@article{Wills2017,
title = {Phenotypic and Genetic Relationship Between BMI and Drinking in a Sample of UK Adults},
author = {AG Wills, LM Evans, C Hopfer C},
url = {https://www.ncbi.nlm.nih.gov/pubmed/?term=Phenotypic+and+Genetic+Relationship+Between+BMI+and+Drinking+in+a+Sample+of+UK+Adults},
year = {2017},
date = {2017-02-25},
journal = {Behaviour Genetics},
abstract = {The health impairments derived from both alcoholism and obesity are well known. However, reports that relate increased alcohol use with increased measures of obesity have been mixed in their findings, especially with respect to genetic factors that could potentially link these two behaviors. Here, using a large sample of adults from the UK (n ≈ 113,000), we report both the observed and genetic correlations between BMI (kg/m2) and two measures of alcohol use: reported quantity (drinks per week) and frequency of use (from never to daily). Overall, both observationally and genetically, alcohol intake is negatively correlated with BMI. Phenotypic correlations ranged from -0.01 to -0.17, and genetic correlations ranged from -0.1 to -0.4. Genetic correlations tended to be stronger than the phenotypic correlations, and these correlations were stronger in females and between BMI and, specifically, frequency of use. Though the mechanisms driving these relationships are yet to be identified, we can conclude that the genetic factors related to drinking both more and more often are shared with those responsible for lower BMI.},
keywords = {alcohol, BMI, Drinking},
pubstate = {published},
tppubtype = {article}
}

@article{Beasley2016,
title = {Is alcohol consumption related to likelihood of reporting chronic widespread pain in people with stable consumption? Results from UK Biobank.},
author = {MJ Beasley, TV Macfarlane, GJ Macfarlane},
url = {http://www.ncbi.nlm.nih.gov/pubmed/27437785},
year = {2016},
date = {2016-07-19},
journal = {Pain },
abstract = {Studies have suggested alcohol consumption is strongly related to reduced reporting of chronic widespread pain (CWP) and level of disability in people with CWP or fibromyalgia. Direction of causality has not been established, that is whether the association is due to people's health influencing their alcohol consumption or vice versa. UK Biobank recruited over 500,000 people aged 40-69 years registered at medical practices nationwide. Participants provided detailed information on health and lifestyle factors including pain and alcohol consumption. Total units consumed per week was calculated for current drinkers. Information was also collected on changes in alcohol consumption and reasons for such changes. Analysis was by logistic regression expressed as odds ratios (ORs) with 95% confidence intervals (CIs), then adjusted for a large number of potential confounding factors (adjORs). In males who reported drinking the same as 10 years previously, there was a U-shaped relationship between amount drunk and odds of reporting CWP (non-drinkers CWP prevalence 2.4%, 19.1-32.1 units/wk 0.4%, >53.6 units/wk 1.0%; adjORs 2.53 95% CI [1.78-3.60] vs 1 vs 1.52 [1.05-2.20]). In females there was a decrease in proportion reporting CWP up to the modal category of alcohol consumption with no further change in those drinking more (non-drinkers CWP prevalence 3.4%, 6.4-11.2 units/wk 0.7%, >32.1 units/wk 0.7%; adjORs 2.11 [1.67-2.66] vs 1 vs 0.86 [0.54-1.39]). This large study has shown a clear relationship between alcohol consumption and reporting of pain even in people who had not reported changing consumption due to health concerns, after adjustment for potential confounding factors.},
keywords = {1144, alcohol, pain},
pubstate = {published},
tppubtype = {article}
}

@article{Dawes2014b,
title = {Cigarette Smoking, Passive Smoking, Alcohol Consumption, and Hearing Loss},
author = {Piers Dawes and Karen J. Cruickshanks and David R. Moore and Mark Edmondson-Jones and Abby McCormack and Heather Fortnum and Kevin J. Munro},
url = {http://link.springer.com/article/10.1007/s10162-014-0461-0},
year = {2014},
date = {2014-05-28},
journal = {Journal of the Association for Research in Otolaryngology},
volume = {15},
number = {4},
pages = {663-674},
abstract = {The objective of this large population-based cross-sectional study was to evaluate the association between smoking, passive smoking, alcohol consumption, and hearing loss. The study sample was a subset of the UK Biobank Resource, 164,770 adults aged between 40 and 69 years who completed a speech-in-noise hearing test (the Digit Triplet Test). Hearing loss was defined as speech recognition in noise in the better ear poorer than 2 standard deviations below the mean with reference to young normally hearing listeners. In multiple logistic regression controlling for potential confounders, current smokers were more likely to have a hearing loss than non-smokers (odds ratio (OR) 1.15, 95 % confidence interval (CI) 1.09–1.21). Among non-smokers, those who reported passive exposure to tobacco smoke were more likely to have a hearing loss (OR 1.28, 95 %CI 1.21–1.35). For both smoking and passive smoking, there was evidence of a dose-response effect. Those who consume alcohol were less likely to have a hearing loss than lifetime teetotalers. The association was similar across three levels of consumption by volume of alcohol (lightest 25 %, OR 0.61, 95 %CI 0.57–0.65; middle 50 % OR 0.62, 95 %CI 0.58–0.66; heaviest 25 % OR 0.65, 95 %CI 0.61–0.70). The results suggest that lifestyle factors may moderate the risk of hearing loss. Alcohol consumption was associated with a protective effect. Quitting or reducing smoking and avoiding passive exposure to tobacco smoke may also help prevent or moderate age-related hearing loss},
keywords = {alcohol, hearing, lung, smoking},
pubstate = {published},
tppubtype = {article}
}