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.
We examined associations between adherence to adaptations of the 2018 World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) cancer prevention recommendations and total, ...exposure-related and site-specific cancer risk.
A total of 20,001 participants ages 40 to 69 years at enrollment into the Melbourne Collaborative Cohort Study in 1990 to 1994, who had diet, body size, and lifestyle reassessed in 2003 to 2007 ("baseline"), were followed-up through June 2021. We constructed diet and standardized lifestyle scores based on core WCRF/AICR recommendations on diet, alcohol intake, body size and physical activity, and additional scores incorporating weight change, sedentary behavior, and smoking. Associations with cancer risk were estimated using Cox regression, adjusting for confounders.
During follow-up (mean = 16 years), 4,710 incident cancers were diagnosed. For highest quintile ("most adherent") of the standardized lifestyle score, compared with lowest ("least adherent"), a HR of 0.82 95% confidence interval (CI): 0.74-0.92 was observed for total cancer. This association was stronger with smoking included in the score (HR = 0.74; 95% CI: 0.67-0.81). A higher score was associated with lower breast and prostate cancer risk for the standardized score, and with lung, stomach, rectal, and pancreatic cancer risk when the score included smoking. Our analyses identified alcohol use, waist circumference and smoking as key drivers of associations with total cancer risk.
Adherence to WCRF/AICR cancer prevention recommendations is associated with lower cancer risk.
With <0.2% of our sample fully adherent to the recommendations, the study emphasizes the vast potential for preventing cancer through modulation of lifestyle habits.
We conducted a systematic review and meta-analysis to estimate the potential association between LCω-3PUFAs and prostate cancer (PC). A comprehensive literature search was performed through 2013 to ...identify prospective studies that examined dietary intakes of long-chain omega-3 polyunsaturated fatty acids (LCω-3PUFA) or blood biomarkers of LCω-3PUFA status and risk of PC. Random-effects meta-analyses were conducted to generate summary relative risk estimates (SRREs) for LCω-3PUFAs and total PC, and by stage and grade. Subgroup analyses were also conducted for specific fatty acids and other study characteristics. Twelve self-reported dietary intake and 9 biomarker studies from independent study populations were included in the analysis, with 446,243 and 14,897 total participants, respectively. No association between LCω-3PUFAs and total PC was observed (SRRE = 1.00, 95% CI: 0.93–1.09) for the dietary intake studies (high vs. low LCω-3PUFAs category comparison) or for the biomarker studies (SRRE of 1.07, 95% CI: 0.94–1.20). In general, most summary associations for the dietary intake studies were in the inverse direction, whereas the majority of summary associations for the biomarker studies were in the positive direction, but all were weak in magnitude. The results from this meta-analysis do not support an association between LCω-3PUFAs and PC.
Purpose
This study prospectively investigates associations between fatty acids assessed in plasma phospholipids (PPL) and diet, and breast cancer risk, including subgroups defined by hormone receptor ...status.
Methods
We performed a case-cohort analysis within the Melbourne Collaborative Cohort Study using a random sample of 2,021 women and 470 breast cancer cases. At baseline, fatty acids were assessed in PPL and estimated from diet using a 121-item food frequency questionnaire. Hazard ratios (HR) and 95 % confidence intervals (CI) were estimated using Cox regression.
Results
Breast cancer risk was positively associated with %PPL saturated fatty acids (SFA); HR
Q5vsQ1
= 1.64 (95 % CI 1.17–2.30);
p
trend = 0.004. Positive associations were found for ER+ or PR+ tumors for %PPL SFA and palmitic acid and for ER−/PR− tumors for %PPL n-6 polyunsaturated fatty acid (PUFA), TFA, TFA 16:1, and TFA 18:1n-7 (all
p
homogeneity <0.05). Breast cancer risk was inversely associated with dietary docosapentaenoic acid (DPA); HR
Q5vsQ1
= 0.57 (95 % CI 0.40–0.82);
p
trend = 0.001 with similar inverse associations observed for dietary docosahexaenoic (DHA) and eicosapentaenoic acid (EPA) and positively associated with dietary n-6:n-3 PUFA. Inverse associations for ER−/PR− tumors were found for dietary dihomo-γ-linolenic acid (DGLA) for older women (
p
homogeneity = 0.04).
Conclusions
Breast cancer risk was positively associated with %PPL SFA and the ratio of dietary n-6 to n-3 PUFA and inversely associated with dietary long-chain n-3 PUFA intake. Some associations between fatty acids and breast cancer varied by age and tumor phenotype defined by hormone receptor status. Increased intake of fish and other foods rich in long-chain n-3 PUFAs and reduced n-6 PUFA intake might reduce breast cancer risk.
Animal and experimental studies have demonstrated that long‐chain n‐3 fatty acids inhibit the development of prostate cancer, whereas n‐6 fatty acids might promote it. We performed a case–cohort ...analysis within the Melbourne Collaborative Cohort Study using a random sample of 1,717 men and 464 prostate cancer cases to investigate associations between fatty acids assessed in plasma phospholipids (PPLs) or diet (estimated using a 121‐item food frequency questionnaire) and prostate cancer risk. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression. Prostate cancer risk was positively associated with %PPL saturated fatty acids (SFAs); HR 95% CI = 1.51 1.06, 2.16 (Q5 vs. Q1, fifth vs. first quintile); p‐trend = 0.003. HRs (Q5 to Q2 vs. Q1) were significantly elevated for %PPL palmitic acid. %PPL oleic acid was inversely associated with risk, HR = 0.62 0.43, 0.91 (Q5 vs. Q1); p‐trend = 0.04. No statistically significant linear trends were observed for dietary intakes. The HRs were elevated for moderate intakes of linoleic acid (Q2 and Q3 vs. Q1, 1.58 1.10, 2.28 and 1.70 1.18, 2.46, respectively), but the increase was not significant for higher intakes (Q4 and Q5). No association varied significantly by tumour aggressiveness (all p‐homogeneity > 0.1). Prostate cancer risk was positively associated with %PPL SFA, largely attributable to palmitic acid and inversely associated with %PPL monounsaturated fatty acids, largely attributable to oleic acid. Higher risks were also observed for dietary n‐6 polyunsaturated fats, primarily linoleic acid.
What's new?
Animal and experimental studies have demonstrated that long'chain n'3 fatty acids inhibit the development of prostate cancer, whereas n'6 fatty acids might promote it. Whether similar associations exist for humans, however, has been unclear. This analysis of data from the Melbourne Collaborative Cohort Study suggests that dietary intake of the n'6 linoleic acid and percentage of saturated fatty acid in plasma phospholipids are positively associated with prostate cancer risk. In addition, a higher percentage of n'9 oleic acid in plasma phospholipids was found to possibly reduce prostate cancer risk.
Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation.
We aimed to examine 1) the ...association between plasma markers related to inflammation and derive marker scores for dietary patterns Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI) and 2) the associations of these marker scores with mortality.
Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50–82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y).
The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-γ, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman ρ: –0.74, –0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72–0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66–0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01–1.39). The same magnitude of effect was not observed for the respective dietary patterns.
Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E-DII, and the AHEI, especially kynurenines. Unfavorable marker scores, reflecting poorer-quality diets, were associated with increased mortality.
Identification of risk biomarkers may enhance early detection of smoking-related lung cancer. We measured between 392 and 1,162 proteins in blood samples drawn at most three years before diagnosis in ...731 smoking-matched case-control sets nested within six prospective cohorts from the US, Europe, Singapore, and Australia. We identify 36 proteins with independently reproducible associations with risk of imminent lung cancer diagnosis (all p < 4 × 10
). These include a few markers (e.g. CA-125/MUC-16 and CEACAM5/CEA) that have previously been reported in studies using pre-diagnostic blood samples for lung cancer. The 36 proteins include several growth factors (e.g. HGF, IGFBP-1, IGFP-2), tumor necrosis factor-receptors (e.g. TNFRSF6B, TNFRSF13B), and chemokines and cytokines (e.g. CXL17, GDF-15, SCF). The odds ratio per standard deviation range from 1.31 for IGFBP-1 (95% CI: 1.17-1.47) to 2.43 for CEACAM5 (95% CI: 2.04-2.89). We map the 36 proteins to the hallmarks of cancer and find that activation of invasion and metastasis, proliferative signaling, tumor-promoting inflammation, and angiogenesis are most frequently implicated.
Response to letter from Geoffrey W. Stuart Ellis, Louisa; Milne, Roger L.; Moore, Melissa M. ...
Journal of science and medicine in sport,
06/2024, Volume:
27, Issue:
6
Journal Article
It was previously estimated that 1814 (1.6 % of incident cancers) were attributable to physical inactivity in Australia in 2010, when only three sites were considered. We estimated the burden of ...cancer due to physical inactivity in Australia for 13 sites.
The population attributable fraction estimated site-specific cancer cases attributable to physical inactivity for 13 cancers. The potential impact fraction was used to estimate cancers that could have been prevented in 2015 if Australian adults had increased their physical activity by a modest amount in 2004–05.
We used 2004–05 national physical activity prevalence data, 2015 national cancer incidence data, and contemporary relative-risk estimates for physical inactivity and cancer. We assumed a 10-year latency period.
An estimated 6361 of the cancers observed in 2015 were attributable to physical inactivity, representing 4.8 % of all cancers diagnosed. If Australian adults had increased their physical activity by one category in 2004–05, 2564 cases (1.9 % of all cancers) could have been prevented in 2015.
More than three times as many cancers are attributable to physical inactivity than previously reported. Physical activity promotion should be a central component of cancer prevention programmes in Australia.
Folate and other one-carbon metabolism nutrients are essential to enable DNA methylation to occur, but the extent to which their dietary intake influences methylation in adulthood is unclear.
We ...assessed associations between dietary intake of these nutrients and DNA methylation in peripheral blood, overall and at specific genomic locations.
We conducted a cross-sectional study using baseline data and samples from 5186 adult participants in the Melbourne Collaborative Cohort Study (MCCS). Nutrient intake was estimated from a food-frequency questionnaire. DNA methylation was measured by using the Illumina Infinium HumanMethylation450 BeadChip array (HM450K). We assessed associations of intakes of folate, riboflavin, vitamins B-6 and B-12, methionine, choline, and betaine with methylation at individual cytosine-guanine dinucleotides (CpGs), and with median (genome-wide) methylation across all CpGs, CpGs in gene bodies, and CpGs in gene promoters. We also assessed associations with methylation at long interspersed nuclear element 1 (LINE-1), satellite 2 (Sat2), and Arthrobacter luteus restriction endonuclease (Alu) repetitive elements for a subset of participants. We used linear mixed regression, adjusting for age, sex, country of birth, smoking, energy intake from food, alcohol intake, Mediterranean diet score, and batch effects to assess log-linear associations with dietary intake of each nutrient. In secondary analyses, we assessed associations with low or high intakes defined by extreme quintiles.
No evidence of log-linear association was observed at P < 10−7 between the intake of one-carbon metabolism nutrients and methylation at individual CpGs. Low intake of riboflavin was associated with higher methylation at CpG cg21230392 in the first exon of PROM1 (P = 5.0 × 10−8). No consistent evidence of association was observed with genome-wide or repetitive element measures of methylation.
Our findings suggest that dietary intake of one-carbon metabolism nutrients in adulthood, as measured by a food-frequency questionnaire, has little association with blood DNA methylation. An association with low intake of riboflavin requires replication in independent cohorts. This study was registered at http://www.clinicaltrials.gov as NCT03227003.
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