01 February 2017 In General Health

BACKGROUND: Explicit labelling of lower strength alcohol products could reduce alcohol consumption by attracting more people to buy and drink such products instead of higher strength ones. Alternatively, it may lead to more consumption due to a 'self-licensing' mechanism. Equivalent labelling of food or tobacco (for example "Low fat" or "Low tar") could influence consumption of those products by similar mechanisms. This systematic review examined the effects of 'Low alcohol' and equivalent labelling of alcohol, food and tobacco products on selection, consumption, and perceptions of products among adults.

METHODS: A systematic review was conducted based on Cochrane methods. Electronic and snowball searches identified 26 eligible studies. Evidence from 12 randomised controlled trials (all on food) was assessed for risk of bias, synthesised using random effects meta-analysis, and interpreted in conjunction with evidence from 14 non-randomised studies (one on alcohol, seven on food and six on tobacco). Outcomes assessed were: quantities of the product (i) selected or (ii) consumed (primary outcomes - behaviours), (iii) intentions to select or consume the product, (iv) beliefs associated with it consumption, (v) product appeal, and (vi) understanding of the label (secondary outcomes - cognitions).

RESULTS: Evidence for impacts on the primary outcomes (i.e. amounts selected or consumed) was overall of very low quality, showing mixed effects, likely to vary by specific label descriptors, products and population characteristics. Overall very low quality evidence suggested that exposure to 'Low alcohol' and equivalent labelling on alcohol, food and tobacco products can shift consumer perceptions of products, with the potential to 'self-licence' excess consumption.

CONCLUSIONS: Considerable uncertainty remains about the effects of labels denoting low alcohol, and equivalent labels, on alcohol, food and tobacco selection and consumption. Independent, high-quality studies are urgently needed to inform policies on labelling regulations.

01 February 2017 In Cancer

It is still inconclusive whether alcohol consumption affects the risk of thyroid cancer. We conducted a meta-analysis of available epidemiological data to address this issue. Compared with nondrinkers, the pooled relative risks (RRs) and corresponding 95% confidential intervals (CIs) of thyroid cancer were 0.80 (95% CI 0.71-0.90) for any drinkers, 0.81 (95% CI 0.70-0.93) for light and 0.71 (95% CI 0.63-0.79) for moderate drinkers. The dose-response analysis suggested that there is no evidence of a dose-risk relationship between alcohol intaking and thyroid cancer risk (P = 0.112). Eligible studies were identified by searching PubMed and EMbase databases. A total of 24 studies, included 9,990 cases with thyroid cancer, were included in this meta-analysis. We defined light alcohol intake as one drink/day. The summary risk estimates were calculated by the random effects model. A dose-response analysis was also conducted for modeling the dose-risk relation. This meta-analysis confirmed an inverse association between alcohol consumption and thyroid cancer risk. Further studies are needed to better understand the potential mechanisms underlying this association.

01 February 2017 In Cancer

BACKGROUND We sought to determine by meta-analysis the relationship between drinking alcohol and the risk of gastric cancer.

MATERIAL AND METHODS A systematic Medline search was performed to identify all published reports of drinking alcohol and the associated risk of gastric cancer. Initially we retrieved 2,494 studies, but after applying inclusion and exclusion criteria, only ten studies were found to be eligible for our meta-analysis.

RESULTS Our meta-analysis showed that alcohol consumption elevated the risk of gastric cancer with an odds ratio (OR) of 1.39 (95% CI 1.20-1.61). Additionally, subgroup analysis showed that only a nested case-control report from Sweden did not support this observation. Subgroup analysis of moderate drinking and heavy drinking also confirmed that drinking alcohol increased the risk of gastric cancer. Publication bias analysis (Begg's and Egger's tests) showed p values were more than 0.05, suggesting that the 10 articles included in our analysis did not have a publication bias.

CONCLUSIONS The results from this meta-analysis support the hypothesis that alcohol consumption can increase the risk of gastric cancer; suggesting that effective moderation of alcohol drinking may reduce the risk of gastric cancer.

15 December 2016 In Drinking & Eating Patterns

PURPOSE: We seek answers to three questions about adolescent risk of starting to drink alcoholic beverages: (1) in new United States (US) data, can we reproduce a recently discovered female excess risk? (2) has a female excess risk emerged in European countries? and (3) might the size of country-level female-male differences (FMD) be influenced by macro-level gender equality and development processes?

METHODS: Estimates are from US and European surveys of adolescents, 2010-2014. For US estimates, newly incident drinking refers to consuming the first full drink during the 12-month interval just prior to assessment. For all countries, lifetime cumulative incidence of drinking refers to any drinking before assessment of the sampled 15-16 years.

RESULTS: Cumulative meta-analysis summary estimates from the US show a highly reproducible female excess in newly incident drinking among 12-17 years (final estimated female-male difference in risk, FMD = 2.1%; 95% confidence interval = 1.5%, 2.7%). Several European countries show female excess risk, estimated as lifetime cumulative incidence of drinking onsets before age 17 years. At the country level, the observed magnitude of FMD in risk is positively associated with the Gender Development Index (especially facets related to education and life expectancy of females relative to males), and with residence in a higher income European country.

CONCLUSIONS: New FMD estimates support reproducibility of a female excess risk in the US. In Europe, evidence of a female excess is modest. Educational attainment, life expectancies, and income merit attention in future FMD research on suspected macro-level processes that influence drinking onsets.

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