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Observational studies suggest that 25-hydroxy vitamin D (25(OH)D) concentration is inversely associated with pain. However, findings from intervention trials are inconsistent. We assessed the effect of vitamin D supplementation on pain using data from a large, double-blind, population-based, placebo-controlled trial (the D-Health Trial). 21 315 participants (aged 60–84 years) were randomly assigned to a monthly dose of 60 000 IU vitamin D3 or matching placebo. Pain was measured using the six-item Pain Impact Questionnaire (PIQ-6), administered 1, 2 and 5 years after enrolment. We used regression models (linear for continuous PIQ-6 score and log-binomial for binary categorisations of the score, namely ‘some or more pain impact’ and ‘presence of any bodily pain’) to estimate the effect of vitamin D on pain. We included 20 423 participants who completed ≥1 PIQ-6. In blood samples collected from 3943 randomly selected participants (∼800 per year), the mean (sd) 25(OH)D concentrations were 77 (sd 25) and 115 (sd 30) nmol/l in the placebo and vitamin D groups, respectively. Most (76 %) participants were predicted to have 25(OH)D concentration >50 nmol/l at baseline. The mean PIQ-6 was similar in all surveys (∼50·4). The adjusted mean difference in PIQ-6 score (vitamin D cf placebo) was 0·02 (95 % CI (−0·20, 0·25)). The proportion of participants with some or more pain impact and with the presence of bodily pain was also similar between groups (both prevalence ratios 1·01, 95 % CI (0·99, 1·03)). In conclusion, supplementation with 60 000 IU of vitamin D3/month had negligible effect on bodily pain.
Barrett’s oesophagus (BE) is the precursor of oesophageal adenocarcinoma, which has become the most common type of oesophageal cancer in many Western populations. Existing evidence on diet and risk of BE predominantly comes from case–control studies, which are subject to recall bias in measurement of diet. We aimed to investigate the potential effect of diet, including macronutrients, carotenoids, food groups, specific food items, beverages and dietary scores, on risk of BE in over 20 000 participants of the Melbourne Collaborative Cohort Study. Diet at baseline (1990–1994) was measured using a food frequency questionnaire. The outcome was BE diagnosed between baseline and follow-up (2007–2010). Logistic regression models were used to estimate OR and 95 % CI for diet in relation to risk of BE. Intakes of leafy vegetables and fruit were inversely associated with risk of BE (highest v. lowest quartile: OR = 0·59; CI: 0·38, 0·94; P-trend = 0·02 and OR = 0·58; CI: 0·37, 0·93; P-trend = 0·02 respectively), as were dietary fibre and carotenoids. Stronger associations were observed for food than the nutrients found in them. Positive associations were observed for discretionary food (OR = 1·54; CI: 0·97, 2·44; P-trend = 0·04) and total fat intake (OR per 10 g/d = 1·11; CI: 1·00, 1·23), the association for fat was less robust in sensitivity analyses. No association was observed for meat, protein, dairy products or diet scores. Diet is a potential modifiable risk factor for BE. Public health and clinical guidelines that incorporate dietary recommendations could contribute to reduction in risk of BE and, thereby, oesophageal adenocarcinoma.
To examine associations between diet and risk of developing gastro-oesophageal reflux disease (GERD).
Prospective cohort with a median follow-up of 15·8 years. Baseline diet was measured using a FFQ. GERD was defined as self-reported current or history of daily heartburn or acid regurgitation beginning at least 2 years after baseline. Sex-specific logistic regressions were performed to estimate OR for GERD associated with diet quality scores and intakes of nutrients, food groups and individual foods and beverages. The effect of substituting saturated fat for monounsaturated or polyunsaturated fat on GERD risk was examined.
A cohort of 20 926 participants (62 % women) aged 40–59 years at recruitment between 1990 and 1994.
For men, total fat intake was associated with increased risk of GERD (OR 1·05 per 5 g/d; 95 % CI 1·01, 1·09; P = 0·016), whereas total carbohydrate (OR 0·89 per 30 g/d; 95 % CI 0·82, 0·98; P = 0·010) and starch intakes (OR 0·84 per 30 g/d; 95 % CI 0·75, 0·94; P = 0·005) were associated with reduced risk. Nutrients were not associated with risk for women. For both sexes, substituting saturated fat for polyunsaturated or monounsaturated fat did not change risk. For both sexes, fish, chicken, cruciferous vegetables and carbonated beverages were associated with increased risk, whereas total fruit and citrus were associated with reduced risk. No association was observed with diet quality scores.
Diet is a possible risk factor for GERD, but food considered as triggers of GERD symptoms might not necessarily contribute to disease development. Potential differential associations for men and women warrant further investigation.
To test the hypothesis that more frequent consumption of sugar-sweetened soft drinks would be associated with increased risk of obesity-related cancers. Associations for artificially sweetened soft drinks were assessed for comparison.
Prospective cohort study with cancers identified by linkage to cancer registries. At baseline, participants completed a 121-item FFQ including separate questions about the number of times in the past year they had consumed sugar-sweetened or artificially sweetened soft drinks. Anthropometric measurements, including waist circumference, were taken and questions about smoking, leisure-time physical activity and intake of alcoholic beverages were completed.
The Melbourne Collaborative Cohort Study (MCCS) is a prospective cohort study which recruited 41 514 men and women aged 40–69 years between 1990 and 1994. A second wave of data collection occurred in 2003–2007.
Data for 35 593 participants who developed 3283 incident obesity-related cancers were included in the main analysis.
Increasing frequency of consumption of both sugar-sweetened and artificially sweetened soft drinks was associated with greater waist circumference at baseline. For sugar-sweetened soft drinks, the hazard ratio (HR) for obesity-related cancers increased as frequency of consumption increased (HR for consumption >1/d v. <1/month=1·18; 95 % CI 0·97, 1·45; P-trend=0·007). For artificially sweetened soft drinks, the HR for obesity-related cancers was not associated with consumption (HR for consumption >1/d v. <1/month=1·00; 95 % CI 0·79, 1·27; P-trend=0·61).
Our results add to the justification to minimise intake of sugar-sweetened soft drinks.
To evaluate the reliability and validity of the FFQ administered to participants in the follow-up of the Melbourne Collaborative Cohort Study (MCCS), and to provide calibration coefficients.
A random sample stratified by country of birth, age, sex and BMI was selected from MCCS participants. Participants completed two FFQ and three 24 h recalls over 1 year. Reliability was evaluated by intraclass correlation coefficients (ICC). Validity coefficients (VC) were estimated from structural equation models and calibration coefficients obtained from regression calibration models.
Adults born in Australia, Greece or Italy.
Nine hundred and sixty-five participants consented to the study; of these, 459 participants were included in the reliability analyses and 615 in the validity and calibration analyses.
The FFQ showed good repeatability for twenty-three nutrients with ICC ranging from 0·66 to 0·80 for absolute nutrient intakes for Australian-born and from 0·51 to 0·74 for Greek/Italian-born. For Australian-born, VC ranged from 0·46 (monounsaturated fat) to 0·83 (Ca) for nutrient densities, comparing well with other studies. For Greek/Italian-born, VC were between 0·21 (Na) and 0·64 (riboflavin). Calibration coefficients for nutrient densities ranged from 0·39 (retinol) to 0·74 (Mg) for Australian-born and from 0·18 (Zn) to 0·54 (riboflavin) for Greek/Italian-born.
The FFQ used in the MCCS follow-up study is suitable for estimating energy-adjusted nutrients for Australian-born participants. However, its performance for estimating intakes is poorer for southern European migrants and alternative dietary assessment methods ought to be considered if dietary data are to be measured in similar demographic groups.
To investigate relationships between mortality and circulating 25-hydroxyvitamin D (25(OH)D), 25-hydroxycholecalciferol (25(OH)D3) and 25-hydroxyergocalciferol (25(OH)D2).
Case–cohort study within the Melbourne Collaborative Cohort Study (MCCS). We measured 25(OH)D2 and 25(OH)D3 in archived dried blood spots by LC–MS/MS. Cox regression was used to estimate mortality hazard ratios (HR), with adjustment for confounders.
The MCCS included 29 206 participants, who at recruitment in 1990–1994 were aged 40–69 years, had dried blood spots collected and no history of cancer. For the present study we selected participants who died by 31 December 2007 (n 2410) and a random sample (sub-cohort, n 2996).
The HR per 25 nmol/l increment in concentration of 25(OH)D and 25(OH)D3 were 0·86 (95 % CI 0·78, 0·96; P=0·007) and 0·85 (95 % CI 0·77, 0·95; P=0·003), respectively. Of 5108 participants, sixty-three (1·2 %) had detectable 25(OH)D2; their mean 25(OH)D concentration was 11·9 (95 % CI 7·3, 16·6) nmol/l higher (P<0·001). The HR for detectable 25(OH)D2 was 1·80 (95 % CI 1·09, 2·97; P=0·023); for those with detectable 25(OH)D2, the HR per 25 nmol/l increment in 25(OH)D was 1·06 (95 % CI 0·87, 1·29; P interaction=0·02). HR were similar for participants who reported being in good, very good or excellent health four years after recruitment.
Total 25(OH)D and 25(OH)D3 concentrations were inversely associated with mortality. The finding that the inverse association for 25(OH)D was restricted to those with no detectable 25(OH)D2 requires confirmation in populations with higher exposure to ergocalciferol.
Observational studies have suggested that 25-hydroxyvitamin D (25(OH)D) levels are associated with inflammatory markers. Most trials reporting significant associations between vitamin D intake and inflammatory markers used specific patient groups. Thus, we aimed to determine the effect of supplementary vitamin D using secondary data from a population-based, randomised, placebo-controlled, double-blind trial (Pilot D-Health trial 2010/0423). Participants were 60- to 84-year-old residents of one of the four eastern states of Australia. They were randomly selected from the electoral roll and were randomised to one of three trial arms: placebo (n 214), 750 μg (n 215) or 1500 μg (n 215) vitamin D3, each taken once per month for 12 months. Post-intervention blood samples for the analysis of C-reactive protein (CRP), IL-6, IL-10, leptin and adiponectin levels were available for 613 participants. Associations between intervention group and biomarker levels were evaluated using quantile regression. There were no statistically significant differences in distributions of CRP, leptin, adiponectin, leptin:adiponectin ratio or IL-10 levels between the placebo group and either supplemented group. The 75th percentile IL-6 level was 2·8 pg/ml higher (95 % CI 0·4, 5·8 pg/ml) in the 1500 μg group than in the placebo group (75th percentiles:11·0 v. 8·2 pg/ml), with a somewhat smaller, non-significant difference in 75th percentiles between the 750 μg and placebo groups. Despite large differences in serum 25(OH)D levels between the three groups after 12 months of supplementation, we found little evidence of an effect of vitamin D supplementation on cytokine or adipokine levels, with the possible exception of IL-6.
To identify predictors of increased adiposity for different measures of adiposity.
Prospective cohort study, the Melbourne Collaborative Cohort Study (MCCS), with data at baseline (1990–1994) and wave 2 (2003–2007).
Participants recruited from the community.
Australian-born participants (n 5879) aged 40 to 69 years who were not current smokers and who were free from common chronic diseases at recruitment. At baseline and at wave 2, weight and waist circumference were measured; while demographic and lifestyle variables were obtained at baseline via structured interviews.
Participants who reported any recreational physical activity at baseline had lower weight and smaller waist circumference at wave 2 than those who did not, particularly for younger participants and for vigorous physical activity. Walking for leisure was not associated, and greater physical activity at work was associated, with greater adiposity measures at wave 2. A diet low in carbohydrates and fibre, but high in fat and protein, predicted greater weight and waist circumference at wave 2. Participants were less likely to have elevated weight or waist circumference at wave 2 if they consumed low to moderate amounts of alcohol.
Our findings indicate that promoting vigorous physical activity, encouraging a diet high in carbohydrate and fibre but low in fat and protein, and limiting alcohol intake could be promising approaches for preventing obesity in middle-aged adults. Similar interventions should successfully address the management of both weight and waist circumference, as they were predicted by similar factors.
Background: Anxiety and depression contribute to morbidity in elderly adults and may be associated with diet. We investigated the association between diet and psychological distress as a marker for depression.
Methods: Dietary patterns were defined by factor analysis or the Mediterranean Diet Score (MDS); depression and anxiety were assessed 12 years later. A total of 8,660 generally healthy men and women born in Australia and aged 50–69 years from the Melbourne Collaborative Cohort Study were included. At baseline (1990–1994), diet (food frequency questionnaire), education, Socio-Economic Indexes for Areas (SEIFA) – Index of Relative Socio-economic Disadvantage, medication use, social engagement, physical activity, smoking status, alcohol use, and health conditions were assessed; at follow-up (2003–2007), psychological distress was assessed using the Kessler Psychological Distress Scale (K10). Logistic regression was used to identify associations between diet and a K10 score ≥20, indicative of psychological distress.
Results: The MDS was inversely associated with psychological distress, with the odds ratio in the top-scoring group relative to the lowest scoring group being 0.72 (95% confidence interval = 0.54–0.95). Stronger adherence to a traditional Australian-style eating pattern was also associated with a lower K10 score at follow-up, with the odds ratio for having a K10 score indicative of psychological distress for the top 20% of adherence to this pattern relative to the lowest being 0.61 (95% confidence interval = 0.40–0.91).
Conclusions: A Mediterranean-style diet was associated with less psychological distress, possibly through provision of a healthy nutrient profile. The Australian dietary pattern, which included some foods high in fat and sugar content along with whole foods, also showed a weak inverse association. Adherence to this pattern may reflect a feeling of belonging to the community associated with less psychological distress.
To evaluate FFQ estimates of dietary intake of individual antioxidants, fruit and vegetables in comparison to plasma concentrations of each antioxidant, and to determine which individual foods are associated with plasma antioxidant concentrations.
Dietary (α-carotene, β-carotene, β-cryptoxanthin, lutein/zeaxanthin, lycopene, retinol, and vitamin E) intakes over 12 months were estimated from a 121-item FFQ. Correlation coefficients, corrected for within-person variability in diet and plasma antioxidants, were used to examine associations between antioxidant concentrations in diet and plasma.
Melbourne Collaborative Cohort Study (MCCS).
Men and women (n 3110) who were randomly selected from the MCCS. Participants were aged 36–72 years and were born in Australia, Greece, Italy or the UK.
Correlation coefficients for the carotenoids ranged from 0·28 for lycopene to 0·46 for β-cryptoxanthin. There was no association between dietary and plasma retinol or dietary vitamin E with plasma α- and γ-tocopherol. Individual plasma carotenoid concentrations were associated with intakes of fruit and vegetables.
Our data suggest that the FFQ provides useful information on intakes of each of the carotenoids: α-carotene, β-carotene, β-cryptoxanthin, lycopene and lutein/zeaxanthin. There was no association between diet and plasma markers of retinol or vitamin E; this may reflect the importance of factors other than intake in modifying circulating levels of these nutrients.
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