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Purpose: Diet and body size may affect the risk of aggressive prostate cancer (APC), but current evidence is inconclusive.Methods: A case-control study was conducted in men under 75 years of age recruited from urology practices in Victoria, Australia; 1,254 with APC and 818 controls for whom the presence of prostate cancer had been excluded by biopsy. Dietary intakes were assessed using a validated food frequency questionnaire. Multivariable unconditional logistic regression estimated odds ratios and confidence intervals for hypothesized risk factors, adjusting for age, family history of prostate cancer, country of birth, socioeconomic status, smoking, and other dietary factors.Results: Positive associations with APC (odds ratio, 95% confidence intervals, highest vs. lowest category or quintile) were observed for body mass index (1.34, 1.02-1.78, Ptrend = 0.04), and trouser size (1.54, 1.17-2.04, Ptrend = 0.001). Intakes of milk and all dairy products were inversely associated with APC risk (0.71, 9.53-0.96, Ptrend = 0.05, and 0.64, 0.48-0.87, Ptrend = 0.012, respectively), but there was little evidence of an association with other dietary variables (Ptrend > 0.05).Conclusions: We confirmed previous evidence for a positive association between body size and risk of APC, and suggest that consumption of dairy products, and milk more specifically, is inversely associated with risk. [ABSTRACT FROM AUTHOR]

The article discusses the Melbourne Collaborative Cohort Study on anthropometric measures, such as Body Mass Index (BMI) and fat mass, as predictors of all-cause mortality associated with obesity conducted in Victoria. It says that two sensitivity analyses were carried out to examine the impact of pre-attendance diseases on the relationship between the anthropometric measures and mortality. Characteristics of participants in the study are also described.

Background: Obesity increases the risk of 13 cancer types. Given the long process of carcinogenesis, it is important to determine the impact of patterns of body mass over time., Methods: Using data from 30,377 participants in the Melbourne Collaborative Cohort Study, we identified body mass index (BMI) trajectories across adulthood and examined their association with the risk of obesity-related cancer. Participants completed interviews and questionnaires at baseline (1990-1994, age 40-69 years), follow-up 1 (1995-1998), and follow-up 2 (2003-2005). Body mass was recalled for age 18 to 21 years, measured at baseline, self-reported at follow-up 1, and measured at follow-up 2. Height was measured at baseline. Cancer diagnoses were ascertained from the Victorian Cancer Registry and the Australian Cancer Database. A latent class trajectory model was used to identify BMI trajectories that were not defined a priori . Cox regression was used to estimate HRs and 95% confidence intervals (CI) of obesity-related cancer risks by BMI trajectory., Results: Six distinct BMI trajectories were identified. Compared with people who maintained lower normal BMI, higher risks of developing obesity-related cancer were observed for participants who transitioned from normal to overweight (HR, 1.29; 95% CI, 1.13-1.47), normal to class I obesity (HR, 1.50; 95% CI, 1.28-1.75), or from overweight to class II obesity (HR, 1.66; 95% CI, 1.32-2.08)., Conclusions: Our findings suggest that maintaining a healthy BMI across the adult lifespan is important for cancer prevention., Impact: Categorization of BMI by trajectory allowed us to identify specific risk groups to target with public health interventions., (©2020 American Association for Cancer Research.)

Adiposity increases estrogen receptor (ER)-positive postmenopausal breast cancer risk. While mechanisms underlying this relationship are uncertain, dysregulated sex-steroid hormone production and insulin signaling are likely pathways. Our aim was to quantify mediating effects of fasting insulin and free estradiol in the adiposity and ER-positive postmenopausal breast cancer association. We used data from a case-cohort study of sex hormones and insulin signaling nested within the Melbourne Collaborative Cohort Study. Eligible women, at baseline, were not diagnosed with cancer, were postmenopausal, did not use hormone therapy and had no history of diabetes or diabetes medication use. Women with ER-negative disease or breast cancer diagnosis within the first follow-up year were excluded. We analyzed the study as a cumulative sampling case-control study with 149 cases and 1,029 controls. Missing values for insulin and free estradiol were multiply imputed with chained equations. Interventional direct (IDE) and indirect (IIE) effects were estimated using regression-based multiple-mediator approach. For women with body mass index (BMI) >30 kg/m 2 compared to women with BMI 18.5-25 kg/m 2 , the risk ratio (RR) of breast cancer was 1.75 (95% confidence interval [CI] 1.05-2.91). The estimated IDE (RR) not through the mediators was 1.03 (95% CI 0.43-2.48). Percentage mediated effect through free estradiol was 72% (IIE-RR 1.56; 95% CI 1.11-2.19). There was no evidence for an indirect effect through insulin (IIE-RR 1.12; 95% CI 0.68-1.84; 28% mediated). Our results suggest that circulating free estradiol plays an important mediating role in the adiposity-breast cancer relationship but does not explain all of the association., (© 2019 UICC.)

Objective: Limited research has assessed the association between patterns of body mass index (BMI) change across adulthood and mortality. We aimed to identify groups of individuals who followed specific group-based BMI trajectories across adulthood, using weight collected on three occasions and recalled data from early adulthood, and to examine associations with all-cause and cause-specific mortality., Design: Prospective cohort study., Setting: Melbourne, Australia., Participants: Adults (n=29 881) enrolled in the Melbourne Collaborative Cohort Study, who were aged from 40 to 70 years between 1990 and 1994, and had BMI data for at least three time points., Outcome: Deaths from any cause before 31 March 2017 and deaths from obesity-related cancers, cardiovascular diseases (CVDs) and other causes before 31 December 2013., Results: We identified six group-based BMI trajectories: lower-normal stable (TR1), higher-normal stable (TR2), normal to overweight (TR3), chronic borderline obesity (TR4), normal to class I obesity (TR5) and overweight to class II obesity (TR6). Generally, compared with maintaining lower-normal BMI throughout adulthood, the lowest mortality was experienced by participants who maintained higher-normal BMI (HR 0.90; 95% CI 0.84 to 0.97); obesity during midlife was associated with higher all-cause mortality even when BMI was normal in early adulthood (HR 1.09; 95% CI 0.98 to 1.21) and prolonged borderline obesity from early adulthood was also associated with elevated mortality (HR 1.16; 95% CI 1.01 to 1.33). These associations were stronger for never-smokers and for death due to obesity-related cancers. Being overweight in early adulthood and becoming class II obese was associated with higher CVD mortality relative to maintaining lower-normal BMI (HR 2.27; 95% CI 1.34 to 3.87)., Conclusion: Our findings highlight the importance of weight management throughout adulthood to reduce mortality., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Conventionally, cohort studies have assessed the association between alcohol and all-cause mortality by using alcohol intake at enrolment., Methods: In the Melbourne Collaborative Cohort Study, participants were asked about usual frequency and quantity of beverage-specific alcohol intake for 10-year periods starting at age 20 from which current, past and lifetime intakes were calculated. We used Cox regression to estimate hazard ratios for mortality for 39 577 participants of the Melbourne Collaborative Cohort Study aged 40-69 at baseline., Results: After a mean follow-up of 15 years/person, we identified 4639 deaths. Associations between all-cause mortality and lifetime, current (baseline) and past intake were J shaped, with lower mortality at low intake (e.g. <40 g/day for men and 10 g/day for women using lifetime intake) and elevated mortality at higher intake. For men, consistent light-to-moderate drinking (>0-39/>0-39 g/day) from age 20 to baseline age was associated with a 16% lower mortality, while heavy drinking at both ages (≥80/≥40 and ≥40/0 g/day) was associated with higher mortality compared with stable abstinence., Conclusions: Our findings support a reduced mortality risk associated with low-dose drinking but also highlight a higher mortality risk for consistent heavy drinking from a young age., (© The Author 2014. Published by Oxford University Press on behalf of Faculty of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Objective: To compare all-cause mortality in a surgical weight loss cohort with a similarly aged, obese population-based cohort., Summary Background Data: Significant weight loss following bariatric surgery improves the comorbidities associated with obesity. Improved survival as a result of surgical weight loss has yet to be clearly demonstrated using clinical data., Methods: The surgical weight loss cohort was a series of consecutive patients treated with a laparoscopic adjustable gastric band in Melbourne between June 1994 and April 2005. The Melbourne Collaborative Cohort Study (MCCS) provided a community control cohort, recruited between 1992 and 1994 and followed to June 2005 to determine vital status. Height and weight were recorded at baseline in both studies. Subjects between 37 and 70 years and with a body mass index (BMI) of > or =35 were included. Vital status was determined by follow-up and searching of death registries. Survival time was compared using Kaplan-Meier estimates, and hazard of death was determined using Cox regression, adjusting for sex, age at baseline, and BMI at baseline., Results: Of 966 weight loss patients (mean age 47 years, mean BMI 45 kg/m), the median follow-up time was 4 years. Mean weight loss after 2 years was 22.8% +/- 9% (58% of excess weight). The MCCS cohort included 2119 severely obese members (mean age, 55 years; mean BMI, 38 kg/m; median follow-up time, 12 years). There were 4 deaths in the weight loss cohort and 225 deaths in the MCCS cohort. Weight loss patients had 72% lower hazard of death than the community control cohort (hazard ratio, 0.28; 95% confidence interval, 0.10-0.85)., Conclusions: Substantial surgical weight loss in a morbidly obese population was associated with a significant survival advantage.

Background and Methodology: Late 'age at menopause' is a recognised risk factor for postmenopausal breast cancer and is also associated with decreased use of hormone replacement therapy (HRT). When investigating the association between HRT use and breast cancer risk it is therefore necessary to adjust for the potential confounder, 'age at menopause'. 'Age at menopause', however, cannot be determined for women with a hysterectomy and ovarian conservation. Using data on 13 357 postmenopausal women in whom 396 cases of invasive breast cancer were diagnosed during 9 years of follow-up from the Melbourne Collaborative Cohort Study, we compared the estimates of relative risk of HRT use for breast cancer for three different methods of dealing with missing data: complete-case analysis, single imputation and multiple imputation., Results: 'Age at menopause' was missing for 17% of the data. Both HRT use and 'age at menopause' were significant risk factors for breast cancer, although 'age at menopause' only marginally confounded the estimates of risk for HRT. Women with 'age at menopause' missing did not represent a random sample of the population. Complete-case analyses resulted in higher estimates of the risk associated with HRT use compared with the different methods of imputation., Discussion and Conclusions: We recommend that analyses investigating the association between HRT and breast cancer should present the results in two ways: excluding women with 'age at menopause' missing and including the women using multiple imputation. For both methods, estimates of risk, with and without the adjustment of 'age at menopause', should be given.

Genetic and environmental influences on variation in balance performance were measured in 93 monozygous and 83 dizygous female twin pairs aged 21-82 years (mean age, 50.5 years) in Melbourne, Australia, between 1999 and 2003. The authors administered clinical (Lord's Balance Test and Step Test) and laboratory tests of static and dynamic balance from the Chattecx Balance System with and without distractor tasks. The authors conducted factor analysis and estimated genetic and environmental variance components and heritability (defined as additive genetic variance as a proportion of all variance, after adjustment for age) using a multivariate normal model with the statistical package FISHER. Three factors were identified and adjusted for age. Heritability was 46% (standard error (SE), 9) for the "sensory balance tests" factor and 30% (SE, 9) for the "static and dynamic perturbations" factor. For both factors, the remaining variance was attributed to unique environmental effects. There was no evidence that genetic factors influenced variation in the "dynamic weight shift tests" factor, with environmental effects shared by twins accounting for 38% (SE, 7) of variance. Neither genetic nor environmental proportions of variance differed significantly between twin subgroups by age (50 years). An age-related decline in performance measures was found across the whole sample. These results imply that balance impairments may have a heritable element.

Objective: To determine factors that may modify the association between hormone therapy (HT) and breast cancer risk., Design: Prospective cohort study (the Melbourne Collaborative Cohort Study) of 24,479 women aged 40 to 69 years. History of HT use was collected at baseline and 4 years later by questionnaire. By June 2002, 336 cases of breast cancer were diagnosed among 13,444 women postmenopausal at baseline. Association of breast cancer risk with history of HT use was analyzed using proportional hazards models., Results: The hazard ratio (HR) for recent HT use (current or stopped within the last year) was elevated (HR 1.51; 95% CI, 1.16-1.98) but was not significantly increased for past HT users (HR 1.19; 95% CI, 0.86-1.64). Recent HT use was associated with better differentiated tumors but was not more likely to be associated with estrogen receptor-positive / progesterone receptor-positive tumors. There was little evidence of interactions between recent HT use and body mass index, alcohol intake, parity, and smoking, although the HR for recent HT use in categories of alcohol consumption was greatest in women consuming the most alcohol (HR 2.37; 95% CI, 1.45-3.88 for those consuming > or = 10 g/d versus HR 1.33; 95% CI, 0.85-2.08 for nondrinkers, P interaction = 0.32)., Conclusions: The risk of breast cancer for recent users of HT in this Australian population is increased by approximately 50%. Our results suggest that any potential modifying effect of the association between HT and breast cancer risk by factors such as alcohol intake and body mass index is likely to be modest.

Objectives: To determine whether vitamin D supplementation can reduce the incidence of falls and fractures in older people in residential care who are not classically vitamin D deficient., Design: Randomized, placebo-controlled double-blind, trial of 2 years' duration., Setting: Multicenter study in 60 hostels (assisted living facilities) and 89 nursing homes across Australia., Participants: Six hundred twenty-five residents (mean age 83.4) with serum 25-hydroxyvitamin D levels between 25 and 90 nmol/L., Intervention: Vitamin D supplementation (ergocalciferol, initially 10,000 IU given once weekly and then 1,000 IU daily) or placebo for 2 years. All subjects received 600 mg of elemental calcium daily as calcium carbonate., Measurements: Falls and fractures recorded prospectively in study diaries by care staff., Results: The vitamin D and placebo groups had similar baseline characteristics. In intention-to-treat analysis, the incident rate ratio for falling was 0.73 (95% confidence interval (CI)=0.57-0.95). The odds ratio for ever falling was 0.82 (95% CI=0.59-1.12) and for ever fracturing was 0.69 (95% CI=0.40-1.18). An a priori subgroup analysis of subjects who took at least half the prescribed capsules (n=540), demonstrated an incident rate ratio for falls of 0.63 (95% CI=0.48-0.82), an odds ratio (OR) for ever falling of 0.70 (95% CI=0.50-0.99), and an OR for ever fracturing of 0.68 (95% CI=0.38-1.22)., Conclusion: Older people in residential care can reduce their incidence of falls if they take a vitamin D supplement for 2 years even if they are not initially classically vitamin D deficient.

Reports of associations between body size and composition and risk of lymphohematopoietic malignancies have been inconsistent. In a prospective study of 40,909 people aged 27-75 years and followed up for an average of 8.4 years, we measured fat mass and fat-free mass (using bioelectrical impedance analysis) and measured waist circumference directly. All malignancies were ascertained via the population cancer registry. The risk of myeloid leukemia was positively associated with body mass index (compared with those < 25 kg/m2, overweight and obese persons' hazard ratios [HRs] = 5.3, 95% confidence interval [CI] = 1.9 to 15.2 and HR = 5.0, 95% CI = 1.6 to 15.5, respectively; P = .006), fat-free mass (per 10-kg increase HR = 1.83, 95% CI = 1.15 to 2.90; P = .01), and waist circumference (per 10-cm increase HR = 1.35, 95% CI = 1.06 to 1.72; P = .02). Lymphoproliferative malignancies and subgroups showed little relationship with body size.

Objectives: To determine the accuracy of prostate cancer reports and completeness of the family history provided by unaffected men with a family history of prostate cancer. A positive family history is associated with increased prostate cancer risk and could influence surveillance recommendations and patient selection for genetic testing in the future. However, the accuracy of prostate cancer reports and completeness of the family history provided by unaffected men is poorly understood., Methods: Eligible respondents were ascertained through participation in a population-based study of prostate cancer. The family history was collected by questionnaire and compared with the verified research pedigree. Information about the family history was also independently collected from spouses. A standard statistical method was used to determine the variables associated with accuracy and failure to report cases., Results: A total of 154 unaffected men (51%) responded. Most (82%) reports of prostate cancer cases were verified. Overall, 63% reported a family history that precisely matched the verified family history. The respondents' wives contributed little additional information. Age and degree of relationship to an affected person were associated with both accuracy and completeness of the family history. Verification altered the empirical risk category of 29% of the respondents; however, most (93%) remained at increased risk., Conclusions: Unaffected men with a family history of prostate cancer generally provide a reliable family history. We conclude that surveillance advice can be reasonably based on a man's reported family history. However, the identification of certain high-risk individuals, which may be relevant for selection for genetic testing in the future, requires more extensive ascertainment of the family history.

Background: Several studies of male colon cancer have found positive associations with body size and composition. It is uncertain whether this relationship is due to non-adipose mass, adipose mass, distribution of adipose mass such as central adiposity, or all three., Methods: In a prospective cohort study of men aged 27-75 at recruitment in 1990-1994, body measurements were taken by interviewers. Fat mass and fat-free mass (FFM) were estimated from bioelectrical impedance analysis. Waist circumference and waist-to-hips ratio (WHR) estimated central adiposity. Incident colon cancers were ascertained via the population cancer registry. Altogether, 16,556 men contributed 145,433 person-years and 153 colon cancers., Results: Rate ratios (RRs) comparing men in the fourth quartile with those in the first quartile were as follows: FFM 2.3 [95% confidence interval (CI) 1.4-3.7]; height 1.9 (95% CI 1.1-3.1); waist circumference 2.1 (95% CI 1.3-3.5); WHR 2.1 (95% CI 1.3-3.4); fat mass 1.8 (95% CI 1.1-3.0); and body mass index 1.7 (95% CI 1.1-2.8). When continuous measures of FFM and WHR were modeled together, the RR for FFM per 10 kg was 1.37 (95% CI 1.04-1.80) and the RR for WHR per 0.1 unit was 1.65 (95% CI 1.28-2.13). After adjustment for FFM and WHR, the RRs for fat mass and body mass index were no longer statistically significant., Conclusion: Male colon cancer appears to be related to body size and composition by two different pathways, via central adiposity and via non-adipose mass.