Prospective study of breast cancer in relation to coffee,tea and caffeine in Sweden

Studies of coffee and tea consumption and caffeine intake as risk factors for breast cancer are inconclusive. We assessed coffee and tea consumption, caffeine intake, and possible confounding factors among 42,099 women from the Swedish Women's Lifestyle and Health study, the participants of which were aged 30–49 years at enrollment in 1991–1992. Complete follow‐up for breast cancer incidence was performed through 2012 via linkage to national registries. Poisson regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CIs) for breast cancer. During follow‐up 1,395 breast cancers were diagnosed. The RR was 0.97 (95% CI 0.94–0.99) for a 1‐unit increase in cups of coffee/day, 1.14 (95% CI 1.05–1.24) for a 1‐unit increase in cups of tea/day, and 0.97 (95% CI 0.95–1.00) for a 100 mg/day increase in caffeine intake. Although the RR for no consumption (RR = 0.86, 95% CI 0.69–1.08), a group with a relatively small number of women, was not statistically significant, women with higher consumption had a decreased breast cancer risk (3–4 cups/day: RR = 0.87, 95% CI 0.76–1.00; ≥5 cups/day: RR = 0.81, 95% CI 0.70–0.94) compared to women consuming 1–2 cups of coffee/day. Compared to no consumption, women consuming >1 cups tea/day showed an increased breast cancer risk (RR = 1.19, 95% CI 1.00–1.42). Similar patterns of estimates were observed for breast cancer risk overall, during pre‐ and postmenopausal years, and for ER+ or PR+ breast cancer, but not for ER? and PR? breast cancer. Our findings suggest that coffee consumption and caffeine intake is negatively associated with the risk of overall and ER+/PR? breast cancer, and tea consumption is positively associated with the risk of overall and ER+/PR+ breast cancer.     

Alcohol consumption and incidence of benign breast disease.

We evaluated whether moderate alcohol consumption is associated with increased risk of developing benign breast disease (BBD), a potential "precursor" or marker for breast cancer development. This study evaluated associations between reported alcohol consumption and BBD diagnosis among 75,826 women in the Nurses' Health Study II. Between 1989 and 1997, 16,035 women reported a first diagnosis of BBD (317/10,000 person-years), of which 2,999 diagnoses were confirmed by tissue biopsy (59/10,000 person-years). Of the pathology specimens reviewed, 532 were nonproliferative benign breast conditions, and 932 were proliferative conditions. Person-time models provided estimates of the rate ratio (RR) and 95% confidence interval (CI). Reported recent adult consumption of alcohol was not associated with increased BBD incidence. Compared with women who did not drink alcohol, the age- and body mass index (BMI)-adjusted RRs for any reported BBD were 0.98 (95% CI, 0.95-1.02) for those who consumed <5 g/day, 0.93 (95% CI, 0.89-0.98) for those who consumed 5-14.9 g/day, and 0.90 (95% CI, 0.83-0.98) for those who consumed >or=15 g/day. The adjusted RRs for biopsy confirmed BBD and any proliferative benign condition were similiar. However, reported alcohol consumption of >or=15 g/day between ages 18 and 22 years was associated with higher rates of biopsy-confirmed BBD (age- and body mass index-adjusted RR = 1.14; 95% CI, 1.00-1.30), nonproliferative BBD (RR = 1.46; 95% CI, 1.09-1.96), and any proliferative BBD (RR = 1.33; 95% CI, 1.05-1.69), but not atypical hyperplasia. In this study, recent alcohol consumption was associated with slightly lower rates of reported BBD. However, greater alcohol consumption earlier in life (ages 18-22 years) was associated with higher proliferative BBD rates, suggesting that timing of exposure may be relevant to disease incidence.     

Coffee, tea, caffeine and risk of breast cancer: a 22-year follow-up

The relation between consumption of coffee, tea and caffeine and risk of breast cancer remains unsettled. We examined data from a large, long-term cohort study to evaluate whether high intake of coffee and caffeine is associated with increased risk of breast cancer. This was a prospective cohort study with 85,987 female participants in the Nurses' Health Study. Consumption of coffee, tea and caffeine consumption was assessed in 1980, 1984, 1986, 1990, 1994, 1998 and the follow-up continued through 2002. We documented 5,272 cases of invasive breast cancer during 1,715,230 person-years. The multivariate relative risks (RRs) of breast cancer across categories of caffeinated coffee consumption were: 1.0 for <1 cup/month (reference category), 1.01 (95% confidence interval: 0.92-1.12) for 1 month to 4.9 week, 0.92 (0.84-1.01) for 5 week to 1.9 days, 0.93 (0.85-1.02) for 2-3.9 days, 0.92 (0.82-1.03) for >or=4 cups per day (p for trend = 0.14). Intakes of tea and decaffeinated coffee were also not significantly associated with risk of breast cancer. RRs (95% CI) for increasing quintiles of caffeine intake were 1.00, 0.98 (0.90-1.07), 0.92 (0.84-1.00), 0.94 (0.87-1.03) and 0.93 (0.85-1.01) (p for trend = 0.06). A significant inverse association of caffeine intake with breast cancers was observed among postmenopausal women; for the highest quintile of intake compared to the lowest RR 0.88 (95% CI = 0.79-0.97, p for trend = 0.03). We observed no substantial association between caffeinated and decaffeinated coffee and tea consumption and risk of breast cancer in the overall cohort. However, our results suggested a weak inverse association between caffeine-containing beverages and risk of postmenopausal breast cancer.     

Coffee consumption and risk of colorectal cancer: A systematic review and meta‐analysis of prospective cohort studies

An inverse association between coffee consumption and the risk of colorectal cancer has been found in several case‐control studies, but such an association was not consistent in prospective cohort studies. We conducted a systematic meta‐analysis of prospective cohort studies on coffee consumption and colorectal cancer published up to June 2008. We combined relative risks (RR) for colorectal cancer comparing high vs. low categories of coffee consumption using random‐effects models. We identified 12 eligible cohort studies, which included 646,848 participants and 5,403 cases for colorectal cancer. The summarized result of the meta‐analysis comparing high‐ vs. low‐consumption categories showed no significant effect of coffee consumption on colorectal cancer risk (RR = 0.91; 95% confidence intervals [CI]: 0.81–1.02). The RR was 0.93 (95% CI: 0.71–1.22) when considering 4 studies conducted in the United States of America, 0.91 (95% CI: 0.76–1.10) for 5 studies from Europe, and 0.83 (95% CI: 0.62–1.10) for 3 Japanese studies. No significant differences by sex and cancer‐site were found, but there was a slight suggestion of an inverse association between coffee consumption and colon cancer in women (RR = 0.79; 95% CI: 0.60–1.04), especially Japanese women (RR = 0.62; 95% CI: 0.37–1.05). The suggestive inverse associations were slightly stronger in studies that controlled for smoking and alcohol, and in studies with shorter follow‐up times. Information on coffee type, its serving size, or brewing method may provide a better understanding of this reassuring result and the real role of coffee on colorectal cancer risk. © 2008 Wiley‐Liss, Inc.     

Effects of α‐tocopherol and β‐carotene supplementation on cancer incidence and mortality: 18‐Year postintervention follow‐up of the Alpha‐Tocopherol,Beta‐Carotene Cancer Prevention Study

In the Alpha‐Tocopherol, Beta‐Carotene Cancer Prevention Study among 29,133 Finnish male smokers aged 50–69 years, daily α‐tocopherol (50 mg) for a median of 6.1 years decreased the risk of prostate cancer, whereas β‐carotene (20 mg) increased risk of lung cancer and overall mortality. To determine the postintervention effects of α‐tocopherol and β‐carotene, 25,563 men were followed 18 years for cancer incidence and all causes of mortality through national registers. Neither supplement had significant effects on post‐trial cancer incidence. Relative risk (RR) for lung cancer (n = 2,881) was 1.04 (95% confidence interval [CI], 0.96–1.11) among β‐carotene recipients compared with nonrecipients. For prostate cancer (n = 2,321), RR was 0.97 (95% CI, 0.89–1.05) among α‐tocopherol recipients compared with nonrecipients with the preventive effect of α‐tocopherol continuing ～8 years postintervention. Body mass index significantly modified the effect of α‐tocopherol on prostate cancer (p for interaction = 0.01) RR 1.00 (95% CI, 0.88–1.14) in normal‐weight men, 0.87 (95% CI, 0.77–0.98) in overweight men, and 1.25 (95% CI, 1.01–1.55) in obese men. The post‐trial relative mortality (based on 16,686 deaths) was 1.02 (95% CI, 0.98–1.05) for α‐tocopherol recipients compared with nonrecipients and 1.02 (95% CI, 0.99–1.05) for β‐carotene recipients compared with nonrecipients. α‐Tocopherol decreased post‐trial prostate cancer mortality (RR, 0.84; 95% CI, 0.70–0.99), whereas β‐carotene increased it (RR, 1.20; 95% CI, 1.01–1.42). In conclusion, supplementation with α‐tocopherol and β‐carotene appeared to have no late effects on cancer incidence. The preventive effect of moderate‐dose α‐tocopherol on prostate cancer continued several years post‐trial and resulted in lower prostate cancer mortality.     

Type 2 diabetes mellitus,insulin‐use and risk of bladder cancer in a large cohort study

Type 2 diabetes mellitus (T2DM) is associated with increased bladder cancer incidence in some, but not all, studies. Many studies had limited statistical power and few examined risk by insulin‐use, duration of diabetes or cancer stage. We examined the association between T2DM and bladder cancer incidence in the Cancer Prevention Study II Nutrition Cohort, a large prospective study with information on insulin‐use and duration of diabetes. Diabetes and insulin‐use were ascertained from a questionnaire at study enrollment in 1992 or 1993 and updated in 1997 and every 2 years thereafter. During follow‐up through 2007, 1,852 cases of incident bladder cancer were identified among 172,791 participants. Multivariable adjusted relative risks (RRs) and 95% confidence intervals (CIs) were estimated using extended Cox regression modeling. There were no associations of T2DM with the risk of bladder cancer overall (RR = 1.01, 95% CI: 0.87–1.17), noninvasive disease (RR = 0.93, 95% CI: 0.76–1.14) or invasive disease (RR = 1.13, 95% CI: 0.91–1.40). Compared to participants without T2DM, risk of invasive bladder cancer was higher among participants who had had T2DM for >15 years (RR = 1.63, 95% CI: 1.09–2.43) and among those using insulin (RR = 1.64, 95% CI: 1.18–2.27). These results do not support an association of T2DM with overall bladder cancer incidence, but do suggest positive associations of long‐term T2DM and insulin‐use or other factors correlated with severe diabetes, with invasive bladder cancer incidence.     

Obesity and incidence of lung cancer: A meta‐analysis

To date, the relationship between obesity and the incidence of lung cancer remains unclear and inconclusive. Thus, we conducted a meta‐analysis of published studies to provide a quantitative evaluation of this association. Relevant studies were identified through PubMed and EMBASE databases from 1966 to December 2011, as well as through the reference lists of retrieved articles. A total of 31 articles were included in this meta‐analysis. Overall, excess body weight (body mass index, BMI ≥ 25 kg/m²) was inversely associated with lung cancer incidence (relative risk, RR = 0.79; 95% confidence interval, CI: 0.73–0.85) compared with normal weight (BMI = 18.5‐24.9 kg/m²). The association did not change with stratification by sex, study population, study design, and BMI measurement method. However, when stratified by smoking status, the inverse association between excess body weight and lung cancer incidence in current (RR = 0.63, 95% CI: 0.57–0.70) and former (RR = 0.73, 95% CI: 0.58–0.91) smokers was strengthened. In non‐smokers, the association was also statistically significant (RR = 0.83, 95% CI: 0.70–0.98), although the link was weakened to some extent. The stratified analyses also showed that excess body weight was inversely associated with squamous cell carcinoma (RR = 0.68, 95% CI: 0.58–0.80) and adenocarcinoma (RR = 0.79, 95% CI: 0.65–0.96). No statistically significant link was found between excess body weight and small cell carcinoma (RR = 0.99, 95% CI: 0.66–1.48). The results of this meta‐analysis indicate that overweight and obesity are protective factors against lung cancer, especially in current and former smokers.     

Fluid intake and risk of bladder cancer in the Nurses' Health Studies

Increase in fluid intake may reduce bladder cancer risk by decreasing the contact time between carcinogens in urine and bladder epithelium. However, this association has not been examined in a large cohort of women. The association between total fluid intake and bladder cancer risk in two large prospective women's cohorts with 427 incident bladder cancer cases was examined. Detailed information on total fluid intake was collected by repeated food frequency questionnaires over time. Multivariable relative risks (RRs) and 95% confidence intervals (95% CIs) were estimated by using Cox proportional hazards regression models. Results from the two cohorts were pooled together using the random‐effects model. Using the average values from the earliest two dietary assessments and lowest quartile as reference, a suggestive inverse association was observed between total fluid intake and overall bladder cancer risk (RR: 0.83, 95% CI: 0.61–1.12, p‐value for trend: 0.08), and invasive bladder cancer risk (RR: 0.47, 95% CI: 0.23–0.97, p‐value for trend: 0.04). Among heavy cigarette smokers, women with the highest quartile of total fluid intake had a 38% decrease in bladder cancer risk (RR: 0.62, 95% CI: 0.41–0.93, p‐value for trend: 0.02). The findings suggested that total fluid intake may reduce bladder cancer risk for female smokers, as well as reduce the risk of invasive bladder cancer.     

A meta-analysis of alcohol consumption and the risk of brain tumours

BackgroundAlcohol is capable of traversing the blood–brain barrier and is thus a possible risk factor for brain cancer. Several epidemiological studies have been published on the issue, a number of those during recent years, with inconsistent findings.Materials and methodsWe performed a systematic literature search in the Medline and EMBASE databases. We found a total of 19 studies providing risk estimates for total alcohol or specific alcoholic beverages. Pooled estimates of the relative risks (RR) and 95% confidence intervals (CI) were calculated using random-effects models.ResultsThe pooled RR of brain cancer for alcohol drinkers versus non-drinkers was 0.97 (95% CI 0.82–1.15; based on 12 studies). Moderate (<2 drinks/day) and heavy alcohol drinkers had RRs of 1.01 (95% CI 0.81–1.25) and 1.35 (95% CI 0.85–2.15), respectively. With reference to specific alcoholic beverages, the RRs were 1.01 (95% CI 0.70–1.48) for wine, 0.96 (95% CI 0.82–1.12) for beer, and 1.20 (95% CI 1.01–1.42) for spirit consumption. The RRs for drinkers versus non-drinkers were 0.93 (95% CI 0.81–1.07) for glioma and 0.71 (95% CI 0.45–1.12) for meningioma.ConclusionsAlcohol drinking does not appear to be associated with adult brain cancer, though a potential effect of high doses deserves further study.     

Beta‐carotene supplementation and cancer risk: a systematic review and metaanalysis of randomized controlled trials

The effect of beta‐carotene supplementation on cancer incidence has been investigated in several randomized controlled trials. The objective was to review the effect of beta‐carotene supplementation on cancer incidence in randomized trials by cancer site, beta‐carotene supplementation characteristics and study population. Relevant trials were retrieved by searching PubMed (up to April 2009). Authors involved in selected studies were contacted for additional information. Thirteen publications reporting results from 9 randomized controlled trials were included. Overall, no effect of beta‐carotene supplementation was observed on the incidence of all cancers combined (RR, 1.01; 95% CI, 0.98–1.04), pancreatic cancer (RR, 0.99; 95% CI, 0.73–1.36), colorectal cancer (RR, 0.96; 95% CI, 0.85–1.09), prostate cancer (RR, 0.99; 95% CI, 0.91–1.07), breast cancer (RR, 0.96; 95% CI, 0.85–1.10), melanoma (RR, 0.98; 95% CI, 0.65–1.46) and non melanoma skin cancer (RR, 0.99; 95% CI, 0.93–1.05). The incidence of lung and stomach cancers were significantly increased in individuals supplemented with beta‐carotene at 20–30 mg day⁻¹ (RR, 1.16; 95% CI, 1.06–1.27 and RR, 1.34; 95% CI, 1.06–1.70), in smokers and asbestos workers (RR, 1.20; 95% CI, 1.07–1.34 and RR, 1.54; 95% CI, 1.08–2.19) compared to the placebo group. Beta‐carotene supplementation has not been shown to have any beneficial effect on cancer prevention. Conversely, it was associated with increased risk not only of lung cancer but also of gastric cancer at doses of 20–30 mg day⁻¹, in smokers and asbestos workers. This study adds to the evidence that nutritional prevention of cancer through beta‐carotene supplementation should not be recommended.     

Vegetables and fruits consumption and risk of esophageal and gastric cancer subtypes in the Netherlands Cohort Study

Prospective epidemiologic data on vegetables and fruits consumption and risk of subtypes of esophageal and gastric cancer are sparse. We studied the association between vegetables and fruits consumption and risk of esophageal squamous cell carcinoma (ESCC), esophageal adenocarcinoma (EAC), gastric cardia adenocarcinoma (GCA) and gastric noncardia adenocarcinoma (GNCA) in the Netherlands Cohort Study. In 1986, 120,852 Dutch men and women aged 55-69 filled out a questionnaire on diet and other cancer risk factors. After 16.3 years of follow-up, 101 ESCC, 144 EAC, 156 GCA, 460 GNCA cases and 4,035 subcohort members were available for case-cohort analysis using Cox proportional hazards models. Multivariable adjusted incidence rate ratios (RRs) were generally below unity. Total vegetable consumption was nonsignificantly inversely associated with EAC and ESCC risk, but not with GCA and GNCA risk. Significant inverse associations were observed for raw vegetables and EAC risk [RR per 25 g/day: 0.81, 95% confidence interval (CI) 0.68-0.98], and Brassica vegetables and GCA risk (RR per 25 g/day: 0.72, 95% CI 0.54-0.95). Total fruit consumption was associated with a nonsignificantly decreased EAC risk. Citrus fruits were inversely associated with EAC and GCA risk (RRs for highest vs. lowest intake: 0.55, 95% CI 0.31-0.98 and 0.38, 95% CI 0.21-0.69, respectively). Specifically for current smokers, vegetables and possibly also fruits intake was inversely associated with ESCC and EAC risk. Consumption of (specific groups of) vegetables and fruits may protect against subtypes of esophageal and gastric cancer.     

Dietary acrylamide and cancer risk: An updated meta‐analysis

The debate on the potential carcinogenic effect of dietary acrylamide is open. In consideration of the recent findings from large prospective investigations, we conducted an updated meta‐analysis on acrylamide intake and the risk of cancer at several sites. Up to July 2014, we identified 32 publications. We performed meta‐analyses to calculate the summary relative risk (RR) of each cancer site for the highest versus lowest level of intake and for an increment of 10 µg/day of dietary acrylamide, through fixed‐effects or random‐effects models, depending on the heterogeneity test. Fourteen cancer sites could be examined. No meaningful associations were found for most cancers considered. The summary RRs for high versus low acrylamide intake were 0.87 for oral and pharyngeal, 1.14 for esophageal, 1.03 for stomach, 0.94 for colorectal, 0.93 for pancreatic, 1.10 for laryngeal, 0.88 for lung, 0.96 for breast, 1.06 for endometrial, 1.12 for ovarian, 1.00 for prostate, 0.93 for bladder and 1.13 for lymphoid malignancies. The RR was of borderline significance only for kidney cancer (RR = 1.20; 95% confidence interval, CI, 1.00–1.45). All the corresponding continuous estimates ranged between 0.95 and 1.03, and none of them was significant. Among never‐smokers, borderline associations with dietary acrylamide emerged for endometrial (RR = 1.23; 95% CI, 1.00–1.51) and ovarian (RR = 1.39; 95% CI, 0.97–2.00) cancers. This systematic review and meta‐analysis of epidemiological studies indicates that dietary acrylamide is not related to the risk of most common cancers. A modest association for kidney cancer, and for endometrial and ovarian cancers in never smokers only, cannot be excluded.     

A meta-analysis of coffee and tea consumption and the risk of glioma in adults

Background

Coffee contains many compounds, including antioxidants, which could prevent cancerogenesis, and coffee has been related with lower incidence of cancer at several sites. Tea is also rich in antioxidants, mainly polyphenols. To provide a quantitative overall estimate on the relation between coffee and tea consumption and glioma, we combined all published data, using a meta-analytic approach.

Methods

In September 2012, a bibliography search was carried out in both PubMed and Embase to identify observational studies providing quantitative estimates on the issue. Pooled estimates of the relative risks (RR) and the corresponding 95 % confidence intervals (CI) were calculated using random-effects models.

Results

Six studies (four cohort and two case–control studies) were available for meta-analysis, for a total of about 2100 cases. The summary RRs and 95 % CIs of glioma for drinkers versus non/occasional drinkers were 0.96 (95 % CI: 0.81–1.13) for coffee and 0.86 (95 % CI: 0.78–0.94) for tea, with no heterogeneity between studies. When we compared the highest versus the lowest categories of consumption, the RRs were 1.01 (95 % CI: 0.83–1.22) for coffee, 0.88 (95 % CI: 0.69–1.12) for tea, and 0.75 (95 % CI: 0.54–1.05) for coffee plus tea.

Conclusions

This meta-analysis, although based on few studies, suggests a lack of association between coffee intake and glioma risk, and a tendency, if any, to a lower risk for tea and coffee plus tea drinkers.     

A prospective study of diet and stomach cancer mortality in United States men and women.

Frequent consumption of fruits, vegetables, and whole grains has been associated with a reduced risk of stomach cancer in the majority of case-control studies of these factors: however, prospective studies have been less consistent. We examined the association between selected major food groups (citrus fruits, vegetables, whole grains, and processed meats) and risk of fatal stomach cancer in the Cancer Prevention Study (CPS) II cohort of 1.2 million United States men and women. During 14 years of follow-up, we documented 439 stomach cancer deaths in women and 910 in men after exclusion of individuals with prevalent cancers, inadequate diet information, and recent weight loss at baseline in 1982. After controlling for other risk factors, none of the food groups examined were associated with risk of stomach cancer except for an unexpected increased risk with vegetable consumption in women [relative risk (RR) = 1.25; 95% confidence interval (CI), 0.99-1.58; highest versus lowest tertile, P = 0.06 for trend]. A high overall plant food intake (a sum of vegetables, citrus fruit, and whole grains) was associated with reduced risk in men (RR = 0.79; 95% CI, 0.67-0.93; highest versus lowest tertile, P = 0.003 for trend), but not in women (RR = 1.18; 95% CI, 0.93-1.50; P = 0.16 for trend). Of individual foods examined, liver consumption greater than twice/week was associated with an increased risk of fatal stomach cancer in women (RR = 1.96; 95% CI, 1.09-3.53) and men (RR = 1.63; 95% CI, 1.02-2.62) compared with nonconsumers. This study supports a modest role for plant foods in reducing the risk of fatal stomach cancer in men, but not in women.     

Aspirin and cancer risk: a quantitative review to 2011

BackgroundAspirin has been associated to a reduced risk of colorectal and possibly of a few other common cancers.MethodsTo provide an up-to-date quantification of this association, we conducted a meta-analysis of all observational studies on aspirin and 12 selected cancer sites published up to September 2011.ResultsRegular aspirin is associated with a statistically significant reduced risk of colorectal cancer [summary relative risk (RR) from random effects models = 0.73, 95% confidence interval (CI) 0.67–0.79], and of other digestive tract cancers (RR = 0.61, 95% CI = 0.50–0.76, for squamous cell esophageal cancer; RR = 0.64, 95% CI = 0.52–0.78, for esophageal and gastric cardia adenocarcinoma; and RR = 0.67, 95% CI = 0.54–0.83, for gastric cancer), with somewhat stronger reductions in risk in case–control than in cohort studies. Modest inverse associations were also observed for breast (RR = 0.90, 95% CI = 0.85–0.95) and prostate cancer (RR = 0.90, 95% CI = 0.85–0.96), while lung cancer was significantly reduced in case–control studies (0.73, 95% CI = 0.55–0.98) but not in cohort ones (RR = 0.98, 95% CI = 0.92–1.05). No meaningful overall associations were observed for cancers of the pancreas, endometrium, ovary, bladder, and kidney.ConclusionsObservational studies indicate a beneficial role of aspirin on colorectal and other digestive tract cancers; modest risk reductions were also observed for breast and prostate cancer. Results are, however, heterogeneous across studies and dose–risk and duration–risk relationships are still unclear.     

Alcohol consumption and risk of hematological malignancies: A meta‐analysis of prospective studies

Current convincing evidence suggests that alcohol intake increases the risk of several carcinomas, which might subsequently lead to a recommendation toward limiting alcohol consumption. However, there are accumulating data worth meta‐analyzing that show a different effect on the risk of hematological malignancies. Eligible cohort studies were sought in PubMed database up to August 31, 2016. Separate analyses were performed by subtype of hematological malignancy (non‐Hodgkin lymphoma [NHL] and subtypes, Hodgkin lymphoma [HL], leukemia and subtypes), time status (ever, current, former), level of consumption (light, moderate, heavy), alcoholic beverage (total alcohol, beer, liquor, wine) and gender. Moderate and heavy alcohol consumption were significantly associated with reduced risk of NHL (relative risk [RR] = 0.85, 95% confidence interval [CI]: 0.80–0.90 and RR = 0.73, 95%CI: 0.60–0.89, respectively); a protective trend was also shown for light alcohol intake (RR = 0.93, 95%CI: 0.87–1.00). Specifically, beer consumption was associated with reduced NHL risk (RR = 0.88, 95%CI: 0.81–0.95). However, the association regarding other alcoholic beverages seemed null. The beneficial effects of alcohol mainly pertained to Diffuse Large B‐Cell Lymphoma (DLBCL) (RR = 0.83, 95%CI: 0.77–0.89) and Follicular Lymphoma (FL) (RR = 0.85, 95%CI: 0.78–0.93). There was also no association between alcohol consumption and risk of HL or leukemias. In contrast to most solid malignancies, alcohol seems to confer a protective effect on NHL risk, especially on DLBCL and FL subtypes, with beer being notably beneficial.     

Egg consumption and breast cancer risk: a meta-analysis

The relationship between egg consumption and breast cancer risk has been inconsistent, so it is necessary to conduct a meta-analysis to evaluate the relationship. PubMed, EMBASE and ISI Web of Knowledge were searched to find cohort studies or case control studies that evaluated the relationship between egg consumption and breast cancer risk. A comprehensive meta-analysis software was used to conduct the meta-analysis. 13 studies were included. The meta-analysis results showed that egg consumption was associated with increased breast cancer risk (RR 1.04, 95 % CI 1.01–1.08). Subgroup analyses showed egg consumption was also associated with increased breast cancer risk based on cohort studies (RR 1.04, 95 % CI 1.00–1.08), among European population (RR 1.05, 95 % CI 1.01–1.09), Asian population (RR 1.09, 95 % CI 1.00–1.18), postmenopausal population (RR 1.06, 95 % CI 1.02–1.10), and those who consumed ≥2, ≤5/week (RR 1.10, 95 % CI 1.02–1.17), but not in case–control studies (RR 1.06, 95 % CI 0.97–1.15), among American population (RR 1.04, 95 % CI 0.94–1.16), premenopausal population (RR 1.04, 95 % CI 0.98–1.11) and those who consumed ≥1, <2/week (RR 1.04, 95 % CI 0.97–1.11) or >5 eggs/week (RR 0.97, 95 % CI 0.88–1.06). Egg consumption was associated with increased breast cancer risk among the European, Asian and postmenopausal population and those who consumed ≥2, ≤5/week.     

Coffee drinking and risk of endometrial cancer—A population‐based cohort study

Coffee drinking has been reported to have beneficial effects on insulin resistance, which has been directly associated with endometrial cancer. Although a relationship between coffee consumption and endometrial cancer risk is biologically plausible, this hypothesis has been previously explored in only 2 prospective studies, with a small number of cases. We used data from the Swedish Mammography Cohort, a population‐based prospective cohort study of 60,634 women. During 17.6 years of follow‐up, 677 participants were diagnosed with incident endometrial cancer (adenocarcinoma). We examined the association between self‐reported coffee consumption (at baseline 1987–90 and in 1997) and endometrial cancer risk using Cox proportional hazards models. Each additional cup (200 g) of coffee per day was associated with a rate ratio (RR) of 0.90 [95% confidence interval (CI), 0.83–0.97]. In women drinking 4 or more cups of coffee a day, the RR for the risk reduction of endometrial cancer was 0.75 (95% CI, 0.58–0.97) when compared with those who drank 1 cup or less. The association seemed largely confined to overweight and obese women, who showed a respective risk reduction of 12% (95% CI, 0–23%) and 20% (95% CI, 7–31%) for every cup of coffee, but was not observed among normal‐weight women. There was a statistically significant interaction between coffee consumption and body mass index (p_interaction < 0.001). These data indicate that coffee consumption may be associated with decreased risk of endometrial cancer, especially among women with excessive body weight. If confirmed by other prospective studies, these results are of major public health significance. © 2009 UICC     

Green tea and black tea consumption in relation to colorectal cancer risk: the Singapore Chinese Health Study

The relationships between green tea and black tea consumption and colorectal cancer risk were examined within the Singapore Chinese Health Study, a prospective cohort study of diet and cancer involving >60,000 men and women. Intake of green tea and black tea was assessed through in-person interviews. Incident cancer cases and deaths among cohort members were identified through record linkage of the cohort database with respective databases from the nationwide Singapore Cancer Registry and the Singapore Registry of Births and Deaths. The proportional hazard regression method was used to examine the associations between intake of green and black tea separately and colorectal cancer risk with adjustment for potential confounders. After an average of 8.9 years of follow-up, 845 colorectal cancer cases were identified. Subjects who drank green tea exhibited a statistically non-significant increase in risk [relative risk (RR) = 1.12, 95% confidence interval (CI) = 0.97-1.29] relative to non-drinkers of green tea. This risk increase was mainly confined to men (RR = 1.31, 95% CI = 1.08-1.58); the comparable RR in women was 0.89 (95% CI = 0.71-1.12). In men, the green tea-colorectal cancer association was noted mainly in those with advanced disease (Duke C or D) (RR = 1.53, 95% CI = 1.19-1.97), and the association was dose dependent (P for trend = 0.0002). This latter association was especially strong within the colon subsite (RR = 1.75, 95% CI = 1.24-2.46; P for trend < 0.0001). Irrespective of gender, intake of black tea was not associated with risk of colorectal cancer (RR = 0.92, 95% CI = 0.79-1.07) in this Asian population.     

Factors associated with incident and fatal pancreatic cancer in a cohort of middle‐aged women

Risk factors for pancreatic cancer, other than smoking and diabetes, are not well‐established, especially for women. In a cohort of 1.3 million middle‐aged women, followed for 9.2 million person‐years for cancer incidence and 11.5 million person‐years for mortality, there were 1,338 incident pancreatic cancer cases and 1,710 deaths from the disease. Using proportional hazards models, we calculated adjusted relative risks (RRs) and 95% confidence intervals (CIs) by smoking, height, body mass index (BMI), alcohol consumption, physical activity and history of diabetes. Pancreatic cancer incidence was greater in current than never smokers (RR 2.39, CI 2.10–2.73), the risk increasing with the number of cigarettes smoked. The incidence of pancreatic cancer also increased with increasing BMI (RR 1.34, CI 1.13–1.57 for BMI ≥ 30 vs. 22.5–25 kg/m²), and with a history of diabetes (RR 1.58, CI 1.22–2.03, with vs. without such a history). These factors were also associated with increased mortality from pancreatic cancer. Height, alcohol consumption and physical activity showed little or no association with pancreatic cancer risk. © 2008 Wiley‐Liss, Inc.