The impact of a population-level school food and nutrition policy on dietary intake and body weights of Canadian children

AbstractObjectiveThe objective of this study is to assess population-level trends in children's dietary intake and weight status before and after the implementation of a provincial school nutrition policy in the province of Nova Scotia, Canada.MethodSelf-reported dietary behavior and nutrient intake and measured body mass index were collected as part of a population-level study with grade 5 students in 2003 (n=5215) and 2011 (5508), prior to and following implementation of the policy. We applied random effects regression methods to assess the effect of the policy on dietary and health outcomes.ResultsIn 2011, students reported consuming more milk products, while there was no difference in mean consumption of vegetables and fruits in adjusted models. Adjusted regression analysis revealed a statistically significant decrease in sugar-sweetened beverage consumption. Despite significant temporal decreases in dietary energy intake and increases in diet quality, prevalence rates of overweight and obesity continued to increase.ConclusionThis population-level intervention research suggests a positive influence of school nutrition policies on diet quality, energy intake and healthy beverage consumption, and that more action beyond schools is needed to curb the increases in the prevalence of childhood obesity

Comparison of ICD code-based diagnosis of obesity with measured obesity in children and the implications for health care cost estimates

<p>Abstract</p> <p>Background</p> <p>Administrative health databases are a valuable research tool to assess health care utilization at the population level. However, their use in obesity research limited due to the lack of data on body weight. A potential workaround is to use the ICD code of obesity to identify obese individuals. The objective of the current study was to investigate the sensitivity and specificity of an ICD code-based diagnosis of obesity from administrative health data relative to the gold standard measured BMI.</p> <p>Methods</p> <p>Linkage of a population-based survey with anthropometric measures in elementary school children in 2003 with longitudinal administrative health data (physician visits and hospital discharges 1992-2006) from the Canadian province of Nova Scotia. Measured obesity was defined based on the CDC cut-offs applied to the measured BMI. An ICD code-based diagnosis obesity was defined as one or more ICD-9 (278) or ICD-10 code (E66-E68) of obesity from a physician visit or a hospital stay. Sensitivity and specificity were calculated and health care cost estimates based on measured obesity and ICD-based obesity were compared.</p> <p>Results</p> <p>The sensitivity of an ICD code-based obesity diagnosis was 7.4% using ICD codes between 2002 and 2004. Those correctly identified had a higher BMI and had higher health care utilization and costs.</p> <p>Conclusions</p> <p>An ICD diagnosis of obesity in Canadian administrative health data grossly underestimates the true prevalence of childhood obesity and overestimates the health care cost differential between obese and non-obese children.</p

The Role of Maternal Smoking in Effect of Fetal Growth Restriction on Poor Scholastic Achievement in Elementary School

Fetal growth restriction and maternal smoking during pregnancy are independently implicated in lowering intellectual attainment in children. We hypothesized that only reduction of fetal growth that is attributable to extrinsic causes (e.g., maternal smoking) affects intellectual development of a child. Cross-sectional survey of 3,739 students in Nova Scotia (Canada) in 2003 was linked with the perinatal database, parental interviews on socio-demographic factors and the performance on standardized tests when primarily 11–12 years of age, thereby forming a retrospective cohort. Data was analyzed using hierarchical logistic regression with correction for clustering of children within schools. The risk of poor test result among children born small-for-gestational-age (SGA) to mothers who smoked was 29.4%, higher than in any other strata of maternal smoking and fetal growth. The adjusted odds ratio among SGA children born to mothers who smoked was the only one elevated compared to children who were not growth restricted and born to mothers who did not smoke (17.0%, OR = 1.46, 95% CI 1.02, 2.09). Other perinatal, maternal and socio-demographic factors did not alter this pattern of effect modification. Heterogeneity of etiology of fetal growth restriction should be consider in studies that address examine its impact on health over life course

Evaluation of a health promoting schools program in a school board in Nova Scotia, Canada.

A Health promoting schools (HPS) approach aims to make schools a healthy place through a holistic approach that promotes a supportive 'school ethos' and emphasizes improvements in physical, social, and emotional well-being and educational outcomes. A HPS initiative in rural Nova Scotia (Canada) provided an opportunity for a population-level natural experiment. This study investigated student well-being and health behaviours between schools with and without HPS implementation and schools with high and low school ethos scores. Student well-being, nutrition, and physical activity were examined in a cross-sectional survey of elementary students in Nova Scotia, Canada in 2014. Multiple regression was used to assess the relationship with student well-being using the Quality of Life in School (QoLS) instrument and health behaviours. The main exposure was attending one of the 10 HPS schools; secondary exposure was the school ethos score. The overall QoLS score and its subdomain scores in the adjusted models were higher in students attending HPS schools compared to those in non-HPS schools, but the differences were not statistically significant and the effect sizes were small. Students in schools that scored high on school ethos score had higher scores for the QoLS and its subdomains, but the difference was only significant for the teacher-student relationship domain. Although this study did not find significant differences between HPS and non-HPS schools, our results highlight the complexity of evaluating HPS effects in the real world. The findings suggest a potential role of a supportive school ethos for student well-being in school

CMT2N-causing aminoacylation domain mutants enable Nrp1 interaction with AlaRS

Through dominant mutations, aminoacyl-tRNA synthetases constitute the largest protein family linked to Charcot-Marie-Tooth disease (CMT). An example is CMT subtype 2N (CMT2N), caused by individual mutations spread out in AlaRS, including three in the aminoacylation domain, thereby suggesting a role for a tRNA-charging defect. However, here we found that two are aminoacylation defective but that the most widely distributed R329H is normal as a purified protein in vitro and in unfractionated patient cell samples. Remarkably, in contrast to wild-type (WT) AlaRS, all three mutant proteins gained the ability to interact with neuropilin 1 (Nrp1), the receptor previously linked to CMT pathogenesis in GlyRS. The aberrant AlaRS-Nrp1 interaction is further confirmed in patient samples carrying the R329H mutation. However, CMT2N mutations outside the aminoacylation domain do not induce the Nrp1 interaction. Detailed biochemical and biophysical investigations, including X-ray crystallography, small-angle X-ray scattering, hydrogen-deuterium exchange (HDX), switchSENSE hydrodynamic diameter determinations, and protease digestions reveal a mutation-induced structural loosening of the aminoacylation domain that correlates with the Nrp1 interaction. The b1b2 domains of Nrp1 are responsible for the interaction with R329H AlaRS. The results suggest Nrp1 is more broadly associated with CMT-associated members of the tRNA synthetase family. Moreover, we revealed a distinct structural loosening effect induced by a mutation in the editing domain and a lack of conformational impact with C-Ala domain mutations, indicating mutations in the same protein may cause neuropathy through different mechanisms. Our results show that, as with other CMT-associated tRNA synthetases, aminoacylation per se is not relevant to the pathology

CMT2N-causing aminoacylation domain mutants enable Nrp1 interaction with AlaRS.

Through dominant mutations, aminoacyl-tRNA synthetases constitute the largest protein family linked to Charcot-Marie-Tooth disease (CMT). An example is CMT subtype 2N (CMT2N), caused by individual mutations spread out in AlaRS, including three in the aminoacylation domain, thereby suggesting a role for a tRNA-charging defect. However, here we found that two are aminoacylation defective but that the most widely distributed R329H is normal as a purified protein in vitro and in unfractionated patient cell samples. Remarkably, in contrast to wild-type (WT) AlaRS, all three mutant proteins gained the ability to interact with neuropilin 1 (Nrp1), the receptor previously linked to CMT pathogenesis in GlyRS. The aberrant AlaRS-Nrp1 interaction is further confirmed in patient samples carrying the R329H mutation. However, CMT2N mutations outside the aminoacylation domain do not induce the Nrp1 interaction. Detailed biochemical and biophysical investigations, including X-ray crystallography, small-angle X-ray scattering, hydrogen-deuterium exchange (HDX), switchSENSE hydrodynamic diameter determinations, and protease digestions reveal a mutation-induced structural loosening of the aminoacylation domain that correlates with the Nrp1 interaction. The b1b2 domains of Nrp1 are responsible for the interaction with R329H AlaRS. The results suggest Nrp1 is more broadly associated with CMT-associated members of the tRNA synthetase family. Moreover, we revealed a distinct structural loosening effect induced by a mutation in the editing domain and a lack of conformational impact with C-Ala domain mutations, indicating mutations in the same protein may cause neuropathy through different mechanisms. Our results show that, as with other CMT-associated tRNA synthetases, aminoacylation per se is not relevant to the pathology

Domain collapse and active site ablation generate a widespread animal mitochondrial seryl-tRNA synthetase

Through their aminoacylation reactions, aminoacyl tRNA-synthetases (aaRS) establish the rules of the genetic code throughout all of nature. During their long evolution in eukaryotes, additional domains and splice variants were added to what is commonly a homodimeric or monomeric structure. These changes confer orthogonal functions in cellular activities that have recently been uncovered. An unusual exception to the familiar architecture of aaRSs is the heterodimeric metazoan mitochondrial SerRS. In contrast to domain additions or alternative splicing, here we show that heterodimeric metazoan mitochondrial SerRS arose from its homodimeric ancestor not by domain additions, but rather by collapse of an entire domain (in one subunit) and an active site ablation (in the other). The collapse/ablation retains aminoacylation activity while creating a new surface, which is necessary for its orthogonal function. The results highlight a new paradigm for repurposing a member of the ancient tRNA synthetase family.© The Author(s) 2023. Published by Oxford University Press on behalf of Nucleic Acids Research

Increased serum neurofilament light and thin ganglion cell-inner plexiform layer are additive risk factors for disease activity in early multiple sclerosis

OBJECTIVE: To investigate the association of combined serum neurofilament light chain (sNfL) and retinal optical coherence tomography (OCT) measurements with future disease activity in patients with early multiple sclerosis (MS). METHODS: We analyzed sNfL by single molecule array technology and performed OCT measurements in a prospective cohort of 78 patients with clinically isolated syndrome and early relapsing-remitting MS with a median (interquartile range) follow-up of 23.9 (23.3–24.7) months. Patients were grouped into those with abnormal or normal sNfL levels, defined as sNfL ≥/<80th percentile of age-corrected reference values. Likewise, patients were grouped by a median split into those with thin or thick ganglion cell and inner plexiform layer (GCIP), peripapillary retinal nerve fiber layer, and inner nuclear layer in nonoptic neuritis eyes. Outcome parameters were violation of no evidence of disease activity (NEDA-3) criteria or its components. RESULTS: Patients with abnormal baseline sNfL had a higher risk of violating NEDA-3 (hazard ratio [HR] 2.28, 95% CI 1.27–4.09, p = 0.006) and developing a new brain lesion (HR 2.47, 95% CI 1.30(–4).69, p = 0.006), but not for a new relapse (HR 2.21, 95% CI 0.97–5.03, p = 0.058). Patients with both abnormal sNfL and thin GCIP had an even higher risk for NEDA-3 violation (HR 3.61, 95% CI 1.77–7.36, p = 4.2e−4), new brain lesion (HR 3.19, 95% CI 1.51–6.76, p = 0.002), and new relapse (HR 5.38, 95% CI 1.61–17.98, p = 0.006) than patients with abnormal sNfL alone. CONCLUSIONS: In patients with early MS, the presence of both abnormal sNfL and thin GCIP is a stronger risk factor for future disease activity than the presence of each parameter alone

Serum GFAP and NfL as disease severity and prognostic biomarkers in patients with aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder

BACKGROUND: Neuromyelitis optica spectrum disorder (NMOSD) is a frequently disabling neuroinflammatory syndrome with a relapsing course. Blood-based disease severity and prognostic biomarkers for NMOSD are a yet unmet clinical need. Here, we evaluated serum glial fibrillary acidic protein (sGFAP) and neurofilament light (sNfL) as disease severity and prognostic biomarkers in patients with aquaporin-4 immunoglobulin (Ig)G positive (AQP4-IgG(+)) NMOSD. METHODS: sGFAP and sNfL were determined by single-molecule array technology in a prospective cohort of 33 AQP4-IgG(+) patients with NMOSD, 32 of which were in clinical remission at study baseline. Sixteen myelin oligodendrocyte glycoprotein IgG-positive (MOG-IgG(+)) patients and 38 healthy persons were included as controls. Attacks were recorded in all AQP4-IgG(+) patients over a median observation period of 4.25 years. RESULTS: In patients with AQP4-IgG(+) NMOSD, median sGFAP (109.2 pg/ml) was non-significantly higher than in MOG-IgG(+) patients (81.1 pg/ml; p = 0.83) and healthy controls (67.7 pg/ml; p = 0.07); sNfL did not substantially differ between groups. Yet, in AQP4-IgG(+), but not MOG-IgG(+) patients, higher sGFAP was associated with worse clinical disability scores, including the Expanded Disability Status Scale (EDSS, standardized effect size = 1.30, p = 0.007) and Multiple Sclerosis Functional Composite (MSFC, standardized effect size = - 1.28, p = 0.01). While in AQP4-IgG(+), but not MOG-IgG(+) patients, baseline sGFAP and sNfL were positively associated (standardized effect size = 2.24, p = 0.001), higher sNfL was only non-significantly associated with worse EDSS (standardized effect size = 1.09, p = 0.15) and MSFC (standardized effect size = - 1.75, p = 0.06) in patients with AQP4-IgG(+) NMOSD. Patients with AQP4-IgG(+) NMOSD with sGFAP > 90 pg/ml at baseline had a shorter time to a future attack than those with sGFAP ≤ 90 pg/ml (adjusted hazard ratio [95% confidence interval] = 11.6 [1.3-105.6], p = 0.03). In contrast, baseline sNfL levels above the 75th age adjusted percentile were not associated with a shorter time to a future attack in patients with AQP4-IgG(+) NMOSD. CONCLUSION: These findings suggest a potential role for sGFAP as biomarker for disease severity and future disease activity in patients with AQP4-IgG(+) NMOSD in phases of clinical remission

Biomarkers of Multiple Sclerosis

The search for an ideal multiple sclerosis biomarker with good diagnostic value, prognostic reference and an impact on clinical outcome has yet to be realized and is still ongoing. The aim of this review is to establish an overview of the frequent biomarkers for multiple sclerosis that exist to date. The review summarizes the results obtained from electronic databases, as well as thorough manual searches. In this review the sources and methods of biomarkers extraction are described; in addition to the description of each biomarker, determination of the prognostic, diagnostic, disease monitoring and treatment response values besides clinical impact they might possess. We divided the biomarkers into three categories according to the achievement method: laboratory markers, genetic-immunogenetic markers and imaging markers. We have found two biomarkers at the time being considered the gold standard for MS diagnostics. Unfortunately, there does not exist a single solitary marker being able to present reliable diagnostic value, prognostic value, high sensitivity and specificity as well as clinical impact. We need more studies to find the best biomarker for MS.publishersversionPeer reviewe