before treatment of DKA and the association with severity of illness suggest that prevention of DKA is the key to avoiding this devastating complication.

PURPOSE. To examine the association between metabolic control (HbA(1c)) and the chromatic mechanisms of children with type 1 diabetes (T1D), by using the color visual evoked potential (VEP).METHODS. Fifty children with T1D ( age range, 6 - 12.9 years) and 33 age-matched control subjects were tested. VEPs were recorded by placing five electrodes on the scalp according to the International 10/20 System of Electrode Placement. Active electrodes O1, O2, and Oz were placed over the visual cortex. Short-wavelength ( S), and long-and medium-wavelength (LM) color stimuli consisted of vertical, photometric isoluminant ( 1 cyc/deg) gratings presented in a pattern onset ( 100 ms) - offset ( 400 ms) mode. Achromatic vertical gratings were presented at 3 cyc/deg. Primary outcome measure was VEP latency. The relationship between S, LM, and achromatic VEP latency, and HbA(1c) was determined by ANCOVA regression.RESULTS. S-, LM-, achromatic VEP latencies were not associated significantly with HbA(1c). Pubertal status, however, was associated significantly ( P = 0.0114) and selectively with S- VEP latency. Pubertal children with T1D had delayed ( mean delay, 9.5 ms) S- VEP latencies when compared with the prepubertal children with T1D. However, there was no statistically significant difference ( P = 0.1573) in the effect of pubertal status on S- VEP latency between the T1D and control groups.CONCLUSIONS. Pubertal status rather than HbA(1c) appears to affect selectively the S- VEP latency of preteen children with T1D. Further study is warranted to determine whether the delay in S- VEP latency in pubertal children with T1D changes over time and whether this change could be a predictive marker for future development of background diabetic retinopathy.

Diabetic MedicineVolume 22, Issue 2 p. 115-117 Is the ‘Accelerator Hypothesis’ worthy of our attention? D. Daneman, D. Daneman University of Toronto and The Hospital for Sick Children, Toronto, Ontario, CanadaSearch for more papers by this author D. Daneman, D. Daneman University of Toronto and The Hospital for Sick Children, Toronto, Ontario, CanadaSearch for more papers by this author First published: 19 January 2005 https://doi.org/10.1111/j.1464-5491.2005.01532.xCitations: 13Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Wilkin TJ. The accelerator hypothesis: weight gain as the missing link between Type I and Type II diabetes. Diabetologia 2001; 44: 914–922. 2 Betts PR, Mulligan J, Ward P, Smith B, Wilkin T. Increasing body weight predicts the earlier onset of insulin-dependent diabetes in childhood: testing the ‘accelerator hypothesis.’ Diabet Med 2005; 2: 144–151. 3 Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL. Overweight prevalence and trends for children and adolescents. The National Health and Nutrition Examination Surveys, 1963–91. Arch Pediatr Adolesc Med 1995; 149: 1085–1091. 4 Tremblay MS, Willms JD. Secular trends in the body mass index of Canadian children. CMAJ 2000; 163: 1429–1433. 5 Chinn S, Hughes JM, Rona RJ. Trends in growth and obesity in ethnic groups in Britain. Arch Dis Child 1998; 19: 162–166. 6 Fagot-Campagna A, Pettitt DJ, Engelgau MM, Burrows NR, Geiss LS, Valdez R et al. Type 2 diabetes among North American children and adolescents: an epidemiologic review and a public health perspective. J Pediatr 2000; 136: 664–672. 7 Fagot-Campagna A, Narayan KM, Imperatore G. Type 2 diabetes in children. Br Med J 2001; 322: 377–378. 8 Tuomilehto J, Karvonen M, Pitkaniemi J, Virtala E, Kohtamaki K, Toivanen L et al. Record-high incidence of Type I (insulin-dependent) diabetes mellitus in Finnish children. The Finnish Childhood Type I Diabetes Registry Group. Diabetologia 1999; 42: 655–660. 9 Kautiainen S, Rimpela A, Vikat A, Virtanen SM. Secular trends in overweight and obesity among Finnish adolescents in 1977–1999. Int J Obes Relat Metab Disord 2002; 26: 544–552. 10 Tran VV, Chen G, Newgard CB, Hohmeier HE. Discrete and complementary mechanisms of protection of β-cells against cytokine-induced and oxidative damage achieved by bcl-2 overexpression and a cytokine selection strategy. Diabetes 2003; 52: 1423–1432. 11 Rabinovitch A, Suarez-Pinzon W, Strynadka K, Ju Q, Edelstein D, Brownlee M et al. Transfection of human pancreatic islets with an anti-apoptotic gene (bcl-2) protects β-cells from cytokine-induced destruction. Diabetes 1999; 48: 1223–1229. 12 Drucker DJ. Glucagon-like peptides: regulators of cell proliferation, differentiation, and apoptosis. Mol Endocrinol 2003; 17: 161–171. 13 Amiel SA, Sherwin RS, Simonson DC, Lauritano AA, Tamborlane WV. Impaired insulin action in puberty. A contributing factor to poor glycemic control in adolescents with diabetes. N Engl J Med 1986; 315: 215–219. 14 Hamilton J, Daneman D. Deteriorating diabetes control during adolescence: physiological or psychosocial? J Pediatr Endocrinol Metab 2002; 15: 115–126. 15 Pankow JS, Jacobs DR Jr, Steinberger J, Moran A, Sinaiko AR. Insulin resistance and cardiovascular disease risk factors in children of parents with the insulin resistance (metabolic) syndrome. Diabetes Care 2004; 27: 775–780. 16 Bacha F, Saad R, Gungor N, Janosky J, Arslanian SA. Obesity, regional fat distribution, and syndrome X in obese black versus white adolescents: race differential in diabetogenic and atherogenic risk factors. J Clin Endocrinol Metab 2003; 88: 2534–2540. 17 Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K et al. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med 2002; 346: 802–810. 18 Pundziute-Lycka A, Dahlquist G, Nystrom L, Arnqvist H, Bjork E, Blohme G et al. for the Swedish Childhood Diabetes Study Group. The incidence of Type I diabetes has not increased but shifted to a younger age at diagnosis in the 0–34 years group in Sweden 1983–1998. Diabetologia 2002; 45: 783–791. 19 Moran A, Jacobs DR Jr, Steinberger J, Hong CP, Prineas R, Luepker R et al. Insulin resistance during puberty: results from clamp studies in 357 children. Diabetes 1999; 48: 2039–2044. 20 Hamilton J, Cummings E, Zdravkovic V, Finegood D, Daneman D. Metformin as an adjunct therapy in adolescents with type 1 diabetes and insulin resistance: a randomized controlled trial. Diabetes Care 2003; 26: 138–143. 21 Sarnblad S, Kroon M, Aman J. Metformin as additional therapy in adolescents with poorly controlled type 1 diabetes: randomised placebo-controlled trial with aspects on insulin sensitivity. Eur J Endocrinol 2003; 149: 323–329. 22 Devendra D, Liu E, Eisenbarth GS. Type 1 diabetes: recent developments. Br Med J 2004; 328: 750–754. Citing Literature Volume22, Issue2February 2005Pages 115-117 ReferencesRelatedInformation

AIM:To review the clinical experience of children and teens diagnosed with Type 2 diabetes (T2DM) at a paediatric hospital serving a large urban multi-ethnic population.METHODS:Retrospective chart review of patients with T2DM followed in the diabetes clinic at the Hospital for Sick Children (HSC) over an 8-year period. Patients who were included were younger than 18, referred at the onset of diabetes, and where presentation and/or clinical course was 'typical' of T2DM.RESULTS:Of 1020 children with diabetes followed at HSC, 4% were identified as having T2DM in 2002. There was a sixfold increase in new cases from 1994 to 2002. The mean age at diagnosis was 13.5 +/- 2.2 years (range 8.8-17.5) with a female-to-male ratio of 1.7. Most had a first- or second-degree relative with T2DM. There was an overrepresentation of children with T2DM from Asian and African Canadian ethnic groups relative to the regional population. The majority of teens were asymptomatic at presentation, with a smaller number in diabetic ketoacidosis (DKA) at diagnosis. Mean HbA1c at diagnosis was 10 +/- 3.4%. Approximately one half of patients were initially treated by diet and exercise with many requiring intensification of therapy over a short period of time.CONCLUSIONS:We report a similar increase in T2DM incidence and clinical presentation at HSC to other clinic reports in large North American urban centres. Of note is the high prevalence of children of South/South-East Asian descent.

OBJECTIVE To compare the prevalence of eating disturbances in preteen and early teenage girls with type 1 diabetes to their nondiabetic peers. RESEARCH DESIGN AND METHODS A cross-sectional, case-controlled study of 101 girls with type 1 diabetes, ages 9-14 years, and 303 age-matched, female nondiabetic control subjects was conducted. Participants completed a Children's Eating Disorder Examination interview. Socioeconomic status, BMI, and diabetes-related variables were assessed. Groups were compared using chi(2) analyses. RESULTS Binge eating; the use of intense, excessive exercise for weight control; the combination of two disturbed eating-related behaviors; and subthreshold eating disorders were all more common in girls with type 1 diabetes. Metabolic control was not related to eating behavior in this study population. CONCLUSIONS Eating disturbances, though mostly mild, were significantly more common in preteen and early teenage girls with type 1 diabetes. Screening and prevention programs for this high-risk group should begin in the preteen years.