27 September 2019 In Cancer

BACKGROUND: Alcohol consumption is associated with increased risk of breast cancer; however, its association with subsequent risk of breast cancer death is unclear.

METHODS: We followed 4523 women with complete information on relevant risk factors for mortality; these women were 35 to 64 years of age when diagnosed with incident invasive breast cancer between 1994 and 1998. During follow up (median, 8.6 years), 1055 women died; 824 died from breast cancer. The information on alcohol consumption before diagnosis was collected shortly after breast cancer diagnosis (average: 5.1 months) during an in-person interview which used a structured questionnaire. Multivariable Cox proportional hazards regression models provided hazard ratios (HRs) and 95% confidence intervals (CIs) for breast cancer-specific mortality, mortality due to causes other than breast cancer, and all-cause mortality associated with alcohol consumption from age 15 years until breast cancer diagnosis and during recent periods of time prior to breast cancer diagnosis.

RESULTS: Average weekly alcohol consumption from age 15 years until breast cancer diagnosis was inversely associated with breast cancer-specific mortality (Ptrend = 0.01). Compared to non-drinkers, women in the highest average weekly alcohol consumption category (>/=7 drinks/week) had 25% lower risk of breast cancer-specific mortality (HR = 0.75, 95% CI = 0.56-1.00). Breast cancer mortality risk was also reduced among women in the highest average weekly alcohol consumption category in two recent time periods (5-year period ending 2-years prior to breast cancer diagnosis, HR = 0.74, 95% CI = 0.57-0.95; 2-year period immediately prior to breast cancer diagnosis: HR = 0.73, 95% CI = 0.56-0.95). Furthermore, analyses of average weekly alcohol consumption by beverage type from age 15 years until breast cancer diagnosis suggested that wine consumption was inversely associated with breast cancer-specific mortality risk (wine Ptrend = 0.06, beer Ptrend = 0.24, liquor Ptrend = 0.74). No association with any of these alcohol consumption variables was observed for mortality risk due to causes other than breast cancer.

CONCLUSIONS: Overall, we found no evidence that alcohol consumption before breast cancer diagnosis increases subsequent risk of death from breast cancer.

27 September 2019 In Cancer

Background: Alcohol intake is a leading modifiable cause related to cancer-specific deaths. Various alcohol intake patterns have shown to impact cancer progression differently, however, many studies only evaluated simplified patterns (such as heavy vs. non-heavy drinking) of alcohol intake for cancer survivors. The objective of this study is to provide population-based prevalence of the complex alcohol drinking patterns for cancer survivors, and compare it with that of non-cancer individuals. Additionally, we evaluated the impact of cancer related factors (binary, alcohol-related cancer type, and length of cancer history) to the alcohol intake patterns adjusted for the selected factors. Methods: A total of 193,197 individuals, including 16,504 cancer survivors, with age >/=18 years old in the 2012-2017 National Health Interview Survey (NHIS) were included in this study. The population-based prevalence of alcohol patterns was estimated. To evaluate cancer related factors associated with the alcohol intake patterns, we applied multinomial logistic models with the appropriate sampling weights and adjusted the selected demographic factors and smoking status. Results: There were 62.1% of cancer survivors and 66.0% of non-cancer individuals who were current alcohol drinkers in the past year. The prevalence of heavy drinking was identical for 5.2% of cancer and non-cancer individuals. For frequent binge drinking, cancer survivors tended to have less frequent binge than non-cancer individuals (2.8% vs. 4.9%). After adjusting for the selected demographic factors and smoking status, the cancer survivors were less likely to have the intermediate level of alcohol intake (light/moderate or occasional binge drinking) compared with non-cancer individuals, but no difference for the excessive alcohol intake (heavy or frequent binge drinking) was observed for those with and without cancer. As for cancer type, those with non-alcohol related cancer tended to be a current drinker compared with those with alcohol-related cancer. Compared with cancer survivors with a short cancer history (2-4 years), survivors with a cancer history of 5-9 years were more likely to be current drinkers after adjusting for the selected factors. Cancer status, alcohol-related cancer type and length of cancer history had no impact on excessive alcohol intake.

Conclusions: In summary, cancer survivors have similar excessive alcohol drinking patterns but were less likely to have the intermediate level of alcohol intake compared to non-cancer individuals. Alcohol intake may enhance cancer progression, interfere with cancer treatments and increase cancer-related mortality. To improve cancer survivors' health, custom alcohol interventions and cessation programs should be conducted to minimize alcohol intake for cancer survivors, especially for excessive alcohol drinkers.

12 August 2019 In Cancer

Background: Alcohol is classified as a Group 1 carcinogen by the International Agency for Research on Cancer because it induces hepatocellular carcinoma (among other cancers) in humans. An excessive alcohol intake may result in fatty liver, acute/chronic hepatitis, and cirrhosis and eventually lead to hepatocellular carcinoma. It has been reported that alcohol abuse increases the relative risk of hepatocellular carcinoma by 3- to 10-fold.

Aim and Methods: To clarify the known mechanisms of alcohol-related carcinogenesis, we searched Pubmed using the terms alcohol and immune mechanism, alcohol and cancer, and immune mechanism and cancer and summarized the articles as a qualitative review.

Results: From a clinical perspective, it is well known that alcohol interacts with other factors, such as smoking, viral hepatitis, and diabetes, leading to an increased risk of hepatocellular carcinoma. There are several possible mechanisms through which alcohol may induce liver carcinogenicity, including the mutagenic effects of acetaldehyde and the production of ROS due to the excessive hepatic deposition of iron. Furthermore, it has been reported that alcohol accelerates hepatitis C virus-induced liver tumorigenesis through TLR4 signaling. Despite intense investigations to elucidate the mechanisms, they remain poorly understood.

Conclusion: This review summarizes the recent findings of clinical and pathological studies that have investigated the carcinogenic effects of alcohol in the liver.

24 June 2019 In Cancer

Alcohol consumption is associated with higher risk of breast cancer (BC); however, the biological mechanisms underlying this association are not fully elucidated, particularly the extent to which this relationship is mediated by sex hormone levels. Circulating concentrations of estradiol, testosterone, their free fractions and sex-hormone binding globulin (SHBG), were examined in 430 incident BC cases and 645 matched controls among alcohol-consuming postmenopausal women nested within the European Prospective Investigation into Cancer and Nutrition. Mediation analysis was applied to assess whether individual hormone levels mediated the relationship between alcohol intake and BC risk. An alcohol-related hormonal signature, obtained by partial least square (PLS) regression, was evaluated as a potential mediator. Total (TE), natural direct and natural indirect effects (NIE) were estimated. Alcohol intake was positively associated with overall BC risk and specifically with estrogen receptor-positive tumors with respectively TE = 1.17(95%CI: 1.01,1.35) and 1.36(1.08,1.70) for a 1-standard deviation (1-SD) increase of intake. There was no evidence of mediation by sex steroids or SHBG separately except for a weak indirect effect through free estradiol where NIE = 1.03(1.00,1.06). However, an alcohol-related hormonal signature negatively associated with SHBG and positively with estradiol and testosterone was associated with BC risk (odds ratio [OR] = 1.25 [1.07,1.47]) for a 1-SD higher PLS score, and had a statistically significant NIE accounting for a mediated proportion of 24%. There was limited evidence of mediation of the alcohol-BC association by individual sex hormones. However, a hormonal signature, reflecting lower levels of SHBG and higher levels of sex steroids, mediated a substantial proportion of the association.

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