04 August 2017 In Cancer

PURPOSE: To estimate the Australian cancer burden attributable to lifestyle-related risk factors and their combinations using a novel population attributable fraction (PAF) method that accounts for competing risk of death, risk factor interdependence and statistical uncertainty.

PARTICIPANTS: 365 173 adults from seven Australian cohort studies. We linked pooled harmonised individual participant cohort data with population-based cancer and death registries to estimate exposure-cancer and exposure-death associations. Current Australian exposure prevalence was estimated from representative external sources. To illustrate the utility of the new PAF method, we calculated fractions of cancers causally related to body fatness or both tobacco and alcohol consumption avoidable in the next 10 years by risk factor modifications, comparing them with fractions produced by traditional PAF methods.

FINDINGS TO DATE: Over 10 years of follow-up, we observed 27 483 incident cancers and 22 078 deaths. Of cancers related to body fatness (n=9258), 13% (95% CI 11% to 16%) could be avoided if those currently overweight or obese had body mass index of 18.5-24.9 kg/m2. Of cancers causally related to both tobacco and alcohol (n=4283), current or former smoking explains 13% (11% to 16%) and consuming more than two alcoholic drinks per day explains 6% (5% to 8%). The two factors combined explain 16% (13% to 19%): 26% (21% to 30%) in men and 8% (4% to 11%) in women. Corresponding estimates using the traditional PAF method were 20%, 31% and 10%. Our PAF estimates translate to 74 000 avoidable body fatness-related cancers and 40 000 avoidable tobacco- and alcohol-related cancers in Australia over the next 10 years (2017-2026). Traditional PAF methods not accounting for competing risk of death and interdependence of risk factors may overestimate PAFs and avoidable cancers.

FUTURE PLANS: We will rank the most important causal factors and their combinations for a spectrum of cancers and inform cancer control activities.

22 June 2017 In Drinking & Eating Patterns

BACKGROUND: In a survey taken in Germany in 2015, 14.1% of the 12- to 17-year-olds surveyed had practiced binge drinking at least once in the preceding 30 days. The school program "Klar bleiben" ("Keep a Clear Head") was designed for and implemented among 10th graders. The participants committed themselves to abstain from binge drinking for 9 weeks. We studied whether this intervention influenced the frequency and intensity of binge drinking.

METHODS: This cluster-randomized controlled trial was carried out in 196 classes of 61 schools, with a total of 4163 participants with a mean age of 15.6 years (standard deviation 0.73 years). Data were collected by questionnaire in late 2015, before the intervention and again six months later. The primary endpoints were the frequency of consumption of at least 4 or 5 alcoholic drinks (for girls and boys, respectively) and the typical quantity consumed. This trial was registered in the German Clinical Trials Registry (Deutsches Register Klinischer Studien, DRKS) with the DRKS ID number DRKS00009424.

RESULTS: At the beginning of the trial, there was no difference between the intervention group and the control group with respect to the primary endpoints. After the intervention, differences were found among participants who had consumed alcohol before the trial (73.2% of the overall sample): binge drinking at least once in the preceding month was reported by 49.4% of the control group and by 44.2% in the intervention group (p = 0.028). The mean number of alcoholic drinks consumed in each drinking episode was 5.20 in the control group and 5.01 in the intervention group (p = 0.047).

CONCLUSION: The intervention was effective only in the large subgroup of adolescents who had previously consumed alcohol: they drank alcohol less often and in smaller amounts than their counterparts in the control group.

27 February 2017 In Cancer

It is not clear whether alcohol consumption is associated with lung cancer risk. The relationship is likely confounded by smoking, complicating the interpretation of previous studies. We examined the association of alcohol consumption and lung cancer risk in a large pooled international sample, minimizing potential confounding of tobacco consumption by restricting analyses to never smokers. Our study included 22 case-control and cohort studies with a total of 2548 never-smoking lung cancer patients and 9362 never-smoking controls from North America, Europe and Asia within the International Lung Cancer Consortium (ILCCO) and SYNERGY Consortium. Alcohol consumption was categorized into amounts consumed (grams per day) and also modelled as a continuous variable using restricted cubic splines for potential non-linearity. Analyses by histologic sub-type were included. Associations by type of alcohol consumed (wine, beer and liquor) were also investigated. Alcohol consumption was inversely associated with lung cancer risk with evidence most strongly supporting lower risk for light and moderate drinkers relative to non-drinkers (>0-4.9g per day: OR=0.80, 95% CI=0.70-0.90; 5-9.9g per day: OR=0.82, 95% CI=0.69-0.99; 10-19.9g per day: OR=0.79, 95% CI=0.65-0.96). Inverse associations were found for consumption of wine and liquor, but not beer. The results indicate that alcohol consumption is inversely associated with lung cancer risk, particularly among subjects with low to moderate consumption levels, and among wine and liquor drinkers, but not beer drinkers. Although our results should have no relevant bias from the confounding effect of smoking we cannot preclude that confounding by other factors contributed to the observed associations. Confounding in relation to the non-drinker reference category may be of particular importance.

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01 February 2017 In Cancer

Genome-wide association studies (GWAS) have identified many genetic susceptibility loci for colorectal cancer (CRC). However, variants in these loci explain only a small proportion of familial aggregation, and there are likely additional variants that are associated with CRC susceptibility. Genome-wide studies of gene-environment interactions may identify variants that are not detected in GWAS of marginal gene effects. To study this, we conducted a genome-wide analysis for interaction between genetic variants and alcohol consumption and cigarette smoking using data from the Colon Cancer Family Registry (CCFR) and the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Interactions were tested using logistic regression. We identified interaction between CRC risk and alcohol consumption and variants in the 9q22.32/HIATL1 (Pinteraction = 1.76x10-8; permuted p-value 3.51x10-8) region. Compared to non-/occasional drinking light to moderate alcohol consumption was associated with a lower risk of colorectal cancer among individuals with rs9409565 CT genotype (OR, 0.82 [95% CI, 0.74-0.91]; P = 2.1x10-4) and TT genotypes (OR,0.62 [95% CI, 0.51-0.75]; P = 1.3x10-6) but not associated among those with the CC genotype (p = 0.059). No genome-wide statistically significant interactions were observed for smoking. If replicated our suggestive finding of a genome-wide significant interaction between genetic variants and alcohol consumption might contribute to understanding colorectal cancer etiology and identifying subpopulations with differential susceptibility to the effect of alcohol on CRC risk.

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