Search

Abstract Provision of non-invasive vascular imaging results to individuals has been shown to improve cardiovascular disease risk factor control: its impact on diet remains uncertain. In this two-arm, single-blind, parallel, 12-week randomized controlled trial, 240 participants, 57.5% females aged 60–80 y had abdominal aortic calcification and clinical assessments performed at a hospital clinic. Participants were randomized 1:1 to receive (intervention n = 121) or not (control n = 119) their calcification results. Both groups received educational resources on cardiovascular disease risk control and were unblinded to the intervention. Outcome measures were performed at baseline and 12 weeks. The primary outcomes of the study were changes in fruit and vegetable intake measures over 12 weeks assessed using plasma carotenoid concentrations (biomarkers of FV intake) and a food frequency questionnaire. Secondary outcomes included 12-week changes in other aspects of the diet, physical activity, body weight, blood pressure, heart rate, lipid profile, glucose concentrations, estimated cardiovascular disease risk score, and medication use. Between-group differences were tested using linear mixed-effects regression. There were no between-group differences in the primary outcomes at 12 weeks: plasma carotenoids (mean difference +0.03 µg/mL [95%CI −0.06, 0.13]) and fruit and vegetable intakes (+18 g/d [−37, 72]). However, the provision of calcification results led to between-group differences in serum total (−0.22 mmol/L [−0.41, −0.04]) and non-HDL (−0.19 mmol/L [−0.35, −0.03]) cholesterol, and estimated cardiovascular disease risk score (−0.24% [−0.47, −0.02]). No between-group differences were seen for other secondary outcomes. In this work, providing vascular imaging results did not improve diet but did improve some cardiovascular disease risk factors (Australian and New Zealand Clinical Trials Registry ACTRN12618001087246).

Abstract Background Vegan and vegetarian dietary patterns are known to beneficially modulate risk factors for cardiovascular disease; however, the current literature does not differentiate between various plant-based diets. This study aimed to examine the association between various plant-based diets and plasma lipids and glycaemic indices compared to a regular meat-eating diet. Methods A cross-sectional study of Australian adults (n = 230) aged 30-75yrs habitually consuming the following were recruited: vegan, lacto-vegetarian, pesco-vegetarian, semi-vegetarian, or regular meat-eater. Multivariable regression analysis was used to adjust for covariates. Results Compared to regular meat-eaters, vegans had significantly lower total cholesterol (-0.77mmol/L,95% CI -1.15, -0.39, P

Abstract Background Higher cruciferous vegetable intake is associated with lower cardiovascular disease risk in observational studies. The pathways involved remain uncertain. We aimed to determine whether cruciferous vegetable intake (active) lowers 24-h brachial systolic blood pressure (SBP; primary outcome) compared to root and squash vegetables (control) in Australian adults with mildly elevated BP (SBP 120–160 mmHg inclusive). Methods In this randomized, controlled, crossover trial, participants completed two 2-week dietary interventions separated by a 2-week washout. Cruciferous vegetables were compared to root and squash vegetables (~ 300 g/day) consumed with lunch and dinner meals. Participants were blinded to which interventions were the active and control. Adherence was assessed using food diaries and biomarkers (S-methyl cysteine sulfoxide (SMCSO, active) and carotenoids (control)). Twenty-four-hour brachial ambulatory SBP and secondary outcomes were assessed pre- and post each intervention. Differences were tested using linear mixed effects regression. Results Eighteen participants were recruited (median (IQR) age: 68 (66–70); female: n = 16/18; mean ± SD clinic SBP: 135.9 ± 10.0 mmHg). For both interventions, 72% participants had 100% adherence (IQR: 96.4–100%). SMCSO and carotenoids were significantly different between interventions (mean difference active vs. control SMCSO: 22.93 mg/mL, 95%CI 15.62, 30.23, P

Background and aimsBone mineral density (BMD) and body composition play an important role in maintaining metabolic health and physical functioning. Plant-based diets (PBDs) are known to be lower in protein and calcium, which can impact BMD and body composition. This study aimed to investigate the relationship between various PBDs compared to regular meat diet and whole-body BMD, body composition, and weight status.MethodsA cross-sectional study was conducted with adults (n = 240) aged 30–75 years, who habitually followed dietary patterns: vegan, lacto-vegetarian, pesco-vegetarian, semi-vegetarian, or regular meat eater (48 per group). Parameters were measured using dual-energy x-ray absorptiometry (DXA), and multivariable regression analyses were used to adjust for lifestyle confounders, socioeconomic factors, and BMI.ResultsAfter adjustments, whole-body BMD and body composition were not significantly different between those following PBDs and regular meat diets, except for lacto-ovo vegetarians, who had significantly lower lean mass by −1.46 kg (CI: −2.78, −0.13). Moreover, lacto-ovo vegetarians had a significantly lower T-score by −0.41 SD (CI: −0.81, −0.01) compared to regular meat eaters. Waist circumference was significantly lower in individuals adhering to a PBD compared to a regular meat diet: vegans by −4.67 cm (CI: −8.10, −1.24), lacto-ovo vegetarians by −3.92 cm (CI: −6.60, −1.23), pesco-vegetarians by −3.24 cm (CI: −6.09, −0.39), and semi-vegetarians by −5.18 cm (CI: −7.79, −2.57). There were no significant differences in lean mass (%), fat mass (% and total), android/gynoid measures, body weight, or BMI across dietary patterns. All dietary patterns met the recommended dietary intake for calcium and protein, and 25-hydroxy-vitamin D status was comparable across groups.ConclusionsThis cross-sectional study found that adhering to a PBD characterized by varying degrees of dairy and meat restriction is not associated with meaningful changes in BMD or body composition, provided that the dietary patterns are planned appropriately with adequate levels of calcium and protein.

Dietary carotenoids are associated with lower risk of CHD. Assessment of dietary carotenoid intake using questionnaires can be susceptible to measurement error. Consequently, there is a need to validate data collected from FFQs which measure carotenoid intake. This study aimed to assess the performance of the Cardio-Med Survey Tool (CMST)-FFQ-version 2 (v2) as a measure of dietary carotenoid intake over 12-months against plasma carotenoids biomarkers and 7-Day Food Records (7DFR) in an Australian cardiology cohort. Dietary carotenoid intakes (β- and α-carotene, lycopene, β-cryptoxanthin and lutein/zeaxanthin) were assessed using the 105-item CMST-FFQ-v2 and compared to intakes measured by 7DFR and plasma carotenoid concentrations. Correlation coefficients were calculated between each dietary method, and validity coefficients (VCs) were calculated between each dietary method and theoretical true intake using the ‘methods of triads’. Thirty-nine participants aged 37–77 years with CHD participated in the cross-sectional study. The correlation between FFQ and plasma carotenoids were largest and significant for β-carotene (0.39, p=0.01), total carotenoids (0.37, p=0.02) and β-cryptoxanthin (0.33, p=0.04), with weakest correlations observed for α-carotene (0.21, p=0.21) and lycopene (0.21, p=0.21). The FFQ VCs were moderate (0.3–0.6) or larger for all measured carotenoids. The strongest were observed for total carotenoids (0.61) and β-carotene (0.59), while the weakest were observed for α-carotene (0.33) and lycopene (0.37). In conclusion, the CMST-FFQ-v2 measured dietary carotenoids intakes with moderate confidence for most carotenoids, however, there was less confidence in ability to measure α-carotene and lycopene intake, thus further research is warranted using a larger sample.

Chronic obstructive pulmonary disease (COPD) is a progressing disease, with lung but not gut microbiota implicated in its etiology. Here the authors compare the stool from patients with COPD and healthy controls to find specific gut bacteria and metabolites associated with active disease, thereby hinting at a potential role for the gut microbiome in COPD.

Summary: Background: Soluble fibre modulates airway inflammation in animal models. The aim of this study was to investigate the effects of soluble fibre supplementation, with and without a probiotic, on plasma short chain fatty acids (SCFA), airway inflammation, asthma control and gut microbiome in adults with asthma. Methods: A randomised, double-blinded, placebo controlled 3-way cross-over trial in 17 subjects with stable asthma at the Hunter Medical Research Institute, Newcastle, Australia. Subjects received 3 × 7 day oral interventions in random order; soluble fibre (inulin 12 g/day), soluble fibre + probiotic (inulin 12 g/day + multi-strain probiotic >25 billion CFU) and placebo. Plasma SCFA, sputum cell counts and inflammatory gene expression, asthma control gut microbiota, adverse events including gastrointestinal symptoms were measured. Findings: There was no difference in change in total plasma SCFA levels (μmol/L) in the placebo versus soluble fibre (Δmedian [95% CI] 16·3 [−16·9, 49·5], p = 0·335) or soluble fibre+probiotic (18·7 [−14·5, 51·9], p = 0·325) group. Following the soluble fibre intervention there was an improvement in the asthma control questionnaire (ACQ6) (∆median (IQR) -0·35 (−0·5, −0·13), p = 0·006), sputum %eosinophils decreased (−1.0 (−2·5, 0), p = 0·006) and sputum histone deacetylase 9 (HDAC9) gene expression decreased (−0.49 (−0.83, −0.27) 2-ΔCt, p = .008). Individual bacterial operational taxonomic units changed following both inulin and inulin+probiotic arms. Interpretation: Soluble fibre supplementation for 7 days in adults with asthma did not change SCFA levels. Within group analysis showed improvements in airway inflammation, asthma control and gut microbiome composition following inulin supplementation and these changes warrant further investigation, in order to evaluate the potential of soluble fibre as a non-pharmacological addition to asthma management. Fund: John Hunter Hospital Charitable Trust. Keywords: Asthma, Inulin, Soluble fibre, SCFAs, Inflammation, Free fatty acid receptors, Histone deacetylases

BackgroundAsthma is the most frequent cause of hospitalisation among children; however, little is known regarding the effects of asthma on immune responses in children.ObjectiveThe present study aimed to evaluate cytokine responses of peripheral blood mononuclear cells (PBMCs), PBMC composition and lung function in children with and without asthma.MethodsUsing a case-control design, we compared 48 children with asthma aged 3-11 years with 14 age-matched healthy controls. PBMC composition and cytokine production including interferon (IFN)-γ, interleukin (IL)-1β, IL-5 and lL-6 following stimulation with rhinovirus-1B (RV1B), house dust mite (HDM) and lipopolysaccharide (LPS) were measured. Lung function was assessed using impulse oscillometry and nitrogen multiple breath washout.ResultsThe frequency of group 2 innate lymphoid cells were significantly higher in asthmatics and PBMCs from asthmatics had deficient IFN-γ production in response to both RV1B and LPS compared with controls (P

Abstract Background The obesity paradox in COPD describes protective effects of obesity on lung pathology and inflammation. However, the underlying relationships between obesity, diet and disease outcomes in COPD are not fully understood. In this study we measured the response to dietary fatty acids upon markers of inflammation and remodelling in human lung cells from people with and without COPD. Methods Pulmonary fibroblasts were challenged with ω-3 polyunsaturated fatty acids (PUFAs), ω-6 PUFAs, saturated fatty acids (SFAs) or the obesity-associated cytokine TNFα. After 48–72 h release of the pro-inflammatory cytokines interleukin (IL)-6 and CXCL8 was measured using ELISA and mRNA expression and deposition of the extracellular matrix (ECM) proteins fibronectin, type I collagen, tenascin and perlecan were measured using qPCR or ECM ELISA, respectively. Results Challenge with the ω-6 PUFA arachidonic acid (AA), but not ω-3 PUFAs or SFAs, resulted in increased IL-6 and CXCL8 release from fibroblasts, however IL-6 and CXCL8 release was reduced in COPD (n = 19) compared to non-COPD (n = 36). AA-induced cytokine release was partially mediated by downstream mediators of cyclooxygenase (COX)-2 in both COPD and non-COPD. In comparison, TNFα-induced IL-6 and CXCL8 release was similar in COPD and non-COPD, indicating a specific interaction of AA in COPD. In patients with or without COPD, regression analysis revealed no relationship between BMI and cytokine release. In addition, AA, but not SFAs or ω-3 PUFAs reduced the basal deposition of fibronectin, type I collagen, tenascin and perlecan into the ECM in COPD fibroblasts. In non-COPD fibroblasts, AA-challenge decreased basal deposition of type I collagen and perlecan, but not fibronectin and tenascin. Conclusions This study shows that AA has disease-specific effects on inflammation and ECM protein deposition. The impaired response to AA in COPD might in part explain why obesity appears to have less detrimental effects in COPD, compared to other lung diseases.

Abstract Background Long-chain omega-3 polyunsaturated fatty acids (LCn-3PUFAs) may act as an effective adjunct therapy for chronic obstructive pulmonary disease (COPD), a condition characterised by persistent airflow limitation and inflammation. However, the nature of this illness presents challenges for evaluating potential benefits. The aim of this study was to determine the feasibility of undertaking a randomised controlled trial of LCn-3PUFA supplementation in adults with COPD. Methods A 16-week parallel, double-blind, randomised, placebo-controlled dietary supplementation trial was conducted. Participants diagnosed with COPD were randomly allocated to take six 1-g capsules of fish oil (3.6 g LCn-3PUFA) or corn oil (placebo) daily for 16 weeks. Key outcomes used to determine the feasibility of the trial included recruitment rate, participant retention rate and supplement adherence (blood biomarker and returned capsule count). An estimate of the effect size for clinical outcomes such as pulmonary function and functional exercise capacity was calculated. Results None of the key feasibility criteria were met. The enrolment target was 40 participants in 52 weeks; however, only 13 were finally enrolled, with just seven in the first 52 weeks. Eight participants completed the study (retention rate 62%). Targets for compliance were not achieved; red blood cell LCn-3PUFA content (expressed as percentage of total fatty acids) did not increase by more than 2% in the fish oil group; capsule counts were unreliable. As the target sample size was not achieved and only a small number of participants completed the study, it was not possible to use the variance in clinical outcomes to estimate a sample size for a future study. Conclusions This study highlights major difficulties, especially with recruitment, in conducting this LCn-3PUFA supplementation trial in people with COPD, rendering the protocol unfeasible by predetermined criteria. A modified approach is needed to investigate potential health benefits of fish oil in people with COPD. A multicentre study with changes to inclusion and exclusion criteria is recommended. Trial registration Australia and New Zealand Clinical Trials Register (ANZCTR), ACTRN12612000158864

Abstract One of the limitations for ranking foods and meals for healthiness on the basis of the glycaemic index (GI) is that the GI is subject to manipulation by addition of fat. Postprandial lipemia, defined as a rise in circulating triglyceride containing lipoproteins following consumption of a meal, has been recognised as a risk factor for the development of cardiovascular disease and other chronic diseases. Many non-modifiable factors (pathological conditions, genetic background, age, sex and menopausal status) and life-style factors (physical activity, smoking, alcohol and medication use, dietary choices) may modulate postprandial lipemia. The structure and the composition of a food or a meal consumed also plays an important role in the rate of postprandial appearance and clearance of triglycerides in the blood. However, a major difficulty in grading foods, meals and diets according to their potential to elevate postprandial triglyceride levels has been the lack of a standardised marker that takes into consideration both the general characteristics of the food and the food’s fat composition and quantity. The release rate of lipids from the food matrix during digestion also has an important role in determining the postprandial lipemic effects of a food product. This article reviews the factors that have been shown to influence postprandial lipemia with a view to develop a novel index for ranking foods according to their healthiness. This index should take into consideration not only the glycaemic but also lipemic responses.

Asthma is a highly prevalent inflammatory disease of the airways. Bacterial metabolites of soluble fibre fermentation, such as short chain fatty acids (SCFAs), have been shown to exert anti-inflammatory effects via free fatty acid receptor activation and epigenetic regulation through inhibition of histone deacetylases (HDACs). The aim of the present review was to summarise the available evidence for soluble fibre in the treatment and prevention asthma. There is substantial preclinical evidence suggesting soluble fibre may be beneficial in the airways. The clinical evidence in this area is limited, however available studies to date have reported promising evidence for the future of soluble fibre interventions as an adjunct treatment in asthma management. Keywords: Soluble fibre, Dietary fibre, Inflammation, Asthma

Background/Aims: Chronic Obstructive Pulmonary Disease (COPD) is characterized by airway inflammation, in which contributes to loss of lung function. Systemic inflammation is also a feature of COPD contributing to many associated co-morbidities. Statins, omega-3 fatty acids (docosahexanoic acid, DHA and eicosapentanoic acid, EPA) and lycopene have been shown to decrease systemic inflammation; however their combined effects have not been investigated. This study aims to identify changes in systemic and airway inflammation induced by statins alone or in combination with DHA, EPA and lycopene in COPD. Methods: COPD patients (n = 11) received rosuvastatin (20 mg/day) for 4 weeks, then a combination of rosuvastatin (20 mg/day), DHA and EPA (1.5 g/day) and lycopene (45 mg/day) for 8 weeks. Blood and sputum were collected and lung function measured by spirometry at baseline, week 4 and 12. Plasma fatty acids were measured using gas chromatography, while plasma carotenoids were analysed using high-performance liquid chromatography. Plasma CRP and IL-6 concentrations were measured using ELISA; and peripheral blood gene expression was measured using the nCounter™ GX Human Inflammation Kit 2. Results: Following the interventions, clinical characteristics and plasma IL-6 and CRP were unchanged. Sputum neutrophil proportion and absolute count was increased and macrophage proportion decreased by rosuvastatin (P = 0.020 and P = 0.015; respectively). Rosuvastatin increased LTB4R and decreased CXCL10 and AGER gene expression in white blood cells. The addition of lycopene and omega-3 fatty acids decreased LTB4R and increased CXCL10 to basal levels, whilst combined use of interventions increased ALOX15 blood gene expression. Conclusion: This study shows that rosuvastatin, omega-3 fatty acids and lycopene have some anti-inflammatory effects systemically, but rosuvastatin may increase airway neutrophils, which would be undesirable in COPD patients, warranting further investigation.

Asthma is a heterogeneous, chronic inflammatory disease of the airways. It is a complex disease with different clinical phenotypes and results in a substantial socioeconomic burden globally. Poor understanding of pathogenic mechanisms of the disease hinders the investigation into novel therapeutics. Emerging evidence of the unfolded protein response (UPR) in the endoplasmic reticulum (ER) has demonstrated previously unknown functions of this response in asthma development. A worsening of asthmatic condition can be brought on by stimuli such as oxidative stress, pathogenic infections, and allergen exposure. All of which can induce ER stress and activate UPR leading to activation of different inflammatory responses and dysregulate the innate immune functions in the airways. The UPR as a central regulator of asthma pathogenesis may explain several unknown mechanism of the disease onset, which leads us in new directions for future asthma treatments. In this review, we summarize and discuss the causes and impact of ER–UPR in driving the pathogenesis of asthma and highlight its importance in clinical implications.

Background. Innate immune antimicrobial peptides, including β-defensin-1, promote the chemotaxis and activation of several immune cells. The role of β-defensin-1 in asthma and chronic obstructive pulmonary disease (COPD) remains unclear. Methods. Induced sputum was collected from healthy controls and individuals with asthma or COPD. β-defensin-1 protein in sputum supernatant was quantified by ELISA. Biomarker potential was examined using receiver operating characteristic curves. β-defensin-1 release from primary bronchial epithelial cells (pBECs) was investigated in culture with and without cigarette smoke extract (CSE). Results. Airway β-defensin-1 protein was elevated in COPD participants compared to asthma participants and healthy controls. Inflammatory phenotype had no effect on β-defensin-1 levels in asthma or COPD. β-defensin-1 protein was significantly higher in severe asthma compared to controlled and uncontrolled asthma. β-defensin-1 protein could predict the presence of COPD from both healthy controls and asthma patients. Exposure of pBECs to CSE decreased β-defensin-1 production in healthy controls; however in pBECs from COPD participants the level of β-defensin-1 remanied unchanged. Conclusions. Elevated β-defensin-1 protein is a feature of COPD and severe asthma regardless of inflammatory phenotype. β-defensin-1 production is dysregulated in the epithelium of patients with COPD and may be an effective biomarker and potential therapeutic target.

A higher proportion of children with asthma are overweight and obese compared to children without asthma; however, it is unknown whether asthmatic children are at increased risk of weight gain due to modifiable lifestyle factors. Thus, the aim of this cross-sectional study was to compare weight-gain risk factors (sleep, appetite, diet, activity) in an opportunistic sample of children with and without asthma. Non-obese children with (n = 17; age 10.7 (2.4) years) and without asthma (n = 17; age 10.8 (2.3) years), referred for overnight polysomnography, underwent measurement of lung function, plasma appetite hormones, dietary intake and food cravings, activity, and daytime sleepiness. Sleep latency (56.6 (25.5) vs. 40.9 (16.9) min, p = 0.042) and plasma triglycerides (1.0 (0.8, 1.2) vs. 0.7 (0.7, 0.8) mmol/L, p = 0.013) were significantly greater in asthmatic versus non-asthmatic children. No group difference was observed in appetite hormones, dietary intake, or activity levels (p > 0.05). Sleep duration paralleled overall diet quality (r = 0.36, p = 0.04), whilst daytime sleepiness paralleled plasma lipids (r = 0.61, p =0.001) and sedentary time (r = 0.39, p = 0.02). Disturbances in sleep quality and plasma triglycerides were evident in non-obese asthmatic children referred for polysomnography, versus non-asthmatic children. Observed associations between diet quality, sedentary behavior, and metabolic and sleep-related outcomes warrant further investigation, particularly the long-term health implications.

AbstractRespiratory diseases, such as asthma and chronic obstructive pulmonary disease (COPD), are a significant and increasing global health problem. These diseases are characterized by airway inflammation, which develops in response to various stimuli. In asthma, inflammation is driven by exposure to a variety of triggers, including allergens and viruses, which activate components of both the innate and acquired immune responses. In COPD, exposure to cigarette smoke is the primary stimulus of airway inflammation. Activation of airway inflammatory cells leads to the release of excessive quantities of reactive oxygen species (ROS), resulting in oxidative stress. Antioxidants provide protection against the damaging effects of oxidative stress and thus may be useful in the management of inflammatory airways disease. Resveratrol, a polyphenol that demonstrates both antioxidative and anti-inflammatory functions, has been shown to improve outcomes in a variety of diseases, in particular, in cancer. We review the evidence for a protective role of resveratrol in respiratory disease. Mechanisms of resveratrol action that may be relevant to respiratory disease are described. We conclude that resveratrol has potential as a therapeutic agent in respiratory disease, which should be further investigated. Antioxid. Redox Signal.13, 1535–1548. [ABSTRACT FROM AUTHOR]

AbstractDepletion of antioxidants through consumption of a low antioxidant diet has been reported to increase neutrophilic airway inflammation and worsen symptoms of asthma. Using a nutrigenomics approach, this study explores the mechanisms of airway neutrophilic inflammation due to depletion of dietary antioxidants. Induced sputum samples were collected at baseline and after participants consumed a low antioxidant diet for 14 days. Genome-wide gene expression profiles were generated from sputum RNA samples from participants with a >10% change in sputum neutrophils using Illumina Humanref-8 expression microarrays. There were 104 genes differentially expressed following the dietary change. Upregulated genes were involved in the innate immune response and included the innate immune receptors TLR2, IL1R2, CD93,the signaling molecules IRAK2, IRAK3,and neutrophil proteases MMP25and CPD. Downregulated genes included those involved in endogenous antioxidant defenses (GSTA1, GSTA2) and protease inhibition (SLPI, SERPINB3). Altered expression of five genes (TLR2, IRAK2, IL1R2, C20orf114,and SERPINB3) was confirmed using real-time polymerase chain reaction (PCR). These observations suggest that depletion of dietary antioxidants in asthma may result in upregulation of genes involved in the innate immune response. A diet low in antioxidants may be contributing to the development of neutrophilic asthma through activation of the innate immune response. [ABSTRACT FROM AUTHOR]

Introduction Approximately 15%–20% of the adult population self-report symptoms of addictive eating. There are currently limited options for management. Motivational interviewing-based interventions, containing personalised coping skills training, have been found to be effective for behaviour change in addictive disorders (eg, alcohol). This project builds upon foundations of an addictive eating feasibility study previously conducted and co-design process involving consumers. The primary aim of this study is to examine the efficacy of a telehealth intervention targeting addictive eating symptoms in Australian adults compared with passive intervention and control groups.Methods and analysis This three-arm randomised controlled trial will recruit participants 18–85 years, endorsing ≥3 symptoms on the Yale Food Addiction Scale (YFAS) 2.0, with body mass index >18.5 kg/m2. Addictive eating symptoms are assessed at baseline (pre-intervention), 3 months (post-intervention) and 6 months. Other outcomes include dietary intake and quality, depression, anxiety, stress, quality of life, physical activity and sleep hygiene. Using a multicomponent clinician-led approach, the active intervention consists of five telehealth sessions (15–45 min each) delivered by a dietitian over 3 months. The intervention uses personalised feedback, skill-building exercises, reflective activities and goal setting. Participants are provided with a workbook and website access. The passive intervention group receives the intervention via a self-guided approach with access to the workbook and website (no telehealth). The control group receives personalised written dietary feedback at baseline and participants advised to follow their usual dietary pattern for 6 months. The control group will be offered the passive intervention after 6 months. The primary endpoint is YFAS symptom scores at 3 months. A cost–consequence analysis will determine intervention costs alongside mean change outcomes.Ethics and dissemination Human Research Ethics Committee of University of Newcastle, Australia provided approval (H-2021-0100). Findings will be disseminated via publication in peer-reviewed journals, conference presentations, community presentations and student theses.Trial registration number Australia New Zealand Clinical Trials Registry (ACTRN12621001079831).

Many preterm infants require hyperoxic gas for survival, although it can contribute to lung injury. Experimentally, neonatal hyperoxia leads to persistent alterations in lung structure and increases leukocytes in bronchoalveolar lavage fluid (BALF). These effects of hyperoxia on the lungs are considered to be caused, at least in part, by increased oxidative stress. Our objective was to determine if dietary supplementation with a known source of antioxidants (tomato juice, TJ) could protect the developing lung from injury caused by breathing hyperoxic gas. Neonatal mice (C57BL6/J) breathed either 65% O2 (hyperoxia) or room air from birth until postnatal day 7 (P7d); some underwent necropsy at P7d and others were raised in room air until adulthood (P56d). In subsets of both groups, drinking water was replaced with TJ (diluted 50:50 in water) from late gestation to necropsy. At P7d and P56d, we analyzed total antioxidant capacity (TAC), markers of oxidative stress (nitrotyrosine and heme oxygenase-1 expression), inflammation (interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) expression), collagen (COL) and smooth muscle in the lungs; we also assessed lung structure. We quantified macrophages in lung tissue (at P7d) and leukocytes in BALF (at P56d). At P7d, TJ increased pulmonary TAC and COL1α1 expression and attenuated the hyperoxia-induced increase in nitrotyrosine and macrophage influx; however, changes in lung structure were not affected. At P56d, TJ increased TAC, decreased oxidative stress and reversed the hyperoxia-induced increase in bronchiolar smooth muscle. Additionally, TJ alone decreased IL-1β expression, but following hyperoxia TJ increased TNF-α expression and did not alter the hyperoxia-induced increase in leukocyte number. We conclude that TJ supplementation during and after neonatal exposure to hyperoxia protects the lung from some but not all aspects of hyperoxia-induced injury, but may also have adverse side-effects. The effects of TJ are likely due to elevation of circulating antioxidant concentrations.

BackgroundThe common cold questionnaire (CCQ) is used to discriminate those with and without a viral infection. Its usefulness in people with acute asthma is unknown. Our aim was to assess the ability of the CCQ to detect viral infection and to monitor recovery during a viral induced asthma exacerbation and confirmed by virological testing.Methodology/principal findingsWe studied subjects (> or =7 yrs) admitted to hospital with acute asthma and diagnosed as positive (n = 63), or negative to viral infection (n = 27) according to molecular and virological testing from respiratory samples. CCQ, asthma history and asthma control questionnaires were completed and repeated 4-6 weeks later. Sensitivity, specificity, and response to change of the CCQ were assessed by receiver operator curve (ROC) analysis and effect size calculation respectively. The CCQ did not discriminate between viral and non-viral infection for subjects with asthma (sensitivity = 76.2%; specificity = 29.6%). ROC analysis could not differentiate between positive or negative virus in subjects with asthma. The CCQ had a large response to change following recovery (effect size = 1.01). 39% of subjects recovering from viral exacerbation remained positive to virological testing at follow-up despite improvement in clinical symptoms. The CCQ reflected clinical improvement in these subjects, thus providing additional information to complement virological testing.Conclusions/significanceThe CCQ is a useful instrument for monitoring response to viral infection in people with asthma. Reliable differentiation between viral and non-viral asthma exacerbations was not achieved with the CCQ and requires specific virological testing. When combined with virological testing, the CCQ should be a useful outcome measure for evaluating therapies in viral-induced asthma.