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Ballet dancing is a multifaceted activity requiring muscular power, strength, endurance, flexibility, and agility; necessitating demanding training schedules. Furthermore dancers may be under aesthetic pressure to maintain a lean physique, and adolescent dancers require extra nutrients for growth and development. This cross-sectional study investigated the nutritional status of 47 female adolescent ballet dancers (13-18 years) living in Auckland, New Zealand. Participants who danced at least 1 hr per day 5 days per week completed a 4-day estimated food record, anthropometric measurements (Dual-energy X-ray Absorptiometry) and hematological analysis (iron and vitamin D). Mean BMI was 19.7 ± 2.4kg/m² and percentage body fat, 23.5 ± 4.1%. The majority (89.4%) of dancers had a healthy weight (5th-85th percentile) using BMI-for-age growth charts. Food records showed a mean energy intake of 8097.3 ± 2155.6kJ/day (48.9% carbohydrate, 16.9% protein, 33.8% fat, 14.0% saturated fat). Mean carbohydrate and protein intakes were 4.8 ±1.4 and 1.6 ± 0.5g/kg/day respectively. Over half (54.8%) of dancers consumed less than 5g carbohydrate/kg/day, and 10 (23.8%) less than 1.2 g protein/kg/day. Over 60% consumed less than the estimated average requirement for calcium, folate, magnesium and selenium. Thirteen (28.3%) dancers had suboptimal iron status (serum ferritin (SF) <20µg/L). Of these, four had iron deficiency (SF < 12µg/L, hemoglobin (Hb) ≥120g/L) and one iron deficiency anemia (SF < 12µg/L, Hb < 120g/L). Mean serum 25-hydroxy vitamin D was 75.1 ± 18.6nmol/L, 41 (91.1%) had concentrations above 50nmol/L. Female adolescent ballet dancers are at risk for iron deficiency, and possibly inadequate nutrient intakes. [ABSTRACT FROM AUTHOR]

Aim: In New Zealand, there are few adequate food frequency questionnaires for assessing dietary intake. This study aimed to develop and assess the relative validity of a multi‐nutrient, culturally appropriate, semi‐quantitative food frequency questionnaire for use in young adult New Zealand women (the New Zealand Women's Food Frequency Questionnaire (NZWFFQ)). Methods: Women (n = 110) aged 16–45 years of Māori, Pacific or European ethnicity completed a NZWFFQ assessing dietary intake over the previous month, and a 4‐day weighed food record. Relative validity was evaluated by comparing nutrient intakes from the NZWFFQ with the food record using Spearman's rank correlation coefficients, cross‐classification, the weighted kappa statistic and Bland–Altman analysis. Results: Nutrient intake was higher from the NZWFFQ compared with the food record for all nutrients (range: 1%–64% difference) except alcohol (−16% difference). Energy‐adjusted correlations ranged from 0.23 to 0.67 (average 0.48). Correct classification into same and adjacent quartiles was over 70% for all nutrients except folate and vitamin D. Gross misclassification into opposite quartiles ranged from 1% (monounsaturated fat, magnesium, calcium) to 10% (iron). The weighted kappa showed poor agreement for vitamin D and folate, fair agreement for most nutrients, and moderate agreement for fibre, vitamin E, magnesium, calcium and phosphorus. Conclusions: The NZWFFQ overestimated intake of nearly all nutrients. While not suitable for assessing absolute intake, the NZWFFQ is suitable for ranking individuals based on nutrient intake demonstrating reasonable relative validity for this purpose. [ABSTRACT FROM AUTHOR]

We evaluated the efficacy of vitamin D (VID), omega-3 long chain polyunsaturated fatty acids (omega-3 LCPUFA, OM), or both (VIDOM) on core symptoms of ASD. New Zealand children with ASD (n = 73; aged 2.5–8.0 years) received daily 2000 IU vitamin D3, 722 mg docosahexaenoic acid, both, or placebo. Outcome measures were Social Responsiveness Scale (SRS) and Sensory Processing Measure (SPM). Of 42 outcome measures comparisons (interventions vs. placebo), two showed greater improvements (P = 0.03, OM and VIDOM for SRS-social awareness) and four showed trends for greater improvements (P < 0.1, VIDOM for SRS-social communicative functioning, OM for SRS-total, VIDOM for SPM-taste/smell and OM for SPM-balance/motion). Omega-3 LCPUFA with and without vitamin D may improve some core symptoms of ASD but no definitive conclusions can be made. [ABSTRACT FROM AUTHOR]

Low vitamin D status in early development has been hypothesised as an environmental risk factor for Autism Spectrum Disorder (ASD), given the concurrent increase in the prevalence of these two conditions, and the association of vitamin D with many ASD-associated medical conditions. Identification of vitamin D-ASD factors may provide indications for primary and secondary prevention interventions. We systematically reviewed the literature for studies on vitamin D-ASD relationship, including potential mechanistic pathways. We identified seven specific areas, including: latitude, season of conception/birth, maternal migration/ethnicity, vitamin D status of mothers and ASD patients, and vitamin D intervention to prevent and treat ASD. Due to differences in the methodological procedures and inconsistent results, drawing conclusions from the first three areas is difficult. Using a more direct measure of vitamin D status—that is, serum 25(OH)D level during pregnancy or childhood—we found growing evidence for a relationship between vitamin D and ASD. These findings are supported by convincing evidence from experimental studies investigating the mechanistic pathways. However, with few primary and secondary prevention intervention trials, this relationship cannot be determined, unless randomised placebo-controlled trials of vitamin D as a preventive or disease-modifying measure in ASD patients are available. [ABSTRACT FROM AUTHOR]

Background: The role of vitamin D and omega-3 long chain polyunsaturated fatty acids (omega-3 LCPUFA) in improving core symptoms of autism spectrum disorder (ASD) in children has been investigated by a few randomised controlled trials and the results are mixed and inconclusive. The response to treatment with these nutrients is heterogenous and may be influenced by inflammatory state. As an exploratory analysis, we investigated whether inflammatory state would modulate the effect of these nutrients on core symptoms of ASD. Methods: Seventy-three New Zealand children with ASD (2.5–8.0 years) completed a 12-month randomised, double-blind, placebo-controlled trial of vitamin D (VID, 2000 IU/day), omega-3 LCPUFA; (OM, 722 mg/day docosahexaenoic acid), or both (VIDOM). Non-fasting baseline plasma interleukin-1β (IL-1β) was available for 67 children (VID = 15, OM = 21, VIDOM = 15, placebo = 16). Children were categorised as having undetectable/normal IL-1β (<3.2 pg/ml, n = 15) or elevated IL-1β (≥3.2 pg/mL, n = 52). The Social Responsiveness Scale (SRS) questionnaire was used to assess core symptoms of ASD (baseline, 12-month). Mixed model repeated measure analyses (including all children or only children with elevated IL-1β) were used. Results: We found evidence for an interaction between baseline IL-1β and treatment response for SRS-total, SRS-social communicative functioning, SRS-awareness and SRS-communication (all Pinteraction < 0.10). When all children were included in the analysis, two outcome comparisons (treatments vs. placebo) showed greater improvements: VID, no effect (all P > 0.10); OM and VIDOM (P = 0.01) for SRS-awareness. When only children with elevated IL-1β were included, five outcomes showed greater improvements: OM (P = 0.01) for SRS-total; OM (P = 0.03) for SRS-social communicative functioning; VID (P = 0.01), OM (P = 0.003) and VIDOM (P = 0.01) for SRS-awareness. Conclusion: Inflammatory state may have modulated responses to vitamin D and omega-3 LCPUFA intervention in children with ASD, suggesting children with elevated inflammation may benefit more from daily vitamin D and omega-3 LCPUFA supplementation. [ABSTRACT FROM AUTHOR]

Background: There is strong mechanistic evidence to suggest that vitamin D and omega-3 long chain polyunsaturated fatty acids (n-3 LCPUFAs), specifically docosahexaenoic acid (DHA), have the potential to significantly improve the symptoms of autism spectrum disorder (ASD). However, there are no trials that have measured the effect of both vitamin D and n-3 LCPUFA supplementation on autism severity symptoms. The objective of this 2 × 2 factorial trial is to investigate the effect of vitamin D, n-3 LCPUFAs or a combination of both on core symptoms of ASD. Methods/design Children with ASD living in New Zealand (n = 168 children) will be randomised to one of four treatments daily: vitamin D (2000 IU), n-3 LCPUFAs (722 mg DHA), vitamin D (2000 IU) + n-3 LCPUFAs (722 mg DHA) or placebo for 12 months. All researchers, participants and their caregivers will be blinded until the data analysis is completed, and randomisation of the active/placebo capsules and allocation will be fully concealed from all mentioned parties. The primary outcome measures are the change in social-communicative functioning, sensory processing issues and problem behaviours between baseline and 12 months. A secondary outcome measure is the effect on gastrointestinal symptoms. Baseline data will be used to assess and correct basic nutritional deficiencies prior to treatment allocation. For safety measures, serum 25-hydroxyvitamin D 25(OH)D and calcium will be monitored at baseline, 6 and 12 months, and weekly compliance and gastrointestinal symptom diaries will be completed by caregivers throughout the study period. Discussion To our knowledge there are no randomised controlled trials assessing the effects of both vitamin D and DHA supplementation on core symptoms of ASD. If it is shown that either vitamin D, DHA or both are effective, the trial would reveal a non-invasive approach to managing ASD symptoms. Trial registration Australian New Zealand Clinical Trial Registry, ACTRN12615000144516. Registered on 16 February 2015. Electronic supplementary material The online version of this article (doi:10.1186/s13063-016-1428-8) contains supplementary material, which is available to authorized users.