06 May 2014 In Cancer




BACKGROUND: It is well established that drinking alcohol raises the risk of liver cancer (hepatocellular carcinoma). However, it has not been sufficiently established as to whether or not drinking cessation subsequently reduces the risk of liver cancer and if it does reduce the risk how long it takes for this heightened risk to fall to that of never drinkers. This question is important for effective policy design and evaluation, to establish causality and for motivational treatments.

METHODS: A systematic review and meta-analysis using the current available evidence and a specific form of Generalised Least Squares is performed to assess how the risk of liver cancer changes with time for former drinkers.

RESULTS: Four studies are found to have quantified the effect of drinking cessation on the risk of liver cancer. The meta-analysis suggests that the risk of liver cancer does indeed fall after cessation by 6-7% a year, but there remains a large uncertainty around this estimate both statistically and in its interpretation. As an illustration it is estimated that a time period of 23 years is required after drinking cessation, with a correspondingly large 95% confidence interval of 14 to 70 years, for the risk of liver cancer to be equal to that of never drinkers.

CONCLUSION: This is a relatively under researched area and this is reflected in the uncertainty of the findings. It is our view that it is not possible to extrapolate the results found here to the general population. Too few studies have addressed this question and of the studies that have, all have significant limitations. The key issue amongst the relevant studies is that it appears that current drinkers, abstainers and former drinkers are not composed of, or effectively adjusted to be, similar populations making inferences about risk changes impossible. This is a very difficult area to study effectively, but it is an important topic. More work is required to reduce both statistical uncertainty and tackle the various study limitations this paper highlights and until this is done, the current result should be considered preliminary.




06 May 2014 In Cancer




INTRODUCTION: Epidemiological studies have shown that moderate alcohol drinkers have a lower death rate for all causes. Alcohol drinking has also been associated with reduced risk of non-Hodgkin lymphoma (NHL). Here, we examined the role of alcohol consumption on NHL survival by type of alcohol consumed and NHL subtype.

METHODS: A cohort of 575 female NHL incident cases diagnosed during 1996-2000 in Connecticut was followed-up for a median of 7.75 years. Demographic, clinical, and lifestyle information was collected at diagnosis. Survival analyses were conducted with Kaplan-Meier methods, and hazard ratios (HR) were estimated from Cox Proportional Hazards models.

RESULTS: Compared to never drinkers, wine drinkers experienced better overall survival (75% vs. 69% five-year survival rates, p-value for log-rank test = 0.030) and better disease free survival (70% vs. 67% five-year disease-free survival rates, p-value for log-rank test = 0.049). Analysis by NHL subtype shows that the favorable effect of wine consumption was mainly seen for patients diagnosed with diffuse large B-cell lymphoma (DLBCL) (wine drinkers for more than 25 years vs. never drinkers: HR = 0.36, 95% CI 0.14-0.94 for overall survival; HR = 0.38, 95% CI 0.16-0.94 for disease-free survival), and the adverse effect of liquor consumption was also observed among DLBCL patients (liquor drinkers vs. never drinkers: HR=2.49, 95% CI 1.26-4.93 for disease-free survival).

CONCLUSIONS: Our results suggest a moderate relationship between pre-diagnostic alcohol consumption and NHL survival, particularly for DLBCL. The results need to be replicated in larger studies.

IMPLICATIONS FOR CANCER SURVIVORS: Pre-diagnostic behaviors might impact the prognosis and survival of NHL patients.




06 May 2014 In Cancer




PURPOSE OF REVIEW: The data indicating that alcohol is an important factor increasing the risk to develop gastrointestinal cancer are consolidating. The purpose of this review is to summarize current evidence.

RECENT FINDINGS: Acetaldehyde is the first metabolite of ethanol metabolism and has direct carcinogenic and mutagenic effects by modifying DNA via generation of DNA adducts. Oxidative stress has a prominent role in triggering chronic inflammation and carcinogenesis through formation of reactive oxygen species. Recently published large prospective cohort studies with sufficient statistical power and meta-analyses could refine the knowledge regarding the impact of alcohol on gastrointestinal cancer. Functional genetic variants of alcohol-metabolizing enzymes proved to be associated with increased risk for esophageal and gastric cancer.The highest risk increase for malignancy was observed in the upper aerodigestive tract (oral cavity, pharynx, larynx) and esophagus (squamous cell carcinoma), weaker correlations were established regarding gastric, pancreatic, and colorectal neoplasias.

SUMMARY: Alcohol overconsumption is a serious avoidable risk factor for the development of gastrointestinal tract cancer, both alone but even more in combination with other risk factors such as tobacco and obesity.




06 May 2014 In Cancer




Alcohol consumption is postulated to be a risk factor for pancreatic cancer (PCA), but clarification of degree of risk related to consumption characteristics is lacking. We examined the association between alcohol consumption and PCA in a population-based case-control study (532 cases, 1,701 controls) in the San Francisco Bay Area. Population-based controls were frequency-matched by sex, age within 5-year categories and county of residence to cases identified by the cancer registry's rapid case ascertainment. Detailed alcohol consumption data, including binge drinking (>/=5 drinks/day), were collected during in-person interviews. Odds ratios (OR) and 95% confidence intervals (95% CI) were computed using adjusted unconditional logistic regression. Depending on dose, duration, and pattern of drinking, ORs were increased 1.5- to 6-fold among men but not women. In men, ORs increased with increasing overall alcohol consumption (22-35 drinks/week OR = 2.2, 95% CI = 1.1-4.0; >/=35 drinks/week OR = 2.6, 95% CI = 1.3-5.1, p-trend = 0.04). Most notable were effects with a history of binge drinking (OR = 3.5, 95% CI = 1.6-7.5) including increased number of drinks per day (p-trend = 0.002), and increased years of binge drinking (p-trend = 0.0006). In fully adjusted models that included smoking and other confounders, ORs for binge drinking in men were somewhat higher than in age-adjusted models. Results from our detailed analyses provide support for heavy alcohol consumption (including binge drinking) as a risk factor for PCA in men.




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