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.

05 December 2018 In Cancer
To investigate the association of alcohol intake with colorectal cancer risk by race/ethnicity as well as sex, lifestyle-related factors, alcoholic beverage type, and anatomical subsite, we analyzed data from 190,698 African Americans, Native Hawaiians, Japanese Americans, Latinos and whites in the Multiethnic Cohort Study, with 4,923 incident cases during a 16.7-year follow-up period (1993-2013). In multivariate Cox regression models, the hazard ratio (HR) was 1.16 (95% confidence interval (CI): 1.01, 1.34) for 15.029.9 g/day of alcohol and 1.28 (95% CI: 1.12, 1.45) for >/=30.0 g/day in men, and 1.06 (95% CI: 0.85, 1.32) and 1.15 (95% CI: 0.92, 1.43), respectively, in women, compared with nondrinkers (P for heterogeneity by sex = 0.74). An increased risk was apparent in Native Hawaiians, Japanese Americans, Latinos and whites, and in individuals with body mass index <25.0 kg/m2, never use of nonsteroidal anti-inflammatory drugs, and lower intake of dietary fiber and folate. Beer and wine, but not liquor, consumption was positively related to colorectal cancer risk. The association was stronger for rectum and left colon than right colon tumors. Our findings suggest that the positive association between alcohol and colorectal cancer varies by race/ethnicity, lifestyle factors, alcoholic beverage type, and anatomical subsite of tumors
29 October 2018 In Cancer

AIMS: The aim of this study was to clarify the relationship between drinking and metabolically healthy status in men with normal weight, overweight and obesity.

METHODS: The subjects were Japanese men aged from 35 to 60 years (n=31781) and they were divided by daily amount of drinking (g ethanol) into light (< 22), moderate (>/=22 and <44), heavy (>/=44 and <66) and very heavy (>/=66) drinkers. Metabolically healthy subjects were defined as those without hypertension, dyslipidemia and diabetes.

RESULTS: The percentage of metabolically healthy subjects was much lower in the overweight (BMI>/=25 and <30) and obese (BMI>/=30) groups than in the normal weight group (BMI>/=18.5 and <25) and was much lower in the obese group than in the overweight group. In each of the normal weight and overweight groups, percentages of metabolically healthy subjects were significantly lower in heavy and very heavy drinkers than in nondrinkers and were marginally significantly higher in light drinkers than in nondrinkers. The above associations between drinking and metabolically healthy status were confirmed by logistic regression analysis. In the obese group, the percentage of metabolically healthy subjects was significantly lower in regular drinkers (including all drinker categories) than in nondrinkers, and metabolically healthy subjects were rare (0.56%) among regular drinkers.

CONCLUSIONS: Regardless of absence and presence of overweight or obesity, excessive alcohol drinking is inversely associated with metabolically healthy status and should be avoided for prevention of cardiovascular disease.

29 October 2018 In Cancer

Epidemiological studies have been used to show associations between modifiable lifestyle habits and the incidence of breast cancer. Among such factors, a history of alcohol use has been reported in multiple studies and meta-analyses over the past decades. However, associative epidemiological studies that were interpreted as evidence that even moderate alcohol consumption increases breast cancer incidence have been controversial. In this review, we consider the literature on the relationship between moderate or heavy alcohol use, both in possible biological mechanisms and in variations in susceptibility due to genetic or epigenetic factors. We argue that there is a need to incorporate additional approaches to move beyond the associations that are reported in traditional epidemiological analyses and incorporate information on molecular pathologic signatures as a requirement to posit causal inferences. In particular, we point to the efforts of the transdisciplinary field of molecular pathological epidemiology (MPE) to evaluate possible causal relationships, if any, of alcohol consumption and breast cancer. A wider application of the principles of MPE to this field would constitute a giant step that could enhance our understanding of breast cancer and multiple modifiable risk factors, a step that would be particularly suited to the era of "personalized medicine".

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