Energy and nutrient intake by 11-13-year-old young adolescents attending private schools in Delhi, India.

There are no high-quality data on dietary behavior of adolescents in India. This study aimed to assess the intake of energy (E), macronutrients and selected micronutrients in a sample of 11-13-year-old schoolchildren in Delhi, India. Participants from private schools (n=10) recorded dietary intake using a 3-day food diary. Information was entered into the dietary assessment tool, Intake24, to ascertain portion size and convert data into nutrient intake through integrated food tables. Of the 514 consenting participants, 393 (76.4%) (169 girls, 224 boys) aged 11.4 (± 1.8) years completed the study. The median (interquartile range (IQR) daily E intake was 2580 (2139.3-2989.8) kcal [10.8 (9.0 -12.5) MJ] for girls, and 2941.5 (2466.7- 3599.3) kcal [12.3 (10.3- 15.2) MJ] for boys. The median (IQR) daily nutrient intakes for girls and boys respectively were: protein 64.6 (54.8-79.3) g, 74.4 (61.4; 89.4) g; carbohydrate 336.5 (285.3- 393.6) g, 379.6 (317.8-461.8) g; and saturated fat 45.6 (34.8-58.3) g, 54.6 (41.9-69.5) g. There were no significant between-gender differences in percent E from protein (10.2 (9.2 - 11.4)), or carbohydrate (52.4 (48.7- 56.7)). Girls obtained less percent E from saturated fat (16.1 (11.0-18.2) compared with boys 16.3 (14.2 - 19.1) (P<0.05). E from saturated fat was above Food and Agriculture Organization recommendations in >74% participants. The EAR for iron was achieved by < 40% of girls. In conclusion, strategies to optimize dietary intake of adolescents in India should focus on preventing excess intakes of E and saturated fat, and improving iron intake in girls.

Geographical distribution of invasive meningococcal disease and carriage: A spatial analysis.

Little information exists concerning the spatial relationship between invasive meningococcal disease (IMD) cases and Neisseria meningitidis (N. meningitidis) carriage. The aim of this study was to examine whether there is a relationship between IMD and asymptomatic oropharyngeal carriage of meningococci by spatial analysis to identify the distribution and patterns of cases and carriage in South Australia (SA). Carriage data geocoded to participants' residential addresses and meningococcal case notifications using Postal Area (POA) centroids were used to analyse spatial distribution by disease- and non-disease-associated genogroups, as well as overall from 2017 to 2020. The majority of IMD cases were genogroup B with the overall highest incidence of cases reported in infants, young children, and adolescents. We found no clear spatial association between N. meningitidis carriage and IMD cases. However, analyses using carriage and case genogroups showed differences in the spatial distribution between metropolitan and regional areas. Regional areas had a higher rate of IMD cases and carriage prevalence. While no clear relationship between cases and carriage was evident in the spatial analysis, the higher rates of both carriage and disease in regional areas highlight the need to maintain high vaccine coverage outside of the well-resourced metropolitan area.

Sources and determinants of free sugars intake by 5-year-old Australian children in the SMILE cohort.

Reducing free sugars intake is important for the prevention of dental caries and obesity in children. The study aimed to determine the amount and sources of free sugars known to contribute to dental caries, and identify sociodemographic determinants of intake by children aged 5 years in Australia. Cross-sectional analysis of dietary data from a cohort study, collected using a customized food frequency questionnaire were used to calculate free sugars intake as grams/day and percentage contribution to Estimated Energy Requirement (EER). The percent contribution of food sources to free sugars intake was derived. Sociodemographic determinants of achieving intakes within WHO thresholds (i.e., <5% and <10% Energy were explored with multinomial logistic regression. Complete data were available for 641 children (347 boys, 294 girls). Median (IQR) free sugars intake (g/day) was 31.6 (21.3-47.6) in boys and 28.1 (19.6-47.9) in girls. The median (IQR) percentage contribution to EER was 7.9 (5.4-12.7); 21% and 42% of children had intakes <5% EER and between 5% and <10%, respectively. The main sources of free sugars were: (1) Cakes, Biscuits and Cereal Bars; (2) Sweetened Milk Products (predominantly yoghurts) and (3) Desserts. Maternal university education, single-parent household, and maternal place of birth being Australia or New Zealand were associated with free sugars intake <5% EER. In conclusion, less than a quarter of 5-year-old children in the SMILE cohort achieved the WHO recommendations to limit free sugars to <5% EER. Strategies to lower free sugars intake could target priority populations such migrants, populations with lower levels of education or health literacy and identify areas for intervention in the wider food environments that children are exposed to.

Intra-urban risk assessment of occupational injuries and illnesses associated with current and projected climate: Evidence from three largest Australian cities.

BACKGROUND: Increased risk of occupational injuries and illnesses (OI) is associated with ambient temperature. However, most studies have reported the average impacts within cities, states, or provinces at broader scales. METHODS: We assessed the intra-urban risk of OI associated with ambient temperature in three Australian cities at statistical area level 3 (SA3). We collected daily workers' compensation claims data and gridded meteorological data from July 1, 2005, to June 30, 2018. Heat index was used as the primary temperature metric. We performed a two-stage time series analysis: we generated location-specific estimates using Distributed Lag Non-Linear Models (DLNM) and estimated the cumulative effects with multivariate meta-analysis. The risk was estimated at moderate heat (90th percentile) and extreme heat (99th percentile). Subgroup analyses were conducted to identify vulnerable groups of workers. Further, the OI risk in the future was estimated for two projected periods: 2016-2045 and 2036-2065. RESULTS: The cumulative risk of OI was 3.4% in Greater Brisbane, 9.5% in Greater Melbourne, and 8.9% in Greater Sydney at extreme heat. The western inland regions in Greater Brisbane (17.4%) and Greater Sydney (32.3%) had higher risk of OI for younger workers, workers in outdoor and indoor industries, and workers reporting injury claims. The urbanized SA3 regions posed a higher risk (19.3%) for workers in Greater Melbourne. The regions were generally at high risk for young workers and illness-related claims. The projected risk of OI increased with time in climate change scenarios. CONCLUSIONS: This study provides a comprehensive spatial profile of OI risk associated with hot weather conditions across three cities in Australia. Risk assessment at the intra-urban level revealed strong spatial patterns in OI risk distribution due to heat exposure. These findings provide much-needed scientific evidence for work, health, and safety regulators, industries, unions, and workers to design and implement location-specific preventative measures.

A comparison of survival models for prediction of eight-year revision risk following total knee and hip arthroplasty.

BACKGROUND: There is increasing interest in the development and use of clinical prediction models, but a lack of evidence-supported guidance on the merits of different modelling approaches. This is especially true for time-to-event outcomes, where limited studies have compared the vast number of modelling approaches available. This study compares prediction accuracy and variable importance measures for four modelling approaches in prediction of time-to-revision surgery following total knee arthroplasty (TKA) and total hip arthroplasty (THA). METHODS: The study included 321,945 TKA and 151,113 THA procedures performed between 1 January 2003 and 31 December 2017. Accuracy of the Cox model, Weibull parametric model, flexible parametric model, and random survival forest were compared, with patient age, sex, comorbidities, and prosthesis characteristics considered as predictors. Prediction accuracy was assessed using the Index of Prediction Accuracy (IPA), c-index, and smoothed calibration curves. Variable importance rankings from the Cox model and random survival forest were also compared. RESULTS: Overall, the Cox and flexible parametric survival models performed best for prediction of both TKA (integrated IPA 0.056 (95% CI [0.054, 0.057]) compared to 0.054 (95% CI [0.053, 0.056]) for the Weibull parametric model), and THA revision. (0.029 95% CI [0.027, 0.030] compared to 0.027 (95% CI [0.025, 0.028]) for the random survival forest). The c-index showed broadly similar discrimination between all modelling approaches. Models were generally well calibrated, but random survival forest underfitted the predicted risk of TKA revision compared to regression approaches. The most important predictors of revision were similar in the Cox model and random survival forest for TKA (age, opioid use, and patella resurfacing) and THA (femoral cement, depression, and opioid use). CONCLUSION: The Cox and flexible parametric models had superior overall performance, although all approaches performed similarly. Notably, this study showed no benefit of a tuned random survival forest over regression models in this setting.

What Is the Effect of Using a Competing-risks Estimator when Predicting Survivorship After Joint Arthroplasty: A Comparison of Approaches to Survivorship Estimation in a Large Registry.

BACKGROUND: There is increasing interest in the development of statistical models that can be used to estimate risk of adverse patient outcomes after joint arthroplasty. Competing risk approaches have been recommended to estimate risk of longer-term revision, which is often likely to be precluded by the competing risk of death. However, a common approach is to ignore the competing risk by treating death as a censoring event and using standard survival models such as Cox regression. It is well-known that this approach can overestimate the event risk for population-level estimates, but the impact on the estimation of a patient's individualized risk after joint arthroplasty has not been explored. QUESTIONS/PURPOSES: We performed this study to (1) determine whether using a competing risk or noncompeting risk method affects the accuracy of predictive models for joint arthroplasty revision and (2) determine the magnitude of difference that using a competing risks versus noncompeting risks approach will make to predicted risks for individual patients. METHODS: The predictive performance of a standard Cox model, with competing risks treated as censoring events, was compared with the performance of two competing risks approaches, the cause-specific Cox model and Fine-Gray model. Models were trained and tested using data pertaining to 531,304 TKAs and 274,618 THAs recorded in the Australian Orthopaedic Association National Joint Replacement Registry between January 1, 2003 and December 31, 2017. The registry is a large database with near-complete capture and follow-up of all hip and knee joint arthroplasty in Australia from 2003 onwards, making it an ideal setting for this study. The performance of the three modeling approaches was compared in two different prediction settings: prediction of the 10-year risk of all-cause revision after TKA and prediction of revision for periprosthetic fracture after THA. The calibration and discrimination of each approach were compared using the concordance index, integrated Brier scores, and calibration plots. Calibration of 10-year risk estimates was further assessed within subgroups of age by comparing the observed and predicted proportion of events. Estimated 10-year risks from each model were also compared in three hypothetical patients with different risk profiles to determine whether differences in population-level performance metrics would translate into a meaningful difference for individual patient predictions. RESULTS: The standard Cox and two competing risks models showed near-identical ability to distinguish between high-risk and low-risk patients (c-index 0.64 [95% CI, 0.64 to 0.64] for all three modeling approaches for TKAs and 0.66 [95% CI 0.66 to 0.66] for THA). All models performed similarly in patients younger than 75 years, but for patients aged 75 years and older, the standard Cox model overestimated the risk of revision more than the cause-specific Cox and Fine-Gray model did. These results were echoed when predictions were made for hypothetical individual patients. For patients with a low competing risk of mortality, the 10-year predicted risks from the standard Cox, cause-specific Cox, and Fine-Gray models were similar for TKAs and THAs. However, a larger difference was observed for hypothetical 89-year-old patients with increased mortality risk. In TKAs, the revision risk for an 89-year-old patient was so low that this difference was negligible (0.83% from the cause-specific Cox model versus 1.1% from the standard Cox model). However, for THAs, where older age is a risk factor for both death and revision for periprosthetic fracture, a larger difference was observed in the 10-year predicted risks for a hypothetical 89-year-old patient (3.4% from the cause-specific Cox model versus 5.2% from the standard Cox model). CONCLUSION: When developing models to predict longer-term revision of joint arthroplasty, failing to use a competing risks modeling approach will result in overestimating the revision risk for patients with a high risk of mortality during the surveillance period. However, even in an extreme instance, where both the frequency of the event of interest and the competing risk of death are high, the largest absolute difference in predicted 10-year risk for an individual patient was just 1.8%, which may not be of consequence to an individual. Despite these findings, when developing or using risk prediction models, researchers and clinicians should be aware of how competing risks were handled in the modeling process, particularly if the model is intended for use populations where the mortality risk is high. LEVEL OF EVIDENCE: Level III, therapeutic study.

Changes in pancreatic exocrine function in young at-risk children followed to islet autoimmunity and type 1 diabetes in the ENDIA study.

BACKGROUNDS: We aimed to monitor pancreatic exocrine function longitudinally in relation to the development of islet autoimmunity (IA) and type 1 diabetes (T1D) in at-risk children with a first-degree relative with T1D, who were followed prospectively in the Environmental Determinants of Islet Autoimmunity (ENDIA) study. METHODS: Fecal elastase-1 (FE-1) concentration was measured longitudinally in 85 ENDIA children from median age 1.0 (IQR 0.7,1.3) year. Twenty-eight of 85 children (progressors) developed persistent islet autoantibodies at median age of 1.5 (IQR 1.1,2.5) years, of whom 11 went on to develop clinical diabetes. The other 57 islet autoantibody-negative children (non-progressors) followed similarly were age and gender-matched with the progressors. An adjusted linear mixed model compared FE-1 concentrations in progressors and non-progressors. RESULTS: Baseline FE-1 did not differ between progressors and non-progressors, or by HLA DR type or proband status. FE-1 decreased over time in progressors in comparison to non-progressors (Wald statistic 5.46, P = .02); in some progressors the fall in FE-1 preceded the onset of IA. CONCLUSIONS: Pancreatic exocrine function decreases in the majority of young at-risk children who progress to IA and T1D.

Higher frequency of vertebrate-infecting viruses in the gut of infants born to mothers with type 1 diabetes.

BACKGROUND: Microbial exposures in utero and early life shape the infant microbiome, which can profoundly impact on health. Compared to the bacterial microbiome, very little is known about the virome. We set out to characterize longitudinal changes in the gut virome of healthy infants born to mothers with or without type 1 diabetes using comprehensive virome capture sequencing. METHODS: Healthy infants were selected from Environmental Determinants of Islet Autoimmunity (ENDIA), a prospective cohort of Australian children with a first-degree relative with type 1 diabetes, followed from pregnancy. Fecal specimens were collected three-monthly in the first year of life. RESULTS: Among 25 infants (44% born to mothers with type 1 diabetes) at least one virus was detected in 65% (65/100) of samples and 96% (24/25) of infants during the first year of life. In total, 26 genera of viruses were identified and >150 viruses were differentially abundant between the gut of infants with a mother with type 1 diabetes vs without. Positivity for any virus was associated with maternal type 1 diabetes and older infant age. Enterovirus was associated with older infant age and maternal smoking. CONCLUSIONS: We demonstrate a distinct gut virome profile in infants of mothers with type 1 diabetes, which may influence health outcomes later in life. Higher prevalence and greater number of viruses observed compared to previous studies suggests significant underrepresentation in existing virome datasets, arising most likely from less sensitive techniques used in data acquisition.

Re-designing a rapid response system: effect on staff experiences and perceptions of rapid response team calls.

BACKGROUND: Rapid Response Team (RRT) calls are clinical crises. Clinical and time pressures can hinder effective liaison between staff who call the RRT ('users') and those responding as part of the RRT ('members'). Non-technical skills (NTS) training has been shown to improve communication and cooperation but requires time and financial resources that may not be available in acute care hospitals. Rapid Response System (RRS) re-design, aiming to promote use of NTS, may provide an alternative approach to improving interactions within RRTs and between members and users. METHODS: Re-design of an existing mature RRS was undertaken in a tertiary, metropolitan hospital incorporating the addition of: 1) regular RRT meetings 2) RRT role badges and 3) a structured member-to-user patient care responsibility "hand-off" process. To compare experiences and perceptions of calls, users and members were surveyed pre and post re-design. RESULTS: Post re-design there were improvements in members' understanding of RRT roles (P = 0.03) and responsibilities (P < 0.01), and recollection of introducing themselves to users (P = 0.02). For users, after the re-design, there were improvements in identification of the RRT leader (P < 0.01), and in the development of clinical plans for patients remaining on the ward at the end of an RRT call (P < 0.01). However, post-re-design, fewer users agreed that the structured hand-off was useful or that they should be involved in the process. Both members and users reported fewer experiences of conflict at RRT calls post-re-design (both P < 0.01). CONCLUSION: The RRS re-design yielded improvements in interactions between members in RRTs and between RRT members and users. However, some unintended consequences arose, particularly around user satisfaction with the structured hand-off. These findings suggest that refinement and improvement of the RRS is possible, but should be an ongoing iterative effort, ideally supported by staff training. TRIAL REGISTRATION: NCT01551160. Registered: 12th March 2012.

Relationship between birth weight or fetal growth rate and postnatal allergy: A systematic review.

BACKGROUND: Individual susceptibility to allergic diseases is developmentally programmed by early-life exposures. Evidence from preclinical studies suggests that intrauterine growth restriction is protective against later inflammatory responses to allergens. OBJECTIVE: We sought to evaluate whether prenatal growth affects susceptibility to allergy in human subjects. METHODS: We systematically searched for relevant studies in 11 databases, including Web of Science, ProQuest, EMBASE, and PubMed. We included only studies that corrected for gestational age or were restricted to full-term infants to separate effects of fetal growth from those of prematurity. RESULTS: The 42 eligible studies included prospective and retrospective cohort, cross-sectional, and case-control studies. Only 2 studies reported allergic asthma. A birth weight increase of 1 kg was associated with a 44% greater risk of food allergy in children (odds ratio [OR], 1.44; 95% CI, 1.04-1.99; P = .001), a 17% greater risk of ever allergic dermatitis in children (OR, 1.17; 95% CI, 1.04-1.32; P = .008), and a 34% greater risk of ever or current allergic dermatitis in infants up to 2 years of age (OR, 1.34; 95% CI, 1.08-1.68; P = .009). Risks of allergic rhinitis were not associated with birth weight. CONCLUSIONS: The results of these meta-analyses suggest that intrauterine growth restriction protects against allergic diseases in human subjects consistent with preclinical evidence but that effects might differ between allergic diseases. The strongest evidence is available for infancy and early childhood, and additional studies in older children and adults are needed to determine whether the effects of prenatal growth on each allergic disease persist or differ between those with severe and mild phenotypes.

Beta cell function in type 1 diabetes determined from clinical and fasting biochemical variables.

AIMS/HYPOTHESIS: Beta cell function in type 1 diabetes is commonly assessed as the average plasma C-peptide concentration over 2 h following a mixed-meal test (CPAVE). Monitoring of disease progression and response to disease-modifying therapy would benefit from a simpler, more convenient and less costly measure. Therefore, we determined whether CPAVE could be reliably estimated from routine clinical variables. METHODS: Clinical and fasting biochemical data from eight randomised therapy trials involving participants with recently diagnosed type 1 diabetes were used to develop and validate linear models to estimate CPAVE and to test their accuracy in estimating loss of beta cell function and response to immune therapy. RESULTS: A model based on disease duration, BMI, insulin dose, HbA1c, fasting plasma C-peptide and fasting plasma glucose most accurately estimated loss of beta cell function (area under the receiver operating characteristic curve [AUROC] 0.89 [95% CI 0.87, 0.92]) and was superior to the commonly used insulin-dose-adjusted HbA1c (IDAA1c) measure (AUROC 0.72 [95% CI 0.68, 0.76]). Model-estimated CPAVE (CPEST) reliably identified treatment effects in randomised trials. CPEST, compared with CPAVE, required only a modest (up to 17%) increase in sample size for equivalent statistical power. CONCLUSIONS/INTERPRETATION: CPEST, approximated from six variables at a single time point, accurately identifies loss of beta cell function in type 1 diabetes and is comparable to CPAVE for identifying treatment effects. CPEST could serve as a convenient and economical measure of beta cell function in the clinic and as a primary outcome measure in trials of disease-modifying therapy in type 1 diabetes.

Gut microbiome dysbiosis and increased intestinal permeability in children with islet autoimmunity and type 1 diabetes: A prospective cohort study.

AIMS/HYPOTHESIS: To investigate the longitudinal relationship between the gut microbiome, circulating short chain fatty acids (SCFAs) and intestinal permeability in children with islet autoimmunity or type 1 diabetes and controls. METHODS: We analyzed the gut bacterial microbiome, plasma SCFAs, small intestinal permeability and dietary intake in 47 children with islet autoimmunity or recent-onset type 1 diabetes and in 41 unrelated or sibling controls over a median (range) of 13 (2-34) months follow-up. RESULTS: Children with multiple islet autoantibodies (≥2 IA) or type 1 diabetes had gut microbiome dysbiosis. Anti-inflammatory Prevotella and Butyricimonas genera were less abundant and these changes were not explained by differences in diet. Small intestinal permeability measured by blood lactulose:rhamnose ratio was higher in type 1 diabetes. Children with ≥2 IA who progressed to type 1 diabetes (progressors), compared to those who did not progress, had higher intestinal permeability (mean [SE] difference +5.14 [2.0], 95% confidence interval [CI] 1.21, 9.07, P = .006), lower within-sample (alpha) microbial diversity (31.3 [11.2], 95% CI 9.3, 53.3, P = .005), and lower abundance of SCFA-producing bacteria. Alpha diversity (observed richness) correlated with plasma acetate levels in all groups combined (regression coefficient [SE] 0.57 [0.21], 95% CI 0.15, 0.99 P = .008). CONCLUSIONS/INTERPRETATION: Children with ≥2 IA who progress to diabetes, like those with recent-onset diabetes, have gut microbiome dysbiosis associated with increased intestinal permeability. Interventions that expand gut microbial diversity, in particular SCFA-producing bacteria, may have a role to decrease progression to diabetes in children at-risk.

Australian children with type 1 diabetes consume high sodium and high saturated fat diets: Comparison with national and international guidelines.

AIM: We aimed to evaluate the diets of children with type 1 diabetes (T1D) against recommended Australian dietary intakes and international T1D guidelines and compare them to children without T1D. METHODS: A cross-sectional analysis in 143 children (103 children aged 8-18 years with T1D and 40 age- and gender-matched controls) and longitudinal analysis at 0, 3, 6 and 12 months in 90 T1D children were conducted. Diet was assessed using an Australian validated food frequency questionnaire. Diet quality was assessed against recommended servings and nutrient intakes from Australian Dietary Guidelines and International Society for Pediatric and Adolescent Diabetes (ISPAD) Nutritional Guidelines. RESULTS: Diet was evaluated in 478 questionnaires. Diet composition did not differ between T1D and controls, and both groups did not meet the majority of the Australian Dietary Guidelines, except for fruit intake. The majority of T1D children and controls (80-83%) were overconsuming sodium (2837 ± 848 mg/day), discretionary foods (5.9 ± 2.5 serves/day) and saturated fat and trans fatty acids (13.1 ± 2.7% of total daily energy intake) in comparison with Australian and ISPAD guidelines. A total of 84% of T1D children and controls achieved the recommended intake of fibre (34.4 ± 11.0 g/day). Longitudinal analysis in children with T1D showed that total daily energy, macronutrient, micronutrient and food group servings intake did not change over the 12 months. Overconsumption of sodium, discretionary foods and saturated fat persisted over the 12-month study period. CONCLUSIONS: The majority of Australian children, with and without T1D, is not meeting recommended dietary guidelines. Significant overconsumption of sodium, saturated fat and discretionary foods attracts the most concern.

Late-gestation maternal dietary methyl donor and cofactor supplementation in sheep partially reverses protection against allergic sensitization by IUGR.

Perinatal exposures are associated with altered risks of childhood allergy. Human studies and our previous work suggest that restricted growth in utero (IUGR) is protective against allergic disease. The mechanisms are not clearly defined, but reduced fetal abundance and altered metabolism of methyl donors are hypothesized as possible underlying mechanisms. Therefore, we examined whether late-gestation maternal dietary methyl donor and cofactor supplementation of the placentally restricted (PR) sheep pregnancy would reverse allergic protection in progeny. Allergic outcomes were compared between progeny from control pregnancies (CON; n = 49), from PR pregnancies without intervention (PR; n = 28), and from PR pregnancies where the dam was fed a methyl donor plus cofactor supplement from day 120 of pregnancy until delivery (PR + Methyl; n = 25). Both PR and PR + Methyl progeny were smaller than CON; supplementation did not alter birth size. PR was protective against cutaneous hypersensitivity responses to ovalbumin (OVA; P < 0.01 in singletons). Cutaneous hypersensitivity responses to OVA in PR + Methyl progeny were intermediate to and not different from the responses of CON and PR sheep. Cutaneous hypersensitivity responses to house dust mites did not differ between treatments. In singleton progeny, upper dermal mast cell density was greater in PR + Methyl than in PR or CON (each P < 0.05). The differences in the cutaneous allergic response were not explained by treatment effects on circulating immune cells or antibodies. Our results suggest that mechanisms underlying in utero programming of allergic susceptibility by IUGR and methyl donor availability may differ and imply that late-gestation methyl donor supplementation may increase allergy risk.

Dietary sodium intake relates to vascular health in children with type 1 diabetes.

BACKGROUND AND OBJECTIVE: Children with type 1 diabetes (T1D) have vascular dysfunction and frequently struggle to adhere to dietary recommendations. Limited data exist for the vascular consequences of poor diet quality in children. We aimed to evaluate the association between dietary components and vascular function in children with T1D. METHODS: Cross-sectional study including 90 children (13.6 [3.5] years, 41 boys) with T1D. They had evaluation of dietary micro and macronutrients (Australian Child and Adolescent Eating Survey), vascular endothelial and smooth muscle function (flow-mediated dilatation and glyceryl trinitrate mediated dilatation [GTN], respectively), clinical and biochemical variables. RESULTS: Children had a sodium intake of 3.013 (0.76) (mean [SD]) g/day. Vascular smooth muscle dysfunction, as measured by GTN, related to higher daily sodium intake (r = -0.31, P = .003), independent of the inverse relationships between GTN and total energy (r = -0.30, P = .005) and fat intake (r = -0.28, P = .007). Multiregression model showed that an increase in 1 g of daily sodium intake was independently associated with a deterioration of 3 percentage units in GTN (95% CI -4.3, -0.9; P = .003). There was an association between sodium intake and systolic blood pressure after adjustment for age and gender (regression coefficient 2.4; 95% CI 0.5, 4.3; P = .01). CONCLUSIONS: High dietary sodium intake in children with T1D is common and relates to vascular dysfunction, independently of other dietary intake, blood pressure, and glycemic control.

Early atherosclerosis is associated with retinal microvascular changes in adolescents with type 1 diabetes.

BACKGROUND/OBJECTIVE: Adolescents with type 1 diabetes have early macrovascular changes (increased intima-media thickness [IMT]) and early retinal changes that predict clinical disease in adulthood. We hypothesized that early changes in the macrovascular and retinal microvascular beds develop in parallel before retinopathy develops. We therefore aimed to investigate the relationship between changes in atherosclerosis (carotid and aortic IMT) and retinal vascular geometry cross-sectionally and longitudinally in adolescents with type 1 diabetes. METHODS: Ninety adolescents with type 1 diabetes (41 boys, aged 13.6 ± 3.5 years) who were enrolled in a randomized controlled trial had evaluations at baseline; 41 randomized to placebo were also investigated at 12 months for carotid and aortic IMT using ultrasound and retinal vascular geometry was measured from retinal photographs. RESULTS: There were significant associations between thicker mean/maximum carotid IMT and wider retinal arteriolar and venular calibers; for every 0.1 mm increase in mean carotid IMT, retinal arteriolar caliber increased by 7.90 µm (95% confidence interval [CI] 4.50, 11.30, P < 0.0001) and venular caliber by 9.61 µm (95% CI 4.16, 15.06, P = 0.0008). Increased mean aortic IMT was associated with increased arteriolar tortuosity (2.61, 95% CI 0.50, 4.71, P = 0.02). CONCLUSIONS: The early changes of atherosclerosis are associated with retinal microvascular changes in adolescents with type 1 diabetes. This supports parallel adverse changes in the macro and microvascular circulations from early adolescence in type 1 diabetes, and highlights the importance of early intervention.

Factors Influencing Knowledge, Food Safety Practices and Food Preferences During Warm Weather of Salmonella and Campylobacter Cases in South Australia.

OBJECTIVE: To assess food safety practices, food shopping preferences, and eating behaviors of people diagnosed with Salmonella or Campylobacter infection in the warm seasons, and to identify socioeconomic factors associated with behavior and practices. METHODS: A cross-sectional survey was conducted among Salmonella and Campylobacter cases with onset of illness from January 1 to March 31, 2013. Multivariable logistic regression analyses examined relationships between socioeconomic position and food safety knowledge and practices, shopping and food preferences, and preferences, perceptions, and knowledge about food safety information on warm days. RESULTS: Respondents in our study engaged in unsafe personal and food hygiene practices. They also carried out unsafe food preparation practices, and had poor knowledge of foods associated with an increased risk of foodborne illness. Socioeconomic position did not influence food safety practices. We found that people's reported eating behaviors and food preferences were influenced by warm weather. CONCLUSIONS: Our study has explored preferences and practices related to food safety in the warm season months. This is important given that warmer ambient temperatures are projected to rise, both globally and in Australia, and will have a substantial effect on the burden of infectious gastroenteritis including foodborne disease. Our results provide information about modifiable behaviors for the prevention of foodborne illness in the household in the warm weather and the need for information to be disseminated across the general population. An understanding of the knowledge and factors associated with human behavior during warmer weather is critical for public health interventions on foodborne prevention.

Effects of induced placental and fetal growth restriction, size at birth and early neonatal growth on behavioural and brain structural lateralization in sheep.

Poor perinatal growth in humans results in asymmetrical grey matter loss in fetuses and infants and increased functional and behavioural asymmetry, but specific contributions of pre- and postnatal growth are unclear. We therefore compared strength and direction of lateralization in obstacle avoidance and maze exit preference tasks in offspring of placentally restricted (PR: 10M, 13F) and control (CON: 23M, 17F) sheep pregnancies at 18 and 40 weeks of age, and examined gross brain structure of the prefrontal cortex at 52 weeks of age (PR: 14M, 18F; CON: 23M, 25F). PR did not affect lateralization direction, but 40-week-old PR females had greater lateralization strength than CON (P = .021). Behavioural lateralization measures were not correlated with perinatal growth. PR did not alter brain morphology. In males, cross-sectional areas of the prefrontal cortex and left hemisphere correlated positively with skull width at birth, and white matter area correlated positively with neonatal growth rate of the skull (all P < .05). These studies reinforce the need to include progeny of both sexes in future studies of neurodevelopmental programming, and suggest that restricting in utero growth has relatively mild effects on gross brain structural or behavioural lateralization in sheep.

Effect of placental restriction and neonatal exendin-4 treatment on postnatal growth, adult body composition, and in vivo glucose metabolism in the sheep.

Intrauterine growth restriction (IUGR) increases the risk of adult type 2 diabetes (T2D) and obesity. Neonatal exendin-4 treatment can prevent diabetes in the IUGR rat, but whether this will be effective in a species where the pancreas is more mature at birth is unknown. Therefore, we evaluated the effects of neonatal exendin-4 administration after experimental restriction of placental and fetal growth on growth and adult metabolic outcomes in sheep. Body composition, glucose tolerance, and insulin secretion and sensitivity were assessed in singleton-born adult sheep from control (CON; n = 6 females and 4 males) and placentally restricted pregnancies (PR; n = 13 females and 7 males) and in sheep from PR pregnancies that were treated with exendin-4 as neonates (daily sc injections of 1 nmol/kg exendin-4; PR + exendin-4; n = 11 females and 7 males). Placental restriction reduced birth weight (by 29%) and impaired glucose tolerance in the adult but did not affect adult adiposity, insulin secretion, or insulin sensitivity. Neonatal exendin-4 suppressed growth during treatment, followed by delayed catchup growth and unchanged adult adiposity. Neonatal exendin-4 partially restored glucose tolerance in PR progeny but did not affect insulin secretion or sensitivity. Although the effects on glucose tolerance are promising, the lack of effects on adult body composition, insulin secretion, and insulin sensitivity suggest that the neonatal period may be too late to fully reprogram the metabolic consequences of IUGR in species that are more mature at birth than rodents.

Cognitive abilities in preterm and term-born adolescents.

OBJECTIVE: To investigate the influence of a range of prenatal and postnatal factors on cognitive development in preterm and term-born adolescents. STUDY DESIGN: Woodcock-Johnson III Tests of Cognitive Abilities were used to assess general intellectual ability and 6 broad cognitive abilities in 145 young adolescents aged approximately 12.5 years and born 25-41 weeks gestational age (GA). To study potential links between neurophysiologic and cognitive outcomes, corticomotor excitability was measured using transcranial magnetic stimulation and surface electromyography. The influence of various prenatal and postnatal factors on cognitive development was investigated using relative importance regression modeling. RESULTS: Adolescents with greater GA tended to have better cognitive abilities (particularly general intellectual ability, working memory, and cognitive efficiency) and higher corticomotor excitability. Corticomotor excitability explained a higher proportion of the variance in cognitive outcome than GA. But the strongest predictors of cognitive outcome were combinations of prenatal and postnatal factors, particularly degree of social disadvantage at the time of birth, birthweight percentile, and height at assessment. CONCLUSIONS: In otherwise neurologically healthy adolescents, GA accounts for little interindividual variability in cognitive abilities. The association between corticomotor excitability and cognitive performance suggests that reduced connectivity, potentially associated with brain microstructural abnormalities, may contribute to cognitive deficits in preterm children. It remains to be determined if the effects of low GA on cognitive outcomes attenuate over childhood in favor of a concomitant increase in the relative importance of heritability, or alternatively, if cognitive development is more heavily influenced by the quality of the postnatal environment.