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Melbourne, Australia

Scott D.,Menzies Research Institute | Blizzard L.,Menzies Research Institute | Fell J.,University of Tasmania | Giles G.,Cancer Epidemiology Center | Jones G.,Menzies Research Institute
Journal of the American Geriatrics Society

OBJECTIVES: To describe associations between dietary nutrient intake and progression of sarcopenia, the age-related loss of muscle mass and strength. DESIGN: Prospective cohort study of community-dwelling older adults. SETTING: Southern Tasmania, Australia. PARTICIPANTS: Seven hundred forty noninstitutionalized older adults (50% female; mean age 62±7) randomly sampled from electoral rolls. MEASUREMENTS: Dietary nutrient intake was examined at baseline and follow-up (2.6±0.4 years later) using The Cancer Council Victoria's Food Frequency Questionnaire (FFQ). Appendicular lean mass (aLM) was assessed using dual X-ray absorptiometry and muscle strength of the knee extensors using a dynamometer. RESULTS: Failing to meet the recommended dietary intake for protein was associated with significantly lower aLM at baseline (-0.81 kg, 95% confidence interval (CI)=-1.54 to-0.08) and follow-up (-0.79 kg, 95%CI=-1.42 to-0.17). Energy-adjusted protein intake was a positive predictor of change in aLM over 2.6 years (β=0.10, P=.003). Energy-adjusted intake of iron (β=0.07, P=.02), magnesium (β=0.07, P=.02), phosphorus (β=0.07, P=.047), and zinc (β=0.08, P=.02) were positive predictors of change in aLM, whereas retinol (β=-0.09, P=.005) was a negative predictor of change in aLM after adjustment for protein intake. No significant associations were observed between nutrient intake and muscle strength. CONCLUSION: Protein and several other dietary nutrients are associated with muscle mass and rate of muscle loss (but not strength) in older adults, suggesting that multiple dietary components may ameliorate the progression of sarcopenia. © 2010, The American Geriatrics Society. Source

Eckermann S.,University of Wollongong | Coory M.,Cancer Epidemiology Center | Willan A.R.,University of Toronto

Economic analysis and assessment of net clinical benefit often requires estimation of absolute risk difference (ARD) for binary outcomes (e.g. survival, response, disease progression) given baseline epidemiological risk in a jurisdiction of interest and trial evidence of treatment effects. Typically, the assumption is made that relative treatment effects are constant across baseline risk, in which case relative risk (RR) or odds ratios (OR) could be applied to estimate ARD. The objective of this article is to establish whether such use of RR or OR allows consistent estimates of ARD.ARD is calculated from alternative framing of effects (e.g. mortality vs survival) applying standard methods for translating evidence with RR and OR. For RR, the RR is applied to baseline risk in the jurisdiction to estimate treatment risk; for OR, the baseline risk is converted to odds, the OR applied and the resulting treatment odds converted back to risk.ARD is shown to be consistently estimated with OR but changes with framing of effects using RR wherever there is a treatment effect and epidemiological risk differs from trial risk. Additionally, in indirect comparisons, ARD is shown to be consistently estimated with OR, while calculation with RR allows inconsistency, with alternative framing of effects in the direction, let alone the extent, of ARD.OR ensures consistent calculation of ARD in translating evidence from trial settings and across trials in direct and indirect comparisons, avoiding inconsistencies from RR with alternative outcome framing and associated biases. These findings are critical for consistently translating evidence to inform economic analysis and assessment of net clinical benefit, as translation of evidence is proposed precisely where the advantages of OR over RR arise. © 2011 Adis Data Information BV. All rights reserved. Source

Coory M.,Cancer Epidemiology Center | Jordan S.,University of Queensland

A key assumption of indirect comparisons is similarity, which means that, in the face of differences in patient characteristics or study methods, there is no treatment-effect modification across sides of the indirect comparison. We therefore conducted a systematic review of MEDLINE and EMBASE from inception to November 2009 to summarize currently available information about how frequently, on average, treatment-effect modification occurs across trials that might be used on different sides of an indirect comparison.Although similarity is a key assumption, there is currently no published evidence specifically for indirect comparisons about how frequently treatment-effect modification occurs.Six analyses were identified that assessed treatment-effect modification across studies included in direct head-to-head meta-analyses. Such analyses are relevant to indirect comparisons because the phenomenon being investigated would occur with similar frequency. They provide important information because lack of treatment-effect modification across sides of an indirect comparison cannot be directly assessed statistically; this is in contrast to direct head-to-head meta-analyses where Cochranes Q statistic or I2 can be used. For ratio measures such as the odds ratio and relative risk, treatment-effect modification occurred for 1033 of meta-analyses. For the risk difference (an arithmetic measure), the range was 1546.It is not prudent to assume similarity in an indirect comparison, based only on the result that ratio measures such as the odds ratio are reasonably robust to treatment-effect modification. All indirect comparisons should include a thorough narrative comparison of differences in patient characteristics and study methods. This will provide end users with the best evidence with which to make an assessment of the likelihood of treatment-effect modification and the plausibility of the similarity assumption. © 2010 Adis Data Information BV. All rights reserved. Source

Winter J.E.,Deakin University | MacInnis R.J.,Cancer Epidemiology Center | MacInnis R.J.,University of Melbourne | Wattanapenpaiboon N.,Deakin University | Nowson C.A.,Deakin University
American Journal of Clinical Nutrition

Background: Whether the association between body mass index (BMI) and all-cause mortality for older adults is the same as for younger adults is unclear. Objective: The objective was to determine the association between BMI and all-cause mortality risk in adults ≥65 y of age. Design: A 2-stage random-effects meta-analysis was performed of studies published from 1990 to 2013 that reported the RRs of all-cause mortality for community-based adults aged ≥65 y. Results: Thirty-two studies met the inclusion criteria; these studies included 197,940 individuals with an average follow-up of 12 y. With the use of a BMI (in kg/m2) of 23.0-23.9 as the reference, there was a 12% greater risk of mortality for a BMI range of 21.0-21.9 and a 19% greater risk for a range of 20.0-20.9 [BMI of 21.0-21.9; HR (95% CI): 1.12 (1.10, 1.13); BMI of 20.0-20.9; HR (95% CI): 1.19 (1.17, 1.22)]. Mortality risk began to increase for BMI >33.0 [BMI of 33.0-33.9; HR (95% CI): 1.08 (1.00, 1.15)]. Self-reported anthropometric measurements, adjustment for intermediary factors, and exclusion of early deaths or preexisting disease did not markedly alter the associations, although there was a slight attenuation of the association in never-smokers. Conclusions: For older populations, being overweight was not found to be associated with an increased risk of mortality; however, there was an increased risk for those at the lower end of the recommended BMI range for adults. Because the risk of mortality increased in older people with a BMI <23.0, it would seem appropriate to monitor weight status in this group to address any modifiable causes of weight loss promptly with due consideration of individual comorbidities. © 2014 American Society for Nutrition. Source

Park D.J.,University of Melbourne | Southey M.C.,University of Melbourne | Giles G.G.,Cancer Epidemiology Center | Giles G.G.,University of Melbourne | Hopper J.L.,University of Melbourne
Breast Cancer Research and Treatment

Numerous independent groups from a range of countries have reported a high prevalence of Mouse Mammary Tumour Virus (MMTV)-like env sequences in human breast cancer specimens, including a prevalence of almost 40% in Australia. MMTV-like sag sequences and a completely integrated provirus have also been described. Recently, it was reported that MMTV is capable of productive infection of human breast cells in vitro. Conclusive demonstration of an association between MMTV and human breast cancer has remained elusive, and negative findings from a number of independent studies have questioned the role of MMTV as an aetiological agent. We used breast cancer specimens from women in the Australian Breast Cancer Family Study (ABCFS) who were diagnosed with first primary invasive breast cancer before the age of 40 years. Specimens were selected for higher grade cancers and for diagnosis relatively soon after childbirth. We searched for MMTV-like env sequences in tumour-enriched DNA using a nested PCR designed to detect all MMTV variants represented in GenBank, including those reportedly detected in human breast cancers. Forty-two specimens were deemed adequate for testing based on strong β-globin PCR. Despite the MMTV nested PCR regimen consistently detecting five copies of control plasmid against a background of MMTV-negative human genomic DNA, no MMTV env sequence was detected in any of the breast cancer specimens. Our findings appear inconsistent with previous reports on Australian breast cancer specimens but consistent with a growing number of independent negative reports internationally. We recommend caution in inferring a role for MMTV or a closely related virus in human breast cancer and suggest that universally regarded alternative lines of evidence such as highly specific serology data will be required to support such an association. © 2010 Springer Science+Business Media, LLC. Source

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