This study aimed to compare the use of the bioelectrical impedance device (BIA) seca^® mBCA 515 using dual X-ray absorptiometry (DXA) as a reference method, for body composition assessment in adults across the spectrum of body mass indices. It explores the utility of simple anthropometric measures (the waist height ratio (WHtR) and waist circumference (WC)) for the assessment of obesity. In the morning after an overnight fast (10 h), 30 participants underwent a body composition DXA (GE iDXA) scan, BIA (seca 515), and anthropometric measures. Compared to the DXA reference measure, the BIA underestimated fat mass (FM) by 0.32 kg (limits of agreement −3.8 kg, 4.4 kg); overestimated fat free mass (FFM) by 0.43 kg (limits of agreement −8.2 kg, 4.3 kg). Some of the variation was explained by body mass index (BMI), as for FM, the mean difference of the normal range BMI group was smaller than for the overweight/obese group (0.25 kg and 0.35 kg, respectively) with wider limits of agreement (−4.30 kg, 4.81 kg, and −3.61 kg, 4.30 kg, respectively). There were significant differences in visceral adipose tissue (VAT) volume measurements between methods with BIA systematically overestimating VAT compared to DXA. WC was more strongly correlated with DXA FM (rho = 0.90, p < 0.001) than WHtR (rho = 0.83, p < 0.001). BIA had some agreement with DXA; however, they are not equivalent measures for the range of BMIs explored, with DXA remaining the more informative tool. WC is a useful and simple assessment tool for obesity.

The aim of this study was to explore the reliability and precision of body compartment measures, in particular visceral adipose tissue, in weight stable adults over a range of BMIs using GE-Lunar iDXA. Weight-stable participants aged 18–65 years had a total body composition scan on GE-Lunar iDXA either on three separate occasions over a three month period (n = 51), or on a single occasion for duplicate scans with repositioning (n = 30). The coefficient of variation (CV%) and least significant change (LSC) of body compartments were calculated. The CV was higher for all measures over three months (range 0.8–5.9%) compared with same-day precision-scans (all < 2%). The CV for visceral adipose tissue (VAT) was considerably higher than all other body compartments (42.2% three months, 16.2% same day scanning). To accurately measure VAT mass using the GE iDXA it is recommended that participants have a BMI ≥ 25 kg/m², or VAT mass > 500 g. Changes observed in VAT mass levels below 500 g should be interpreted with caution due to lack of precision and reliability. All other compartmental measures demonstrated good reliability, with less than 6% variation over three months.

Due to reduced cost and accessibility, the use of genetic testing has appealed to health professionals for personalising nutrition advice. However, translation of the evidence linking polymorphisms, dietary requirements, and pathology risk proves to be challenging for nutrition and dietetic practitioners. Zinc status and polymorphisms of genes coding for zinc-transporters have been associated with chronic diseases. The present study aimed to systematically review the literature to assess whether recommendations for zinc intake could be made according to genotype. Eighteen studies investigating 31 Single Nucleotide Polymorphisms (SNPs) in relation to zinc intake and/or status were identified. Five studies examined type 2 diabetes; zinc intake was found to interact independently with two polymorphisms in the zinc-transporter gene SLC30A8 to affect glucose metabolism indicators. While the outcomes were statistically significant, the small size of the effect and lack of replication raises issues regarding translation into nutrition and dietetic practice. Two studies assessed the relationship of polymorphisms and cognitive performance; seven studies assessed the association between a range of outcomes linked to chronic conditions in aging population; two papers described the analysis of the genetic contribution in determining zinc concentration in human milk; and two papers assessed zinc concentration in plasma without linking to clinical outcomes. The data extracted confirmed a connection between genetics and zinc requirements, although the direction and magnitude of the dietary modification for carriers of specific genotypes could not be defined. This study highlights the need to summarise nutrigenetics studies to enable health professionals to translate scientific evidence into dietary recommendations.

The aim of this study was to determine the efficacy, safety and acceptability of a 4-week very-low-energy diet (VLED) program for adolescents with obesity. Adolescents (13–17 years) with obesity and ≥1 obesity-related complication were Fast Track to Health 52-week randomized controlled trial participants. Adolescents undertook a 4-week micronutrient-complete VLED (800 kcal/day), with weekly dietitian support. Anthropometric data were recorded at baseline and week-4 and side-effects at day 3–4, week-1, -2, -3 and -4. Adolescents completed an acceptability survey at week-4. A total of 134 adolescents (14.9 ± 1.2 years, 50% male) had a 5.5 ± 2.9 kg (p < 0.001) mean weight loss at week-4: 95% experienced ≥1 and 70% experienced ≥3 side-effects during the VLED program, especially during the first week. Hunger, fatigue, headache, irritability, loose stools, constipation and nausea were most common. Reporting more side-effects at day 3–4 correlated with greater weight loss at week-4 (r = −0.188, p = 0.03). Adolescents reported ‘losing weight’ (34%) and ‘prescriptive structure’ (28%) as the most positive aspects of VLED, while ‘restrictive nature’ (45%) and ‘meal replacement taste’ (20%) were least liked. A dietitian-monitored short-term VLED can be implemented safely and is acceptable for many adolescents seeking weight loss, despite frequent side-effects. Investigating predictors of acceptability and effectiveness could determine adolescents most suited to VLED programs.

Background and objectives: Peripheral blood mononuclear cells (PBMCs) have shown promise as a tissue sensitive to subtle and possibly systemic transcriptomic changes, and as such may be useful in identifying responses to weight loss interventions. The primary aim was to comprehensively evaluate the transcriptomic changes that may occur during weight loss and to determine if there is a consistent response across intervention types in human populations of all ages. Methods: Included studies were randomised control trials or cohort studies that administered an intervention primarily designed to decrease weight in any overweight or obese human population. A systematic search of the literature was conducted to obtain studies and gene expression databases were interrogated to locate corresponding transcriptomic datasets. Datasets were normalised using the ArrayAnalysis online tool and differential gene expression was determined using the limma package in R. Over-represented pathways were explored using the PathVisio software. Heatmaps and hierarchical clustering were utilised to visualise gene expression. Results: Seven papers met the inclusion criteria, five of which had raw gene expression data available. Of these, three could be grouped into high responders (HR, ≥ 5% body weight loss) and low responders (LR). No genes were consistently differentially expressed between high and low responders across studies. Adolescents had the largest transcriptomic response to weight loss followed by adults who underwent bariatric surgery. Seven pathways were altered in two out of four studies following the intervention and the pathway ‘cytoplasmic ribosomal proteins’ (WikiPathways: WP477) was altered between HR and LR at baseline in the two datasets with both groups. Pathways related to ‘toll-like receptor signalling’ were altered in HR response to the weight loss intervention in two out of three datasets. Conclusions: Transcriptomic changes in PBMCs do occur in response to weight change. Transparent and standardised data reporting is needed to realise the potential of transcriptomics for investigating phenotypic features. Registration number: PROSPERO: CRD42019106582