01 February 2017 In General Health

OBJECTIVE: To describe the volume and patterns of alcohol consumption up to and including 2012, and to estimate the burden of disease attributable to alcohol consumption as measured in deaths and disability-adjusted life years (DALYs) lost in the Americas in 2012.

METHODS: Measures of alcohol consumption were obtained from the World Health Organization (WHO) Global Information System on Alcohol and Health (GISAH). The burden of alcohol consumption was estimated in both deaths and DALYs lost based on mortality data obtained from WHO, using alcohol-attributable fractions. Regional groupings for the Americas were based on the WHO classifications for 2004 (according to child and adult mortality).

RESULTS: Regional variations were observed in the overall volume of alcohol consumed, the proportion of the alcohol market attributable to unrecorded alcohol consumption, drinking patterns, prevalence of drinking, and prevalence of heavy episodic drinking, with inhabitants of the Americas consuming more alcohol (8.4 L of pure alcohol per adult in 2012) compared to the world average. The Americas also experienced a high burden of disease attributable to alcohol consumption (4.7% of all deaths and 6.7% of all DALYs lost), especially in terms of injuries attributable to alcohol consumption.

CONCLUSIONS: Alcohol is consumed in a harmful manner in the Americas, leading to a high burden of disease, especially in terms of injuries. New cost-effective alcohol policies, such as increasing alcohol taxation, increasing the minimum legal age to purchase alcohol, and decreasing the maximum legal blood alcohol content while driving, should be implemented to decrease the harmful consumption of alcohol and the resulting burden of disease.

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.

17 May 2016 In Cancer

The objective of this study was to outline the biological pathways of alcohol-attributable breast cancer, the epidemiological risk relationship between alcohol consumption and breast cancer, and the global burden of breast cancer incidence and mortality attributable to alcohol consumption, with a focus on light drinking. First, the literature regarding the biological mechanisms of how alcohol affects the risk of breast cancer was reviewed and summarized. Second, a search of meta-analyses that evaluated the risk relationship between alcohol consumption and breast cancer was conducted. Last, the burden of alcohol-attributable breast cancer incidence and mortality was estimated by means of a Population-Attributable Fraction methodology. Data on alcohol consumption were obtained from the Global Information System on Alcohol and Health, and data on cancer incidence and mortality were obtained from the GLOBOCAN database. Alcohol consumption affects breast cancer risk through the alteration in hormone levels and the associated biological pathways, the metabolism of ethanol resulting in carcinogens, and the inhibition of the one carbon metabolism pathway. The systematic review found 15 meta-analyses on the risk relationship between alcohol consumption (also light consumption) and the risk of breast cancer. All but 2 of these analyses showed a dose-response relationship between alcohol consumption and the risk of breast cancer. An estimated 144,000 (95% confidence interval [CI]: 88,000 to 200,000) breast cancer cases and 38,000 (95% CI: 2,400 to 53,000) breast cancer deaths globally in 2012 were attributable to alcohol, with 18.8% of these cases and 17.5% of these deaths affecting women who were light alcohol consumers. All levels of evidence showed a risk relationship between alcohol consumption and the risk of breast cancer, even at low levels of consumption. Due to this strong relationship, and to the amount of alcohol consumed globally, the incidence of and mortality from alcohol-attributable breast cancer is large.

22 March 2016 In General Health

BACKGROUND: Pancreatitis is a highly prevalent medical condition associated with a spectrum of endocrine and exocrine pancreatic insufficiencies. While high alcohol consumption is an established risk factor for pancreatitis, its relationship with specific types of pancreatitis and a potential threshold have not been systematically examined.

METHODS: We conducted a systematic literature search for studies on the association between alcohol consumption and pancreatitis based on PRISMA guidelines. Non-linear and linear random-effect dose-response meta-analyses using restricted cubic spline meta-regressions and categorical meta-analyses in relation to abstainers were conducted.

FINDINGS: Seven studies with 157,026 participants and 3618 cases of pancreatitis were included into analyses. The dose-response relationship between average volume of alcohol consumption and risk of pancreatitis was monotonic with no evidence of non-linearity for chronic pancreatitis (CP) for both sexes (p = 0.091) and acute pancreatitis (AP) in men (p = 0.396); it was non-linear for AP in women (p = 0.008). Compared to abstention, there was a significant decrease in risk (RR = 0.76, 95%CI: 0.60-0.97) of AP in women below the threshold of 40 g/day. No such association was found in men (RR = 1.1, 95%CI: 0.69-1.74). The RR for CP at 100 g/day was 6.29 (95%CI: 3.04-13.02).

INTERPRETATION: The dose-response relationships between alcohol consumption and risk of pancreatitis were monotonic for CP and AP in men, and non-linear for AP in women. Alcohol consumption below 40 g/day was associated with reduced risk of AP in women. Alcohol consumption beyond this level was increasingly detrimental for any type of pancreatitis.

FUNDING: The work was financially supported by a grant from the National Institute on Alcohol Abuse and Alcoholism (R21AA023521) to the last author.

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