ORCID Profile
0000-0003-3345-7333
Current Organisation
The University of Auckland
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Publisher: BMJ
Date: 03-07-2014
Publisher: BMJ
Date: 03-04-2019
DOI: 10.1136/GUTJNL-2017-315730
Abstract: To systematically identify and validate published colorectal cancer risk prediction models that do not require invasive testing in two large population-based prospective cohorts. Models were identified through an update of a published systematic review and validated in the European Prospective Investigation into Cancer and Nutrition (EPIC) and the UK Biobank. The performance of the models to predict the occurrence of colorectal cancer within 5 or 10 years after study enrolment was assessed by discrimination (C-statistic) and calibration (plots of observed vs predicted probability). The systematic review and its update identified 16 models from 8 publications (8 colorectal, 5 colon and 3 rectal). The number of participants included in each model validation ranged from 41 587 to 396 515, and the number of cases ranged from 115 to 1781. Eligible and ineligible participants across the models were largely comparable. Calibration of the models, where assessable, was very good and further improved by recalibration. The C-statistics of the models were largely similar between validation cohorts with the highest values achieved being 0.70 (95% CI 0.68 to 0.72) in the UK Biobank and 0.71 (95% CI 0.67 to 0.74) in EPIC. Several of these non-invasive models exhibited good calibration and discrimination within both external validation populations and are therefore potentially suitable candidates for the facilitation of risk stratification in population-based colorectal screening programmes. Future work should both evaluate this potential, through modelling and impact studies, and ascertain if further enhancement in their performance can be obtained.
Publisher: American Association for Cancer Research (AACR)
Date: 09-2016
DOI: 10.1158/1940-6207.CAPR-15-0434
Abstract: We previously identified osteopontin (OPN) as a promising marker for the early detection of hepatocellular carcinoma (HCC). In this study, we investigated the association between prediagnostic circulating OPN levels and HCC incidence in a large population-based cohort. A nested case–control study was conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. During a mean follow-up of 4.8 years, 100 HCC cases were identified. Each case was matched to two controls and OPN levels were measured in baseline plasma s les. Viral hepatitis, liver function, and α-fetoprotein (AFP) tests were also conducted. Conditional logistic regression models were used to calculate multivariable odds ratio (OR) and 95% confidence intervals (95% CI) for OPN levels in relation to HCC. Receiver operating characteristics curves were constructed to determine the discriminatory accuracy of OPN alone or in combination with other liver biomarkers in the prediction of HCC. OPN levels were positively associated with HCC risk (per 10% increment, ORmultivariable = 1.30 95% CI, 1.14–1.48). The association was stronger among cases diagnosed within 2 years of follow-up. Adding liver function tests to OPN improved the discriminatory performance for subjects who developed HCC (AUC = 0.86). For cases diagnosed within 2 years, the combination of OPN and AFP was best able to predict HCC risk (AUC = 0.88). The best predictive model for HCC in this low-risk population is OPN in combination with liver function tests. Within 2 years of diagnosis, the combination of OPN and AFP best predicted HCC development, suggesting that measuring OPN and AFP could identify high-risk groups independently of a liver disease diagnosis. Cancer Prev Res 9(9) 758–65. ©2016 AACR.
Publisher: Springer Science and Business Media LLC
Date: 11-06-2019
Publisher: BMJ
Date: 03-2017
Publisher: MDPI AG
Date: 20-01-2011
DOI: 10.3390/NU3010152
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 18-06-2019
DOI: 10.1161/CIRCULATIONAHA.118.038813
Abstract: There is uncertainty about the relevance of animal foods to the pathogenesis of ischemic heart disease (IHD). We examined meat, fish, dairy products, and eggs and risk for IHD in the pan-European EPIC cohort (European Prospective Investigation Into Cancer and Nutrition). In this prospective study of 409 885 men and women in 9 European countries, diet was assessed with validated questionnaires and calibrated with 24-hour recalls. Lipids and blood pressure were measured in a subs le. During a mean of 12.6 years of follow-up, 7198 participants had a myocardial infarction or died of IHD. The relationships of animal foods with risk were examined with Cox regression with adjustment for other animal foods and relevant covariates. The hazard ratio (HR) for IHD was 1.19 (95% CI, 1.06–1.33) for a 100-g/d increment in intake of red and processed meat, and this remained significant after exclusion of the first 4 years of follow-up (HR, 1.25 [95% CI, 1.09–1.42]). Risk was inversely associated with intakes of yogurt (HR, 0.93 [95% CI, 0.89–0.98] per 100-g/d increment), cheese (HR, 0.92 [95% CI, 0.86–0.98] per 30-g/d increment), and eggs (HR, 0.93 [95% CI, 0.88–0.99] per 20-g/d increment) the associations with yogurt and eggs were attenuated and nonsignificant after exclusion of the first 4 years of follow-up. Risk was not significantly associated with intakes of poultry, fish, or milk. In analyses modeling dietary substitutions, replacement of 100 kcal/d from red and processed meat with 100 kcal/d from fatty fish, yogurt, cheese, or eggs was associated with ≈20% lower risk of IHD. Consumption of red and processed meat was positively associated with serum non–high-density lipoprotein cholesterol concentration and systolic blood pressure, and consumption of cheese was inversely associated with serum non–high-density lipoprotein cholesterol. Risk for IHD was positively associated with consumption of red and processed meat and inversely associated with consumption of yogurt, cheese, and eggs, although the associations with yogurt and eggs may be influenced by reverse causation bias. It is not clear whether the associations with red and processed meat and cheese reflect causality, but they were consistent with the associations of these foods with plasma non–high-density lipoprotein cholesterol and for red and processed meat with systolic blood pressure, which could mediate such effects.
Publisher: Oxford University Press (OUP)
Date: 12-12-2014
DOI: 10.1093/JNCI/DJU367
Abstract: There is limited evidence on the association between dietary folate intake and the risk of breast cancer (BC) by hormone receptor expression in the tumors. We investigated the relationship between dietary folate and BC risk using data from the European Prospective Investigation into Cancer and Nutrition (EPIC). A total of 367993 women age 35 to 70 years were recruited in 10 European countries. During a median follow-up of 11.5 years, 11575 women with BC were identified. Dietary folate intake was estimated from country-specific dietary questionnaires. Cox proportional hazards regression models were used to quantify the association between dietary variables and BC risk. BC tumors were classified by receptor status. Subgroup analyses were performed by menopausal status and alcohol intake. Intake of other B vitamins was considered. All statistical tests were two-sided. A borderline inverse association was observed between dietary folate and BC risk (hazard ratio comparing top vs bottom quintile [HRQ5-Q1] = 0.92, 95% CI = 0.83 to 1.01, P trend = .037). In premenopausal women, we observed a statistically significant trend towards lower risk in estrogen receptor-negative BC (HRQ5-Q1 = 0.66, 95% CI = 0.45 to 0.96, P trend = .042) and progesterone receptor-negative BC (HRQ5-Q1 = 0.70, 95% CI = 0.51 to 0.97, P trend = .021). No associations were found in postmenopausal women. A 14% reduction in BC risk was observed when comparing the highest with the lowest dietary folate tertiles in women having a high (>12 alcoholic drinks/week) alcohol intake (HRT3-T1 = 0.86, 95% CI = 0.75 to 0.98, P interaction = .035). Higher dietary folate intake may be associated with a lower risk of sex hormone receptor-negative BC in premenopausal women.
Publisher: Elsevier BV
Date: 02-2010
Abstract: The use of serum fatty acid biomarkers in nutritional epidemiology is increasingly common however, there is an absence of scientific evidence to substantiate whether the measurement of fatty acids as molecular percentages (which is the conventional approach) or as absolute concentrations is more informative. To advance understanding about this fundamental concept, we examined the ability of serum myristic acid and linoleic acid, expressed as molecular percentages or as concentrations, to predict dietary fat and serum cholesterol concentrations. A cross-sectional analysis of a population-based survey of New Zealand adults (n = 2732) was undertaken. The association of myristic and linoleic acids in serum cholesterol ester and phospholipid with dietary fat or serum cholesterol was assessed. Intake of saturated fat, dairy fat, and polyunsaturated fat was predicted similarly with the use of both units of measurement. After adjustment for confounders, mean total cholesterol decreased by 0.18 mmol/L from the lowest to the highest quintile of serum cholesteryl-linoleate as a molecular percentage (P = 0.027). In contrast, mean total cholesterol increased by 1.09 mmol/L from the lowest to the highest quintile of serum cholesteryl-linoleate concentration (P < 0.001). The molecular percentage and concentration of serum cholesteryl-myristate were positively associated with total cholesterol (P < 0.001). Results for serum phospholipid fatty acids were similar. Serum myristic acid and linoleic acid measured as molecular percentages, but not as concentrations, predict serum total cholesterol in a manner that distinguishes between the differential cholesterolemic effects of dietary saturated and polyunsaturated fats.
Publisher: Elsevier BV
Date: 04-2020
Publisher: MDPI AG
Date: 08-06-2021
DOI: 10.3390/CARDIOGENETICS11020010
Abstract: Background. Each year, approximately 5000 New Zealanders are admitted to hospital with first-time acute coronary syndrome (ACS). The Multi-Ethnic New Zealand Study of Acute Coronary Syndromes (MENZACS) is a prospective longitudinal cohort study embedded within the All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry in six hospitals. The objective of MENZACS is to examine the relationship between clinical, genomic, and cardiometabolic markers in relation to presentation and outcomes post-ACS. Methods. Patients with first-time ACS are enrolled and study-specific research data is collected alongside the ANZACS-QI registry. The research blood s les are stored for future genetic/biomarker assays. Dietary information is collected with a food frequency questionnaire and information about physical activity, smoking, and stress is also collected via questionnaire. Detailed family history, ancestry, and ethnicity data are recorded on all participants. Results. During the period between 2015 and 2019, there were 2015 patients enrolled. The mean age was 61 years, with 60% of patients aged years and 21% were female. Ethnicity and cardiovascular (CV) risk factor distribution was similar to ANZACS-QI: 13% Māori, 5% Pacific, 5% Indian, and 74% NZ European. In terms of CV risk factors, 56% were ex-/current smokers, 42% had hypertension, and 19% had diabetes. ACS subtype was ST elevation myocardial infarction (STEMI) in 41%, non-ST elevation myocardial infarction (NSTEM) in 54%, and unstable angina in 5%. Ninety-nine percent of MENZACS participants underwent coronary angiography and 90% had revascularization there were high rates of prescription of secondary prevention medications upon discharge from hospital. Conclusion. MENZACS represents a cohort with optimal contemporary management and will be a significant epidemiological bioresource for the study of environmental and genetic factors contributing to ACS in New Zealand’s multi-ethnic environment. The study will utilise clinical, nutritional, lifestyle, genomic, and biomarker analyses to explore factors influencing the progression of coronary disease and develop risk prediction models for health outcomes.
Publisher: American Association for Cancer Research (AACR)
Date: 31-05-2017
DOI: 10.1158/1055-9965.EPI-16-0886
Abstract: Background: Emerging evidence from cohort studies indicates that adiposity is associated with greater incidence of head and neck cancer. However, most studies have used self-reported anthropometry which is prone to error. Methods: Among 363,094 participants in the European Prospective Investigation into Cancer and Nutrition study (EPIC) with measured anthropometry, there were 837 incident cases of head and neck cancer. Head and neck cancer risk was examined in relation to body mass index (BMI) [lean: & .5 kg/m2, normal weight (reference): 22.5–24.9 kg/m2, overweight 25–29.9 kg/m2, obese: ≥30 kg/m2], waist circumference (WC), hip circumference (HC), and waist-to-hip ratio (WHR) using Cox proportional hazards models. Results: Among men, a BMI & 22.5 kg/m2 was associated with higher head and neck cancer risk [HR 1.62 95% confidence interval (CI), 1.23–2.12)] BMI was not associated with head and neck cancer among women. WC and WHR were associated with greater risk of head and neck cancer among women (WC per 5 cm: HR, 1.08 95% CI, 1.02–1.15 WHR per 0.1 unit: HR, 1.64 95% CI, 1.38–1.93). After stratification by smoking status, the association for WHR was present only among smokers (Pinteraction = 0.004). Among men, WC and WHR were associated with head and neck cancer only upon additional adjustment for BMI (WC per 5 cm: HR 1.16 95% CI, 1.07–1.26 WHR per 0.1 unit: HR, 1.42 95% CI, 1.21–1.65). Conclusions: Central adiposity, particularly among women, may have a stronger association with head and neck cancer risk than previously estimated. Impact: Strategies to reduce obesity may beneficially impact head and neck cancer incidence. Cancer Epidemiol Biomarkers Prev 26(6) 895–904. ©2017 AACR.
Publisher: Elsevier BV
Date: 08-2016
Publisher: Wiley
Date: 24-09-2014
DOI: 10.1002/IJC.29214
Publisher: Springer Science and Business Media LLC
Date: 21-12-2014
Publisher: Wiley
Date: 29-09-2014
DOI: 10.1002/IJC.29223
Abstract: Prospective studies examining the association between coffee and tea consumption and gastric cancer risk have shown inconsistent results. We investigated the association between coffee (total, caffeinated and decaffeinated) and tea consumption and the risk of gastric cancer by anatomical site and histological type in the European Prospective Investigation into Cancer and Nutrition study. Coffee and tea consumption were assessed by dietary questionnaires at baseline. Adjusted hazard ratios (HRs) were calculated using Cox regression models. During 11.6 years of follow up, 683 gastric adenocarcinoma cases were identified among 477,312 participants. We found no significant association between overall gastric cancer risk and consumption of total coffee (HR 1.09, 95%-confidence intervals [CI]: 0.84-1.43 quartile 4 vs. non/quartile 1), caffeinated coffee (HR 1.14, 95%-CI: 0.82-1.59 quartile 4 vs. non/quartile 1), decaffeinated coffee (HR 1.07, 95%-CI: 0.75-1.53 tertile 3 vs. non/tertile 1) and tea (HR 0.81, 95%-CI: 0.59-1.09 quartile 4 vs. non/quartile 1). When stratified by anatomical site, we observed a significant positive association between gastric cardia cancer risk and total coffee consumption per increment of 100 mL/day (HR 1.06, 95%-CI: 1.03-1.11). Similarly, a significant positive association was observed between gastric cardia cancer risk and caffeinated coffee consumption (HR 1.98, 95%-CI: 1.16-3.36, p-trend=0.06 quartile 3 vs. non/quartile 1) and per increment of 100 mL/day (HR 1.09, 95%-CI: 1.04-1.14). In conclusion, consumption of total, caffeinated and decaffeinated coffee and tea is not associated with overall gastric cancer risk. However, total and caffeinated coffee consumption may be associated with an increased risk of gastric cardia cancer. Further prospective studies are needed to rule out chance or confounding.
Publisher: Oxford University Press (OUP)
Date: 04-06-2019
DOI: 10.1093/IJE/DYY065
Publisher: Elsevier BV
Date: 08-2019
DOI: 10.1093/AJCN/NQZ072
Publisher: Elsevier BV
Date: 09-2014
Publisher: BMJ
Date: 17-07-2023
DOI: 10.1136/HEARTJNL-2023-322412
Abstract: To examine the associations between specific dietary patterns and incident atrial fibrillation (AF). Using data from the UK Biobank, dietary intakes were calculated from 24-hour diet recall questionnaires. Indices representing adherence to dietary patterns (Mediterranean-style, Dietary Approaches to Stop Hypertension (DASH) and plant-based diets) were scored, and ultra-processed food consumption was studied as a percentage of total food mass consumed. Incident AF hospitalisations were assessed in Cox regression models. A total of 121 300 in iduals were included, with 4 579 incident AF cases over a median follow-up of 8.8 years. Adherence to Mediterranean-style or DASH diets was associated with a lower incidence of AF in minimally adjusted analyses (HR for highest vs lowest quintile 0.87 (95% CI 0.80–0.96) and HR 0.78 (95% CI 0.71–0.86), respectively). However, associations were no longer significant after accounting for lifestyle factors (HR 0.95 (95% CI 0.87–1.04) and 0.94 (95% CI 0.86–1.04) respectively), with adjustment for body mass index responsible for approximately three-quarters of the effect size attenuation. Plant-based diets were not associated with AF risk in any models. Greatest ultra-processed food consumption was associated with a significant increase in AF risk even in fully adjusted models (HR 1.13 (95% CI 1.02–1.24)), and a 10% increase in absolute intake of ultra-processed food was associated with a 5% increase in AF risk (HR 1.05 (95% CI 1.01–1.08)). With the possible exception of reducing ultra-processed food consumption, these findings suggest that attention to other modifiable risk factors, particularly obesity, may be more important than specific dietary patterns for the primary prevention of AF.
Publisher: Elsevier BV
Date: 09-2012
Abstract: Daily supplementation with folate increases erythrocyte folate concentrations however, the time to reach steady-state concentrations has not been empirically demonstrated. Previous predictions of time to steady state or time to 90% steady-state concentration, based on modeling changes in erythrocyte folate during short-term trials, range widely from 40 to 86 wk. We sought to determine the time to steady-state erythrocyte folate concentrations following the initiation of daily folate supplementation using data collected from a 2-y, double-blind, placebo-controlled, randomized trial involving 276 participants aged 65 y or older. The daily supplement contained 1 mg of folate. Erythrocyte folate concentrations were measured, using a microbiological assay, at baseline and at 6, 12, 18, and 24 mo. The mean plasma and erythrocyte folate concentrations in the folate-supplemented group were higher than in the placebo group at 6, 12, 18, and 24 mo (P < 0.001). Adjusted for baseline differences, the difference in erythrocyte folate concentrations between the folate and placebo group at 6 mo was 1.78 μmol/L (95% CI: 1.62-1.95 μmol/L). The difference increased significantly to 2.02 μmol/L (95% CI: 1.85-2.18 μmol/L) at 12 mo. This difference (between the folate and placebo groups) did not significantly change after a further year of folate supplementation at 18 mo, it was 2.09 μmol/L (95% CI: 1.92-2.27 μmol/L) and at 24 mo it was 1.98 μmol/L (95% CI: 1.18-2.15 μmol/L). Twelve months of daily folate supplementation with 1 mg is sufficient time to cause erythrocyte folate concentrations to reach a new steady state.
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Kathryn Bradbury.