Antioxidant vitamins have attracted considerable attention in previous studies of esophageal squamous-cell carcinoma, but dietary studies of adenocarcinoma of the esophagus and gastric cardia remain sparse. Treating these tumors as distinct diseases, we studied intakes of vitamin C, beta-carotene and alpha-tocopherol in a nationwide population-based case-control study in Sweden, with 185, 165, and 258 cases of esophageal adenocarcinoma, esophageal squamous-cell carcinoma, and gastric cardia adenocarcinoma, respectively, and 815 controls. Subjects with a high parallel intake of vitamin C, beta-carotene, and alpha-tocopherol showed a 40-50% decreased risk of both histological types of esophageal cancer compared with subjects with a low parallel intake. Antioxidant intake was not associated with the risk of gastric cardia adenocarcinoma. Separately, vitamin C and beta-carotene reduced the risk of esophageal cancers more than alpha-tocopherol. We found that antioxidant intake is associated with similar risk reductions for both main histological types of esophageal cancer. Our findings indicate that antioxidants do not explain the diverging incidence rates of the 2 histological types of esophageal cancer. Moreover, our data suggest that inverse associations with esophageal squamous-cell carcinoma and adenocarcinoma may be stronger among subjects under presumed higher oxidative stress due to smoking or gastroesophageal reflux, respectively. Our results may be relevant for the implementation of focused, cost-effective preventive measures.
The strong male predominance in esophageal and gastroesophageal junctional adenocarcinoma remains unexplained. Sex hormonal influence has been suggested, but not proven. A protective role of dietary phytoestrogen lignans was hypothesized.
A Swedish nationwide population-based case-control study was conducted in 1995-1997, including 181 cases of esophageal adenocarcinoma, 255 cases of gastroesophageal junctional adenocarcinoma, 158 cases of esophageal squamous cell carcinoma, and 806 control subjects. Data on various exposures, including dietary data, were collected through personal interviews and questionnaires. Dietary intake of lignans was assessed using a food frequency questionnaire and categorized into quartiles based on the consumption among the control participants. Unconditional logistic regression was used to calculate odds ratios (ORs) with 95?% confidence intervals (CIs), including adjustment for all established risk factors.
Participants in the highest quartile of intake of lignans compared with the lowest quartile were at a decreased risk of esophageal adenocarcinoma (OR, 0.65; 95?% CI, 0.38-1.12; p for trend =0.03), gastroesophageal junctional adenocarcinoma (OR, 0.37; 95?% CI, 0.23-0.58; p for trend
BACKGROUND: Long-term deleterious effects of repeated blood donations may be masked by the donors' healthy lifestyle. To investigate possible effects of blood donation and iron loss through blood donation on cancer incidence while minimizing "healthy donor effects," we made dose-response comparisons within a cohort of Swedish and Danish blood donors. METHODS: We used a nested case-control study design, in which case patients were defined as all donors who were diagnosed with a malignancy between their first recorded blood donation and study termination (n = 10866). Control subjects (n = 107140) were individually matched on sex, age, and county of residence. Using conditional logistic regression, we estimated relative risks of cancer according to number of blood donations made or estimated iron loss 3-12 years before a case patient was diagnosed with cancer. All statistical tests were two-sided. RESULTS: No clear association was observed between number of donations and risk of cancer overall. However, between the lowest ( 90th percentile, > 2.7 g) categories of estimated iron loss, there was a trend (P(trend) 25 vs 0 donations, OR = 2.14, 95% CI = 1.22 to 3.74). CONCLUSIONS: Repeated blood donation was not associated with increased or decreased risk of cancer overall. The lack of consistency across latency periods casts doubt on an apparent association between reduced cancer risk and iron loss in men. The positive association between frequent plasma donation and risk of non-Hodgkin lymphoma deserves further exploration.
A rising incidence and a poor survival rate make esophageal cancer a major health issue, hence the need for chemoprevention. We investigated the effects of the selective cyclooxygenase 2 inhibitors (coxibs), rofecoxib and celecoxib, the nonselective nonsteroidal anti-inflammatory drugs (NSAIDs), and aspirin on esophageal cancer.
This nested case-control study used data from a government-run insurance database on patients 66 years and older who underwent esophageal imaging (esophagogastroduodenoscopy or barium swallow) between January 1999 and September 2002. Logistic regression models were used to determine the effect of chronic exposure, by using as proxy at least 30 days of use of the drugs of interest in the past year, on the occurrence of esophageal cancer.
The study included 251 cases and all 86,644 eligible control subjects. Patients more likely to have esophageal cancer (odds ratio, 95% confidence interval) were men (3.42, 2.62-4.48) and older subjects (those 75-84 years and those > or =85 years: 1.40, 1.08-1.82 and 1.69, 1.05-2.72, respectively). Chronic exposure to coxibs or NSAIDs was associated with a significant risk reduction for esophageal cancer (0.63, 0.40-0.98 and 0.47, 0.24-0.93, respectively). Assessed separately, the point estimates were slightly lower for rofecoxib than for celecoxib when examining a possible duration-response effect, although all 95% confidence intervals overlapped (celecoxib: 0.51, 0.27-0.98; 0.30, 0.11-0.82; 0.39, 0.14-1.05; rofecoxib: 0.39, 0.16-0.96; 0.37, 0.12-1.16; 0.33, 0.08-1.36 for exposures of > or =30, > or =60, and > or =90 days, respectively).
Chronic intake of rofecoxib and celecoxib and of nonselective NSAIDs appears to be associated with a decreased incidence of esophageal cancer.
Few prospective studies have investigated the association between whole-grain consumption and incidence of oesophageal cancer. In the Scandinavian countries, consumption of whole grains is high and the incidence of oesophageal cancer comparably low. The aim of this paper was to study the associations between consumption of whole grains, whole-grain products and oesophageal cancer, including its two major histological subtypes. The HELGA cohort is a prospective cohort study consisting of three sub-cohorts in Norway, Sweden and Denmark. Information regarding whole-grain consumption was collected through country-specific food frequency questionnaires. Cancer cases were identified through national cancer registries. Cox proportional hazards ratios were calculated in order to assess the associations between whole grains and oesophageal cancer risk. The analytical cohort had 113,993 members, including 112 cases, and median follow-up time was 11 years. When comparing the highest tertile of intake with the lowest, the oesophageal cancer risk was approximately 45 % lower (adjusted HR 0.55, 95 % CI 0.31-0.97 for whole grains, HR 0.51, 95 % CI 0.30-0.88 for whole-grain products). Inverse associations were also found in continuous analyses. Whole-grain wheat was the only grain associated with lower risk (HR 0.32, 95 % CI 0.16-0.63 highest vs. lowest tertile). Among whole-grain products, the results were less clear, but protective associations were seen for the sum of whole-grain products, and whole-grain bread. Lower risk was seen in both histological subtypes, but particularly for squamous cell carcinomas. In this study, whole-grain consumption, particularly whole-grain wheat, was inversely associated with risk of oesophageal cancer.