06 May 2014 In Cancer

 

 

 

Despite numerous investigations, the correlation between alcohol consumption and prostate cancer risk remains uncertain. This report investigated the association between alcohol use and prostate cancer risk in a prospective cohort study of 294,707 US men aged 50-71 years in 1995-1996. Cox proportional hazards regression models with hazard ratios and 95% confidence intervals were adjusted for characteristics including age, race, body mass index, physical activity, and family history of prostate cancer, as well as testing for prostate-specific antigen and a digital rectal examination. There were 15,327 nonadvanced and 1,900 advanced prostate cancers identified through 2003 and 514 fatal cases through 2005. Risk of nonadvanced prostate cancer was 25% higher for men consuming >/=6 drinks daily (hazard ratio = 1.25, 95% confidence interval: 1.13, 1.37), 19% higher for men consuming 3-60% of respondents). The authors observed no association between alcohol intake and advanced prostate cancer and an inverse association with fatal prostate cancer among heavy drinkers. These findings suggest that higher alcohol consumption modestly increases nonadvanced prostate cancer risk.

 

 

 

06 May 2014 In Cancer

 

 

 

Study results on the association of alcohol consumption with breast cancer survival are inconsistent, partly due to the use of different survival outcomes. We assessed the association of pre-diagnostic alcohol consumption with survival and recurrence in a prospective cohort study in Germany including 2,522 postmenopausal breast cancer patients aged 50-74 years. Patients were diagnosed between 2001 and 2005 and vital status, causes of death, and recurrences were verified through the end of 2009. Cox proportional hazards models were stratified by age at diagnosis and study center and adjusted for relevant prognostic factors. Alcohol consumption was non-linearly associated with increased breast cancer-specific mortality [e.g., >/=12 vs. <0.5 g/day: hazard ratio (HR) = 1.74, 95 % confidence interval (CI): 1.13, 2.67]. Results were independent of estrogen receptor status. A non-significantly decreased risk of mortality due to other causes was found (>/=12 vs. <0.5 g/day: HR = 0.67, 95 % CI: 0.35, 1.29). Alcohol consumption was not associated with overall mortality (>/=12 vs. <0.5 g/day: HR = 1.28, 95 % CI: 0.90, 1.81) and breast cancer recurrence (>/=12 vs. <0.5 g/day: HR = 1.08, 95 % CI: 0.73, 1.58). In conclusion, our findings show that consumption of alcohol before diagnosis is non-linearly associated with increased breast cancer-specific mortality but may be associated with decreased risk of mortality due to other causes.

 

 

 

06 May 2014 In Cancer

 

 

 

Studies of the association between polyphenols dietary intake and breast cancer risk have been limited due to the lack of detailed food composition tables. In addition, none has examined this association according to alcohol intake, despite the facts that alcohol is an established risk factor for breast cancer and that the contribution of alcoholic beverages to polyphenol intake varies according to the level of alcohol consumption. Our objectives were (1) to estimate the associations between breast cancer risk and a wide range of dietary polyphenols using the recently published Phenol-Explorer database; and (2) to evaluate if/how alcohol intake modulates these relationships. 4,141 women from the SU.VI.MAX prospective cohort were followed from 1994 to 2007 (median followup: 12.6 years); 152 developed a first incident invasive primary breast cancer. Dietary intakes were assessed by repeated 24-h records. The Phenol-Explorer database was used to estimate polyphenol intake. Multivariable Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95 % confidence intervals (CIs) for quartiles of polyphenol intake. Analyses were stratified by median alcohol intake (< vs. >/= 6.5 g/d). In non-to-low alcohol drinkers, intakes of some classes of polyphenols were associated with decreased breast cancer risk: hydroxybenzoic acids (HR(Q4vsQ1) = 0.38, 95 % CI: 0.17-0.86, P (trend) = 0.005), flavonoids (0.35, 0.17-0.75, P (trend) = 0.02), flavonols (0.36, 0.18-0.74, P (trend) = 0.002), catechins (0.48, 0.22-1.05, P (trend) = 0.02), theaflavins (0.42, 0.19-0.93, P (trend) = 0.02), and proanthocyanidins (0.39, 0.18-0.84, P (trend) = 0.02). In contrast, in women with higher alcohol use, intakes of hydroxybenzoic acids (2.28, 1.16-4.49, P (trend) = 0.04), flavonoids (2.46, 1.23-4.92, P (trend) = 0.01), anthocyanins (2.94, 1.32-6.53, P (trend) = 0.01), catechins (2.28, 1.19-4.36, P (trend) = 0.02), and proanthocyanidins (2.98, 1.40-6.33, P (trend) = 0.006) were associated with increased breast cancer risk. In conclusion, this prospective study suggests that several classes of polyphenols could potentially contribute to breast cancer prevention among non-to-low alcohol drinkers, but some may increase breast cancer risk among women with higher alcohol intake.

 

 

 

06 May 2014 In Cancer

 

 

 

BACKGROUND: Barrett's esophagus (BE) is a precursor lesion of esophageal adenocarcinoma. Besides gastroesophageal reflux, possible risk factors for BE include overweight, cigarette smoking, and alcohol consumption. Our objective was to study these associations using prospective data.

METHODS: The prospective Netherlands Cohort Study, initiated in 1986, consists of 120,852 men and women, aged 55-69 years at baseline. At baseline, all subjects completed a questionnaire on dietary habits and lifestyle. After 16.3 years of follow-up, 370 BE cases with specialized intestinal metaplasia and 3866 subcohort members were available for case-cohort analysis. Cox proportional hazards models were used to calculate incidence rate ratios (RR) and 95% confidence intervals (CI).

RESULTS: Body mass index at baseline was associated with risk of BE in women [multivariable adjusted RR per 1 kg/m2, 1.07 (1.03-1.11)] but not in men [RR per 1 kg/m2, 0.99 (0.93-1.05)]. The association in women was not specifically due to abdominal overweight. Former cigarette smokers were at increased risk of BE (RR=1.33, 95% CI 1.00-1.77), but current smokers were not. Smoking duration showed a positive association with BE risk (p trend=0.03). For alcohol consumption, the RR per 10 grams ethanol/day was 0.95 (0.87-1.03).

CONCLUSIONS: Increased body mass index was a risk factor for BE in women, but not in men. Several aspects of cigarette smoking were positively associated with BE risk. Alcohol consumption was not associated with an increased risk of BE.Impact: Future research should focus on risk factors for development as well as for progression of BE to esophageal adenocarcinoma.

 

 

 

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