Introduction and Objective: Maternal caregivers of adolescents with type 1 diabetes (T1D) experience elevated levels of depressive symptoms and diabetes distress, which are established risk factors for poor psychosocial and glycemic outcomes in adolescents. We evaluated the effects of a cognitive behavioral intervention for distressed caregivers in a randomized controlled trial. Methods: Maternal caregivers of adolescents with T1D (n=151, mean adolescent age=14+2yrs, 56% female, 85% non-Hispanic White, mean HbA1c=9.0+2.1%), were randomized to receive a cognitive behavioral intervention (Communication & Coping) targeting coping skills and positive parenting strategies or an Enhanced Diabetes Education intervention. Participants in both groups received intervention materials and completed up to 7 phone sessions with a trained interventionist over 3 months, with concurrent daily Facebook posts designed to reinforce the concepts for each intervention. Psychosocial and glycemic data were collected over 12 months. Results: Caregivers in both groups reported significant decreases in depressive symptoms (effect size d=3.5, p<.001) and diabetes distress (d=0.6, p<.001) over 12 months, with no significant differences between groups. Adolescents experienced improvements in quality of life (d =-2.95, p<.001), with marginally higher scores in the Education group (p=.048). Adolescents maintained HbA1c (8.9% at 12 months), with no significant difference between groups. Conclusion: Interventions for caregivers are effective in treating maternal distress and improving quality of life in adolescents with T1D. Specific intervention materials may be less critical than repeated interactions with trained interventionists that address maternal caregivers' concerns about raising an adolescent child with T1D. S.S. Jaser: None. J.H. Simmons: Consultant; Boehringer-Ingelheim. Research Support; Kyowa Kirin Co., Ltd. Consultant; Kyowa Kirin Co., Ltd. Advisory Panel; Ultragenyx. Research Support; Ultragenyx, Alexion. National Institutes of Health (R01DK115545)
In elite global soccer, professional clubs own and operate academy programs for talent identification and development purposes. The development of a youth player into an adult professional is a long-term process, requiring a combination of competitive match play and intensive training. Although developing maximum sprinting and acceleration are crucial, their physical development may be hindered by congested fixtures in youth soccer. Players compete for 40–50 games over 9 months of the in-season, including extremely dense/congested-schedule tournaments. Because of the different competition formats across the world, it is important to understand how youth players physically develop to reach from early development to the senior level and to maximize the efficacy of age-appropriate strength and conditioning programs. The purpose of the narrative review is to identify the physical performance in elite youth soccer players, spanning early to late stages of development and to discuss physical development plans aimed at supporting players transitioning from the youth to first team.
Introduction and Objective: Genetic screening can guide management of pediatric obesity, but it is unclear how results affect health care behaviors by patients and clinicians. We hypothesize that children and adolescents receiving genetic testing for obesity will have a positive perception of the role of genetic testing. Methods: We invited 123 families of patients aged 2-19 years who had genetic testing with the Uncovering Rare Obesity Gene Panel to participate. One parent/guardian and children over the age of 13 from this group were asked to complete age-appropriate surveys about their experience, followed by qualitative interviews. Results: Surveys were completed by 28 participants (21 parents, 7 adolescents). Patients were primarily female (n=12, 57%) and aged 12.47 years (range 4-19y). Self-reported race was white (76.2%), black (14.3%), American Indian/Alaskan Native (4.8%), and multiple or unknown (10%). Weight z-score was 3.33±0.86 and BMI Z-score was 3.88±1.69. Clinically significant variants were found in 81% (17/21) with no difference in BMI or weight in those with positive and negative genetic findings. Participants had early-onset obesity; 80% of parents saw weight gain before the child was in the 2nd grade. Most (71%) parents reported receiving genetic counseling, but only 52% understood these results. Those with negative results more frequently reported not receiving genetic counseling (p = <0.001). Still, 86% of parents recommended genetic testing for obesity to others. Conversely, 29% of adolescents reported receiving genetic counseling and understanding their test results; only 43% of them recommended genetic testing to others. Conclusion: Families have a favorable view of genetic testing for pediatric obesity, but adequate counseling is lacking. Adolescents were less impacted by their results, possibly because genetic counseling was completed only with their parents. A prospective study is underway to correlate patient perceptions of genetic testing with clinical care outcomes. Disclosure R.S. Massa: None. A.H. Shoemaker: Advisory Panel; Rhythm Pharmaceuticals, Inc. Consultant; Soleno Therapeutics. Funding National Institutes of Health (5T32DK007061-50)
Introduction and Objective: Inflammation is associated with progression of diabetic retinopathy (DR). Inflammatory cytokines tumor necrosis factor alpha (TNFα), interleukin-1β (IL-1β), and interleukin-6 (IL-6) are elevated in DR and trigger retinal microvascular leakage. RMEC tight junction complexes include the transmembrane proteins occludin and ZO-1. Diabetic relevant stimuli cause changes in occludin and ZO-1 localization and content. Our goal was to compare the effects of TNFα, IL-1β, and IL-6 on ZO-1 and occludin in RMECs and on RMEC permeability. Methods: Human RMECs (HRMECs) were treated with TNFα, or IL-1β, or IL-6 + soluble IL-6 receptor, or vehicle, and used to perform Western blotting for ZO-1 and Occludin. HRMECs treated as above were immunostained for ZO-1 and occludin and imaged at 40x with a confocal microscope. Transendothelial electrical resistance (TEER) of HRMEC monolayers treated as above was measured with the electrical cell-substrate impedance sensing (ECIS) method. Wild-type C57bl6 mice received intravitreal injections of TNFα, or IL-1β, or IL6 + soluble IL-6 receptor, or vehicle and quantitative fluorescein angiography (qFA) was performed to evaluate the effect of cytokines on retinal vascular permeability. Results: TNFα and IL-6 decreased the occludin protein content of HRMECs (TNFα: p= 0.0129, n=8, IL-6: p=0.0162, n=8) without changing the ZO-1 content (TNFα: p= 0.0724, n=8, IL-6: p=0.1706, n=8). IL-1β treatment decreased the ZO-1 protein content of HRMECs (p= 0.0174, n=8) but did not change the occludin protein content (p=0.6073, n=8). ECIS experiments showed decreased barrier resistance of HRMEC monolayers treated with TNFα, IL-1β, and IL-6. All 3 inflammatory cytokines induced retinal vascular hyperpermeability in vivo on qFA. Conclusion: TNFα, IL-1β, and IL-6 differentially alter HRMEC tight junctional complex proteins ZO-1 and occludin to increase retinal microvascular permeability. I. De la Huerta: None. National Institutes of Health (EY032620)
Introduction and Objective: We asked if a binary endpoint for change (∆) from baseline to a fixed timepoint of 1 year could be useful in future trials. Methods: We used 2hr-OGTT data from the negative abatacept prevention trial and the positive teplizumab prevention trial, and from participants in the observational TrialNet Pathway to Prevention Study (PTP) with similar characteristics. Glucose and C-peptide response curves were plotted and vectors for curve movement from baseline to 1 year were used to categorize simultaneous glucose ∆ and C-peptide ∆ as metabolic treatment failure vs. success. Results: PTP participants with ∆glucose>0 and ∆C-peptide<0 from baseline to 1 year were at substantially higher risk for stage 3 T1D than those with ∆glucose<0 and ∆C-peptide>0 (p<0.0001). Based on this, we compared placebo vs. treatment groups in both trials for failure (∆glucose>0 with ∆C-peptide<0) vs. success (∆glucose<0 with ∆C-peptide>0) after 1 year. In the table, the failure vs. success endpoint at 1 year revealed more treatment efficacy than the original endpoints used for each trial, which required 8.0 years to implement for abatacept and 10.5 years to implement for teplizumab. Conclusion: An analytic approach using a binary metabolic endpoint of failure vs. success at a fixed time interval appears to detect treatment effects at least as well as standard primary endpoints with shorter follow-up. E.K. Sims: Consultant; Sanofi. Speaker's Bureau; Med Learning Group. Other Relationship; American Diabetes Association. W.E. Russell: None. K.C. Herold: Consultant; Sanofi, Dompé, Vertex Pharmaceuticals Incorporated, Sonoma, NexImmune. D.D. Cuthbertson: None. H.M. Ismail: Consultant; Rise Therapeutics. L.M. Jacobsen: Advisory Panel; Sanofi. B.M. Nathan: None. M.J. Redondo: None. J. Sosenko: None.
