06 May 2014 In Cancer

 

 

 

BACKGROUND: In the Bagnardi et al. (2001) meta-analysis, it was found that alcohol consumption increases the risk of stomach cancer (OR = 1.32 for heavy drinkers). However, it is unknown if drinking cessation reverses this alcohol-elevated risk. METHODS: A systematic literature review was performed to provide the information for a meta-analysis where the dose-risk trend was estimated for years since drinking cessation and the risk of stomach cancer. A random effect generalised least squares model for trend estimation was used, employing study characteristics to control for heterogeneity. RESULTS: Nineteen observational studies were identified in the literature review, of which five studies quantified duration of cessation and risk of stomach cancer, giving a total of 1947 cancer cases. No significant effect of drinking cessation on the risk of stomach cancer could be found (OR = 0.99 CI: 0.97-1.02). CONCLUSIONS: This result should be interpreted with caution due to the limited number of studies in this area. Recent findings suggest a link between heavy drinking and stomach cancer, especially gastric noncardia, but not for moderate drinking. Since all but one of the included studies in this meta-analysis failed to control for consumption level, the current study could not test if the risk decline following drinking cessation differs between moderate and high consumers.

 

 

 

06 May 2014 In Cancer

 

 

 

BACKGROUND: Increased exposure to endogenous estrogen and/or insulin may partly explain the relationship of obesity, physical inactivity, and alcohol consumption and postmenopausal breast cancer. However, these potential mediating effects have not been formally quantified in a survival analysis setting. METHODS: We combined data from two case-cohort studies based in the Women's Health Initiative-Observational Study with serum estradiol levels, one of which also had insulin levels. A total of 1,601 women (601 cases) aged 50 to 79 years who were not using hormone therapy at enrollment were included. Mediating effects were estimated by applying a new method based on the additive hazard model. RESULTS: A five-unit increase in body mass index (BMI) was associated with 50.0 [95% confidence interval (CI), 23.2-76.6] extra cases per 100,000 women at-risk per year. Of these, 23.8% (95% CI, 2.9-68.4) could be attributed to estradiol and 65.8% (95% CI, 13.6-273.3) through insulin pathways. The mediating effect of estradiol was greater (48.8%; 95% CI, 18.8-161.1) for BMI when restricted to estrogen receptor positive (ER(+)) cases. Consuming 7+ drinks/wk compared with abstinence was associated with 164.9 (95% CI, 45.8-284.9) breast cancer cases per 100,000, but no significant contribution from estradiol was found. The effect of alcohol on breast cancer was restricted to ER(+) breast cancers. CONCLUSIONS: The relation of BMI with breast cancer was partly mediated through estradiol and, to a greater extent, through insulin. Impact: The findings provide support for evaluation of interventions to lower insulin and estrogen levels in overweight and obese postmenopausal women to reduce breast cancer risk.

Cancer Epidemiol Biomarkers Prev; 21(7); 1203-12. (c)2012 AACR

 

 

 

06 May 2014 In Cancer

 

 

 

Colorectal cancer is a major cause of cancer mortality and is considered to be largely attributable to inappropriate lifestyle and behavior patterns. The purpose of this review was to undertake a comparison of the strength of the associations between known and putative risk factors for colorectal cancer by conducting 10 independent meta-analyses of prospective cohort studies. Studies published between 1966 and January 2008 were identified through EMBASE and MEDLINE, using a combined text word and MESH heading search strategy. Studies were eligible if they reported estimates of the relative risk for colorectal cancer with any of the following: alcohol, smoking, diabetes, physical activity, meat, fish, poultry, fruits and vegetables. Studies were excluded if the estimates were not adjusted at least for age. Overall, data from 103 cohort studies were included. The risk of colorectal cancer was significantly associated with alcohol: individuals consuming the most alcohol had 60% greater risk of colorectal cancer compared with non- or light drinkers (relative risk 1.56, 95% CI 1.42-1.70). Smoking, diabetes, obesity and high meat intakes were each associated with a significant 20% increased risk of colorectal cancer (compared with individuals in the lowest categories for each) with little evidence of between-study heterogeneity or publication bias. Physical activity was protective against colorectal cancer. Public-health strategies that promote modest alcohol consumption, smoking cessation, weight loss, increased physical activity and moderate consumption of red and processed meat are likely to have significant benefits at the population level for reducing the incidence of colorectal cancer.

 

 

 

06 May 2014 In Cancer

 

 

 

Results from epidemiological studies suggest that alcohol drinkers have a decreased risk of lymphoid neoplasms, whereas results for myeloid neoplasms are inconsistent. However, most of these studies have used retrospective data. We examined prospectively whether alcohol consumption decreases the risk of both lymphoid and myeloid neoplasms, including most common subtypes. Moreover, we investigated whether this decreased risk is due to ethanol or other contents of specific alcoholic beverages (i.e., beer, wine and liquor). The Netherlands cohort study consisted of 120,852 individuals who completed a baseline questionnaire in 1986. After 17.3 years of follow-up, 1,375 cases of lymphoid and 245 cases of myeloid neoplasms with complete exposure information were available for analysis. Compared with abstinence, we observed for plasma cell neoplasms hazard rate ratios (HR) of 1.66 (95% confidence interval (CI), 1.21-2.29), 1.63 (95% CI, 1.17-2.27), 1.11 (95% CI, 0.75-1.64) and 0.85 (95% CI, 0.51-1.42) with daily ethanol consumption of 0.1-<5, 5-<15, 15-/=30 g, respectively. A similar pattern was observed for chronic lymphocytic leukemia/small lymphocytic lymphoma. No associations were observed for other subtypes and for myeloid neoplasms. When results were analyzed by beverage type, no clear associations were observed. In conclusion, our study did not show an inverse association between alcohol consumption and lymphoid neoplasms. Also, no inverse association was observed with myeloid neoplasms. If any association between alcohol consumption and lymphoid neoplasms exists, our study suggests an increased risk rather than a decreased risk.

 

 

 

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