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Epidemiological studies have identified increased colorectal cancer (CRC) risk with high red meat (HRM) intakes, whereas dietary fibre intake appears to be protective. In the present study, we examined whether a HRM diet increased rectal O6-methyl-2-deoxyguanosine (O6MeG) adduct levels in healthy human subjects, and whether butyrylated high-amylose maize starch (HAMSB) was protective. A group of twenty-three individuals consumed 300 g/d of cooked red meat without (HRM diet) or with 40 g/d of HAMSB (HRM+HAMSB diet) over 4-week periods separated by a 4-week washout in a randomised cross-over design. Stool and rectal biopsy samples were collected for biochemical, microbial and immunohistochemical analyses at baseline and at the end of each 4-week intervention period. The HRM diet increased rectal O6MeG adducts relative to its baseline by 21 % (P< 0·01), whereas the addition of HAMSB to the HRM diet prevented this increase. Epithelial proliferation increased with both the HRM (P< 0·001) and HRM+HAMSB (P< 0·05) diets when compared with their respective baseline levels, but was lower following the HRM+HAMSB diet compared with the HRM diet (P< 0·05). Relative to its baseline, the HRM+HAMSB diet increased the excretion of SCFA by over 20 % (P< 0·05) and increased the absolute abundances of the Clostridium coccoides group (P< 0·05), the Clostridiumleptum group (P< 0·05), Lactobacillus spp. (P< 0·01), Parabacteroides distasonis (P< 0·001) and Ruminococcus bromii (P< 0·05), but lowered Ruminococcus torques (P< 0·05) and the proportions of Ruminococcus gnavus, Ruminococcus torques and Escherichia coli (P< 0·01). HRM consumption could increase the risk of CRC through increased formation of colorectal epithelial O6MeG adducts. HAMSB consumption prevented red meat-induced adduct formation, which may be associated with increased stool SCFA levels and/or changes in the microbiota composition.
Objectives: The aim of this study was to develop a decision support tool to assess the potential benefits and costs of new healthcare interventions.
Methods: The Canadian Partnership Against Cancer (CPAC) commissioned the development of a Cancer Risk Management Model (CRMM)—a computer microsimulation model that simulates individual lives one at a time, from birth to death, taking account of Canadian demographic and labor force characteristics, risk factor exposures, and health histories. Information from all the simulated lives is combined to produce aggregate measures of health outcomes for the population or for particular subpopulations.
Results: The CRMM can project the population health and economic impacts of cancer control programs in Canada and the impacts of major risk factors, cancer prevention, and screening programs and new cancer treatments on population health and costs to the healthcare system. It estimates both the direct costs of medical care, as well as lost earnings and impacts on tax revenues. The lung and colorectal modules are available through the CPAC Web site (www.cancerview.ca/cancerrriskmanagement) to registered users where structured scenarios can be explored for their projected impacts. Advanced users will be able to specify new scenarios or change existing modules by varying input parameters or by accessing open source code. Model development is now being extended to cervical and breast cancers.
The material characterization toolbox has recently experienced a number of parallel revolutionary advances, foreshadowing a time in the near future when material scientists can quantify material structure evolution across spatial and temporal space simultaneously. This will provide insight to reaction dynamics in four-dimensions, spanning multiple orders of magnitude in both temporal and spatial space. This study presents the authors’ viewpoint on the material characterization field, reviewing its recent past, evaluating its present capabilities, and proposing directions for its future development. Electron microscopy; atom probe tomography; x-ray, neutron and electron tomography; serial sectioning tomography; and diffraction-based analysis methods are reviewed, and opportunities for their future development are highlighted. Advances in surface probe microscopy have been reviewed recently and, therefore, are not included [D.A. Bonnell et al.: Rev. Modern Phys. in Review]. In this study particular attention is paid to studies that have pioneered the synergetic use of multiple techniques to provide complementary views of a single structure or process; several of these studies represent the state-of-the-art in characterization and suggest a trajectory for the continued development of the field. Based on this review, a set of grand challenges for characterization science is identified, including suggestions for instrumentation advances, scientific problems in microstructure analysis, and complex structure evolution problems involving material damage. The future of microstructural characterization is proposed to be one not only where individual techniques are pushed to their limits, but where the community devises strategies of technique synergy to address complex multiscale problems in materials science and engineering.
There is some evidence that plasma insulin levels might influence ovarian cancer risk. Glyacemic index (GI) and glycaemic load (GL) are measures that allow the carbohydrate content of individual foods to be classified according to their postprandial glycaemic effects and hence their effects on circulating insulin levels. Therefore, we examined ovarian cancer risk in association with GI and GL, and intake of dietary carbohydrate and sugar.
The study was conducted in a prospective cohort of 49 613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food-frequency questionnaire (FFQ) between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. Data from the FFQ were used to estimate overall GI and GL, and Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between energy-adjusted quartile levels of GL, overall GI, total carbohydrates, total sugar and ovarian cancer risk.
During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases. GI and total carbohydrate and sugar intakes were not associated with ovarian cancer risk in the total cohort. GL was positively associated with a 72% increase in risk of ovarian cancer (HR = 1.72, 95% CI = 1.13–2.62, Ptrend = 0.01) and the magnitude of the association was slightly greater among postmenopausal (HR = 1.89, 95% CI = 0.98–3.65, Ptrend = 0.03) than among premenopausal women (HR = 1.64, 95% CI = 0.95–2.88, Ptrend = 0.07).
Our data suggest that consumption of diets with high GL values may be associated with increased risk of ovarian cancer.
High-glycaemic-load diets may increase endometrial cancer risk by increasing circulating insulin levels and, as a consequence, circulating oestrogen levels. Given the paucity of epidemiological data regarding the relationship between dietary glycaemic index and glycaemic load and endometrial cancer risk, we sought to examine these associations using data from a prospective cohort study.
We examined the association between dietary glycaemic load and endometrial cancer risk in a cohort of 49 613 Canadian women aged between 40 and 59 years at baseline who completed self-administered food-frequency questionnaires between 1982 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000.
During a mean of 16.4 years of follow-up, we observed 426 incident cases of endometrial cancer. Hazard ratios for the highest versus the lowest quartile level of overall glycaemic index and glycaemic load were 1.47 (95% confidence interval (CI) = 0.90–2.41; P for trend = 0.14) and 1.36 (95% CI = 1.01–1.84; P for trend = 0.21), respectively. No association was observed between total carbohydrate or total sugar consumption and endometrial cancer risk. Among obese women (body mass index > 30 kg m−2) the hazard ratio for the highest versus the lowest quartile level of glycaemic load was 1.88 (95% CI = 1.08–3.29; P for trend = 0.54) and there was a 55% increased risk for the highest versus the lowest quartile level of glycaemic load among premenopausal women. There was also evidence to support a positive association between glycaemic load and endometrial cancer risk among postmenopausal women who had used hormone replacement therapy.
Our data suggest that diets with high glycaemic index or high glycaemic load may be associated with endometrial cancer risk overall, and particularly among obese women, premenopausal women and postmenopausal women who use hormone replacement therapy.