05 December 2018 In Cancer

Alcohol has consistently been shown to increase breast cancer (BC) risk. This association may be modified by single nucleotide polymorphisms in alcohol dehydrogenase isoenzymes ADH1B and ADH1C. The Netherlands Cohort Study comprises 62 573 women, aged 55-69 years at baseline (1986). Follow-up for postmenopausal BC for 20.3 years was available. Genotyping of 6 tag SNPs in ADH1B and ADH1C, respectively, was performed on DNA from toenails. A case-cohort approach was used for analysis (complete data available for: nsubcohort= 1301; ncases= 1630). Cox regression models for postmenopausal BC were applied to determine marginal effects of alcohol intake and SNPs using a dominant genetic model, as well as multiplicative interaction of the two. Results were also obtained for subtypes by estrogen (ER) and progesterone receptor (PR) status. Multiple testing was adjusted for by applying the false discovery rate (FDR). Alcohol intake (categorical) increased the risk of postmenopausal BC (ptrend=0.031). Trends for ER and PR subgroups followed a similar pattern. Continuous modelling of alcohol resulted in a hazard rate ratio (HR) for overall postmenopausal BC of 1.09 (95% CI: 1.01 - 1.19) per 10g/d of alcohol. SNPs were not associated with BC risk. No effect modification of the alcohol-BC association by SNP genotype was seen after FDR-correction in overall BC and ER/PR subgroups. In conclusion, alcohol was shown to increase the risk of postmenopausal BC. This association was not significantly modified by common ADH1B and ADH1C SNPs, neither in overall BC nor in hormone receptor defined subtypes.

27 September 2018 In Drinking Patterns

BACKGROUND AND AIMS: Studies examining the next-day cognitive effects of heavy alcohol consumption have produced mixed findings, which may reflect inconsistencies in definitions of 'hangover'. Recent consensus has defined hangover as 'mental and physical symptoms, experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration (BAC) approaches zero'. In light of this, we aimed to review the literature systematically to evaluate and estimate mean effect sizes of the next-day effects of heavy alcohol consumption on cognition.

METHODS: Embase, PubMed and PsycNET databases were searched between December 2016 and May 2018 using terms based on 'alcohol' and 'hangover'. Studies of experimental designs which reported the next-day cognitive effects of heavy alcohol consumption in a 'hangover' group with BAC < 0.02% were reviewed. A total of 805 articles were identified. Thirty-nine full-text articles were screened by two independent reviewers and 19 included in the systematic review; 11 articles provided sufficient data to be included in the meta-analysis; 1163 participants across 19 studies conducted since 1970 were included in the analysis. Data for study design, hangover severity, BAC at testing and cognitive performance were extracted and effect estimates calculated.

RESULTS: The systematic review suggested that sustained attention and driving abilities were impaired during hangover. Mixed results were observed for: psychomotor skills, short- (STM) and long-term memory (LTM) and divided attention. The meta-analysis revealed evidence of impairments in STM [g = 0.64, 95% confidence interval (CI) = 0.15-1.13], LTM (Hedges' g = 0.59, 95% CI = 0.01-1.17) sustained attention (g = 0.47, 95% CI = 0.07-0.87) and psychomotor speed (Hedges' g = 0.66, 95% CI = 0.31-1.00) during alcohol hangover.

CONCLUSION: The research literature suggests that alcohol hangovers may involve impaired cognitive functions and performance of everyday tasks such as driving.

27 July 2018 In Social and Cultural Aspects

Young people frequently display alcohol-related posts ("alcoholposts") on social networking sites such as Facebook and Instagram. Although evidence exists that such posts may be linked with increases in alcohol consumption, hardly any studies have focused on the content of such posts. This study addresses this gap by applying and extending the alcoholpost-typology previously proposed by Hendriks, Gebhardt, and van den Putte. A content analysis assessed the extent to which alcoholposts were displayed on Facebook and/or Instagram profiles of young participants (12-30 years; N = 192), and which type of alcoholpost these posts most strongly resembled. Moderate alcoholposts (e.g., in which alcohol was in the background) were most often posted. At times, textual alcoholposts and commercial alcoholposts were also displayed; however, extreme posts (e.g., about drunk people or drinking-games) were almost nonexistent. These findings confirm the previous results by Hendriks et al. that moderate posts are more frequently posted than extreme posts. This could imply that positive associations with alcohol consumption are more visible on social media than negative associations, potentially leading to an underestimation of alcohol-related risks.

27 July 2018 In Cardiovascular System

OBJECTIVE: To investigate the association between alcohol consumption (at baseline and over lifetime) and non-fatal and fatal coronary heart disease (CHD) and stroke.

DESIGN: Multicentre case-cohort study.

SETTING: A study of cardiovascular disease (CVD) determinants within the European Prospective Investigation into Cancer and nutrition cohort (EPIC-CVD) from eight European countries.

PARTICIPANTS: 32 549 participants without baseline CVD, comprised of incident CVD cases and a subcohort for comparison.

MAIN OUTCOME MEASURES: Non-fatal and fatal CHD and stroke (including ischaemic and haemorrhagic stroke).

RESULTS: There were 9307 non-fatal CHD events, 1699 fatal CHD, 5855 non-fatal stroke, and 733 fatal stroke. Baseline alcohol intake was inversely associated with non-fatal CHD, with a hazard ratio of 0.94 (95% confidence interval 0.92 to 0.96) per 12 g/day higher intake. There was a J shaped association between baseline alcohol intake and risk of fatal CHD. The hazard ratios were 0.83 (0.70 to 0.98), 0.65 (0.53 to 0.81), and 0.82 (0.65 to 1.03) for categories 5.0-14.9 g/day, 15.0-29.9 g/day, and 30.0-59.9 g/day of total alcohol intake, respectively, compared with 0.1-4.9 g/day. In contrast, hazard ratios for non-fatal and fatal stroke risk were 1.04 (1.02 to 1.07), and 1.05 (0.98 to 1.13) per 12 g/day increase in baseline alcohol intake, respectively, including broadly similar findings for ischaemic and haemorrhagic stroke. Associations with cardiovascular outcomes were broadly similar with average lifetime alcohol consumption as for baseline alcohol intake, and across the eight countries studied. There was no strong evidence for interactions of alcohol consumption with smoking status on the risk of CVD events.

CONCLUSIONS: Alcohol intake was inversely associated with non-fatal CHD risk but positively associated with the risk of different stroke subtypes. This highlights the opposing associations of alcohol intake with different CVD types and strengthens the evidence for policies to reduce alcohol consumption.

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