25 August 2020 In Cancer

Alcohol drinking is a risk factor for cancer. The degree of risk is increased in subjects showing the flushing response, which is due to aldehyde dehydrogenase 2 (ALDH2) polymorphism. The attributable risk of alcohol drinking for cancer in Japan has not been sufficiently investigated with consideration of flushing response. We followed 78,825 Japanese in JPHC study cohort II. The association between alcohol consumption and cancer incidence was assessed according to self-reported flushing response using Cox proportional hazards regression models.

The population-attributable fraction (PAF) of cancer incidence was also estimated. During 1993-2013 (average follow-up, 16.8 years), 8486 incident cancers (included 4386 alcohol-related cancers) were reported. Half of men and 36% of women had flushing response. In men with flushing response, moderate or higher alcohol drinking increased the risk of alcohol-related cancers compared with non-drinkers (150-299 g/week, HR 1.63, 95% CI, 1.43-1.99; 300-449 g/week, HR 2.02 95% CI, 1.67-2.44; >/=450 g/week, HR 1.75, 95% CI, 1.39-2.21).

When flushing response was considered in comparisons between non-drinkers and non-flushers, non-flushing heavy drinkers had a slightly higher PAF than flushers (all cancers: flushers, 2.0% and non-flushers, 2.2%; alcohol-related cancers: flushers, 3.8% and non-flushers, 5.8%).

Although the risk of alcohol-related cancer in men with flushing response increased with increasing alcohol consumption, heavy drinkers were also at high risk regardless of flushing response. Considering the PAF of alcohol consumption on cancer, efforts to discourage heavy alcohol consumption to reduce the incidence of alcohol-related cancers appear warranted regardless of flushing response.

04 May 2020 In Cardiovascular System

BACKGROUND/AIM: The association between alcohol consumption and subclinical atherosclerosis is still unclear. Using data from a European multicentre study, we assess subclinical atherosclerosis and its 30-month progression by carotid intima-media thickness (C-IMT) measurements, and correlate this information with self-reported data on alcohol consumption.

METHODS: Between 2002-2004, 1772 men and 1931 women aged 54-79 years with at least three risk factors for cardiovascular disease (CVD) were recruited in Italy, France, Netherlands, Sweden, and Finland. Self-reported alcohol consumption, assessed at baseline, was categorized as follows: none (0 g/d), very-low (0 - 5 g/d), low (> 5 to 10 to 10 to 20 g/d for women, > 30 g/d for men). C-IMT was measured in millimeters at baseline and after 30 months. Measurements consisted of the mean and maximum values of the common carotids (CC), internal carotid artery (ICA), and bifurcations (Bif) and whole carotid tree. We used quantile regression to describe the associations between C-IMT measures and alcohol consumption categories, adjusting for sex, age, physical activity, education, smoking, diet, and latitude.

RESULTS: Adjusted differences between median C-IMT values in different levels of alcohol consumption (vs. very-low) showed that moderate alcohol consumption was associated with lower C-IMTmax[- 0.17(95%CI - 0.32; - 0.02)], and Bif-IMTmean[- 0.07(95%CI - 0.13; - 0.01)] at baseline and decreasing C-IMTmean[- 0.006 (95%CI - 0.011; - 0.000)], Bif-IMTmean[- 0.016(95%CI - 0.027; - 0.005)], ICA-IMTmean[- 0.009(95% - 0.016; - 0.002)] and ICA-IMTmax[- 0.016(95%: - 0.032; - 0.000)] after 30 months. There was no evidence of departure from linearity in the association between alcohol consumption and C-IMT.

CONCLUSION: In this European population at high risk of CVD, findings show an inverse relation between moderate alcohol consumption and carotid subclinical atherosclerosis and its 30-month progression, independently of several potential confounders.

27 March 2020 In Cancer

Alcohol drinking is a risk factor for cancer. The degree of risk is increased in subjects showing the flushing response, which is due to aldehyde dehydrogenase 2 (ALDH2) polymorphism. The attributable risk of alcohol drinking for cancer in Japan has not been sufficiently investigated with consideration of flushing response. We followed 78,825 Japanese in JPHC study cohort II. The association between alcohol consumption and cancer incidence was assessed according to self-reported flushing response using Cox proportional hazards regression models. The population-attributable fraction (PAF) of cancer incidence was also estimated. During 1993-2013 (average follow-up, 16.8 years), 8486 incident cancers (included 4386 alcohol-related cancers) were reported. Half of men and 36% of women had flushing response. In men with flushing response, moderate or higher alcohol drinking increased the risk of alcohol-related cancers compared with non-drinkers (150-299 g/week, HR 1.63, 95% CI, 1.43-1.99; 300-449 g/week, HR 2.02 95% CI, 1.67-2.44; >/=450 g/week, HR 1.75, 95% CI, 1.39-2.21). When flushing response was considered in comparisons between non-drinkers and non-flushers, non-flushing heavy drinkers had a slightly higher PAF than flushers (all cancers: flushers, 2.0% and non-flushers, 2.2%; alcohol-related cancers: flushers, 3.8% and non-flushers, 5.8%). Although the risk of alcohol-related cancer in men with flushing response increased with increasing alcohol consumption, heavy drinkers were also at high risk regardless of flushing response. Considering the PAF of alcohol consumption on cancer, efforts to discourage heavy alcohol consumption to reduce the incidence of alcohol-related cancers appear warranted regardless of flushing response.

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