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Common habitual behaviors and synchronous colorectal cancer risk: a retrospective case-control study. Int J Colorectal Dis 2019; 34:1421-1430. [PMID: 31278528 DOI: 10.1007/s00384-019-03326-x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 05/30/2019] [Indexed: 02/04/2023]
Abstract
PURPOSE The association of habitual behaviors with the prevalence of synchronous colorectal cancer (sCRC) is unknown. Here, we investigated whether these behaviors, which are known risk factors for colorectal polyps, may be related to sCRC risk. METHODS We enrolled 17,093 patients who underwent cancer treatment between January 1995 and December 2016 and examined the association of age, sex, familial history of hereditary colorectal cancer (CRC), and status of three common habitual behaviors (smoking and alcohol and coffee consumption) with the prevalence of sCRC. RESULTS Of the enrolled patients, 960 (5.6%) patients had sCRC. The independent risk factors for sCRC prevalence included advanced age, male sex, hereditary CRC, smoking, and daily alcohol consumption of more than one bottle (> 600 mL). Contrary to these factors, daily coffee consumption of more than one cup seemed to provide a protection from sCRC. In the Kaplan-Meier test, the significantly worse 5-year overall survival (OS) was noted in smokers with stage 0-III CRC. The effect of alcohol consumption on 5-year OS was significant in stages II and III. Compared with those without daily coffee consumption, patients with daily coffee consumption had significantly higher 5-year OS in stages I (93.0% vs. 86.4%), II (87.1% vs. 77.2%), III (71.5% vs. 61.9%), and IV (18.0% vs. 13.0%). CONCLUSIONS sCRC prevalence was significantly associated with habitual behaviors. Patients with smoking or with daily alcohol consumption of one bottle had higher sCRC prevalence than did those without these habits. Coffee consumption could be a protective factor for lowering sCRC risk.
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Rossi M, Jahanzaib Anwar M, Usman A, Keshavarzian A, Bishehsari F. Colorectal Cancer and Alcohol Consumption-Populations to Molecules. Cancers (Basel) 2018; 10:E38. [PMID: 29385712 PMCID: PMC5836070 DOI: 10.3390/cancers10020038] [Citation(s) in RCA: 122] [Impact Index Per Article: 17.4] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2017] [Revised: 01/22/2018] [Accepted: 01/24/2018] [Indexed: 12/11/2022] Open
Abstract
Colorectal cancer (CRC) is a major cause of morbidity and mortality, being the third most common cancer diagnosed in both men and women in the world. Several environmental and habitual factors have been associated with the CRC risk. Alcohol intake, a common and rising habit of modern society, is one of the major risk factors for development of CRC. Here, we will summarize the evidence linking alcohol with colon carcinogenesis and possible underlying mechanisms. Some epidemiologic studies suggest that even moderate drinking increases the CRC risk. Metabolism of alcohol involves ethanol conversion to its metabolites that could exert carcinogenic effects in the colon. Production of ethanol metabolites can be affected by the colon microbiota, another recently recognized mediating factor to colon carcinogenesis. The generation of acetaldehyde and alcohol's other metabolites leads to activation of cancer promoting cascades, such as DNA-adduct formation, oxidative stress and lipid peroxidation, epigenetic alterations, epithelial barrier dysfunction, and immune modulatory effects. Not only does alcohol induce its toxic effect through carcinogenic metabolites, but alcoholics themselves are predisposed to a poor diet, low in folate and fiber, and circadian disruption, which could further augment alcohol-induced colon carcinogenesis.
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Affiliation(s)
- Marco Rossi
- Division of Digestive Diseases, Hepatology, and Nutrition, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
| | - Muhammad Jahanzaib Anwar
- Division of Digestive Diseases, Hepatology, and Nutrition, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
| | - Ahmad Usman
- Division of Digestive Diseases, Hepatology, and Nutrition, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
| | - Ali Keshavarzian
- Division of Digestive Diseases, Hepatology, and Nutrition, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
| | - Faraz Bishehsari
- Division of Digestive Diseases, Hepatology, and Nutrition, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
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Alcohol Consumption-Related Metabolites in Relation to Colorectal Cancer and Adenoma: Two Case-Control Studies Using Serum Biomarkers. PLoS One 2016; 11:e0150962. [PMID: 26967509 PMCID: PMC4788441 DOI: 10.1371/journal.pone.0150962] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/19/2015] [Accepted: 02/21/2016] [Indexed: 01/12/2023] Open
Abstract
Alcohol is a known carcinogen that may be associated with colorectal cancer. However, most epidemiologic studies assess alcoholic beverage consumption using self-reported data, leading to potential exposure misclassification. Biomarkers of alcohol consumption may provide an alternative, complementary approach that reduces misclassification and incorporates individual differences in alcohol metabolism. Therefore, we evaluated the relationship between previously identified alcohol consumption-related metabolites and colorectal cancer and adenoma using serum metabolomics data from two studies. Data on colorectal cancer were obtained from a nested case-control study of 502 US adults (252 cases, 250 controls) within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Data on colorectal adenoma were obtained from a case-control study of 197 US adults (120 cases, 77 controls) from the Navy Colon Adenoma Study. Unconditional multivariable logistic regression models were fit to calculate odds ratios (OR) and 95% confidence intervals (CI) for eight alcohol consumption-related metabolites identified in a previous analysis: ethyl glucuronide; 4-androstene-3beta,17beta-diol disulfate 1; 5-alpha-androstan-3beta,17beta-diol disulfate; 16-hydroxypalmitate; bilirubin (E,Z or Z,E); cyclo (-leu-pro); dihomo-linoleate (20:2n6); and palmitoleate (16:1n7). We found no clear association between these alcohol consumption-related metabolites and either endpoint. However, we did observe an inverse association between cyclo (-leu-pro) and colorectal adenoma that was only observed in the highest metabolite quantile (OR 4th vs. 1st Quantile = 0.30, 95% CI: 0.12–0.78; P-trend = 0.047), but no association for colorectal cancer. In conclusion, there were no adverse associations between alcohol consumption-related metabolites and colorectal cancer or adenoma.
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He XF, Wei J, Liu ZZ, Xie JJ, Wang W, Du YP, Chen Y, Si HQ, Liu Q, Wu LX, Wei W. Association between CYP1A2 and CYP1B1 polymorphisms and colorectal cancer risk: a meta-analysis. PLoS One 2014; 9:e100487. [PMID: 25115775 PMCID: PMC4130485 DOI: 10.1371/journal.pone.0100487] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/23/2013] [Accepted: 05/25/2014] [Indexed: 12/31/2022] Open
Abstract
Background The previous published data on the association between CYP1A2*F (rs762551), CYP1B1 Leu432Val (rs1056836), Asn453Ser (rs180040), and Arg48Gly (rs10012) polymorphisms and colorectal cancer risk remained controversial. Methodology/Principal Findings The purpose of this study is to evaluate the role of CYP1A2*F, CYP1B1 Leu432Val, Asn453Ser, and Arg48Gly genotypes in colorectal cancer susceptibility. We performed a meta-analysis on all the eligible studies that provided 5,817 cases and 6,544 controls for CYP1A2*F (from 13 studies), 9219 cases and 10406 controls for CYP1B1 Leu432Val (from 12 studies), 6840 cases and 7761 controls for CYP1B1 Asn453Ser (from 8 studies), and 4302 cases and 4791 controls for CYP1B1Arg48Gly (from 6 studies). Overall, no significant association was found between CYP1A2*F, CYP1B1 Leu432Val, Asn453Ser, and Arg48Gly and colorectal cancer risk when all the eligible studies were pooled into the meta-analysis. And in the subgroup by ethnicity and source of controls, no evidence of significant association was observed in any subgroup analysis. Conclusions/Significance In summary, this meta-analysis indicates that CYP1A2*F, CYP1B1 Leu432Val, Asn453Ser, and Arg48Gly polymorphisms do not support an association with colorectal cancer, and further studies are needed to investigate the association. In addition, our work also points out the importance of new studies for CYP1A2*F polymorphism in Asians, because high heterogeneity was found (dominant model: I2 = 81.3%; heterozygote model: I2 = 79.0).
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Affiliation(s)
- Xiao-Feng He
- Department of Research, Peace Hospital of Changzhi Medical College, Changzhi, Shanxi Province, China
- * E-mail:
| | - Jie Wei
- Department of Clinical laboratory, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong Province, China
| | - Zhi-Zhong Liu
- Department of Gastroenterology, The Second People's Hospital of Zhuhai, Zhuhai, Guangdong Province, China
| | - Jian-Jun Xie
- Department of Gastroenterology, The Second People's Hospital of Zhuhai, Zhuhai, Guangdong Province, China
| | - Wei Wang
- Department of Gastroenterology, The Second People's Hospital of Zhuhai, Zhuhai, Guangdong Province, China
| | - Ya-Ping Du
- Department of Gastroenterology, The Second People's Hospital of Zhuhai, Zhuhai, Guangdong Province, China
| | - Yu Chen
- Department of Gastroenterology, The Second People's Hospital of Zhuhai, Zhuhai, Guangdong Province, China
| | - Hui-Qiang Si
- Department of Gastroenterology, The Second People's Hospital of Zhuhai, Zhuhai, Guangdong Province, China
| | - Qing Liu
- Department of Gastroenterology, The Second People's Hospital of Zhuhai, Zhuhai, Guangdong Province, China
| | - Li-Xia Wu
- Department of Research, Peace Hospital of Changzhi Medical College, Changzhi, Shanxi Province, China
| | - Wu Wei
- Department of Hematology, Peace Hospital of Changzhi Medical College, Changzhi, Shanxi Province, China
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Zhu JZ, Wang YM, Zhou QY, Zhu KF, Yu CH, Li YM. Systematic review with meta-analysis: alcohol consumption and the risk of colorectal adenoma. Aliment Pharmacol Ther 2014; 40:325-337. [PMID: 24943329 DOI: 10.1111/apt.12841] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/09/2014] [Revised: 05/23/2014] [Accepted: 05/26/2014] [Indexed: 12/12/2022]
Abstract
BACKGROUND Studies on the relation between alcohol consumption and risk of colorectal adenoma (CRA), a precursor of colorectal cancer, have been inconsistent. AIM A systematic review with meta-analysis was conducted to investigate the association and the dose-response of alcohol with CRA. METHODS A literature search was performed on PubMed to identify relevant studies published up to January 2014. A fixed or random effects model was used to estimate summarised relative risks (RRs) and 95% confidence intervals (CIs) for the association between alcohol intake and CRA risk. Statistical heterogeneity between studies was assessed with the χ(2) statistic and quantified by I². RESULTS Twenty-three case-control studies and two cohort studies were included in the meta-analysis. All drinkers were associated with 17% increased risk for CRA, compared with nondrinkers or occasional alcohol drinkers. The dose-response analysis demonstrated that for drinkers of 10, 25, 50 and 100 g/day alcohol consumption, the estimated RRs of CRA were 1.02 (95% CI 0.89-1.16), 1.06 (95% CI 0.92-1.20), 1.16 (95% CI 1.02-1.33) and 1.61 (95% CI 1.42-1.84) respectively, in comparison with non-/occasional drinkers. The risks were consistent in the subgroup analyses of gender and site of adenoma, while it was stronger in European studies than the studies in the US and Asia. CONCLUSIONS This study suggests that alcohol intake is related to a significant increase of risk for colrectal adenoma.
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Affiliation(s)
- J-Z Zhu
- Department of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China
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Kim MC, Kim CS, Chung TH, Park HO, Yoo CI. Metabolic syndrome, lifestyle risk factors, and distal colon adenoma: A retrospective cohort study. World J Gastroenterol 2011; 17:4031-7. [PMID: 22046093 PMCID: PMC3199563 DOI: 10.3748/wjg.v17.i35.4031] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/26/2010] [Revised: 05/19/2011] [Accepted: 05/26/2011] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate relationships between colorectal adenoma incidence, metabolic syndrome (MS) components and lifestyle factors.
METHODS: We conducted a retrospective cohort study using data from individuals who had multiple sigmoidoscopies for colon cancer at the Health Promotion Center of Ulsan University Hospital in Korea from 1998 to 2007.
RESULTS: By multivariate analysis, the incidence of distal colon adenoma was increased by more than 1.76 times in individuals with at least one component of MS compared to those without a component of MS. After adjustment for age, gender, smoking, drinking, and physical exercise, only high body mass index (BMI) was significantly associated with the incidence of distal colon adenoma (Hazard ratio 1.66, 95% confidence interval 1.05-2.62).
CONCLUSION: Our results suggest that high BMI may increase the risk of colorectal adenoma in Korean adults.
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Shin A, Hong CW, Sohn DK, Chang Kim B, Han KS, Chang HJ, Kim J, Oh JH. Associations of cigarette smoking and alcohol consumption with advanced or multiple colorectal adenoma risks: a colonoscopy-based case-control study in Korea. Am J Epidemiol 2011; 174:552-62. [PMID: 21791710 DOI: 10.1093/aje/kwr098] [Citation(s) in RCA: 39] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/07/2023] Open
Abstract
The associations between alcohol consumption and cigarette smoking habits and the risk for colorectal adenomatous polyps according to the detailed clinical information about polyps were assessed in a large colonoscopy-based study. The study enrolled participants who visited the National Cancer Center of the Republic of Korea for cancer screening between April 2007 and April 2009. In 1,242 newly diagnosed colorectal adenoma patients and 3,019 polyp-free controls, past smokers (odds ratio (OR) = 1.31, 95% confidence interval (CI): 1.04, 1.65) and current smokers (OR = 1.70, 95% CI: 1.37, 2.11) had increased risks for adenomas compared with nonsmokers. Cigarette smoking conferred an even higher risk for advanced adenomas and 3 or more adenomas than for low-risk adenomas or a single adenoma. Dose-response relations were observed among the daily number of cigarettes smoked, the duration of smoking, the pack-years of smoking, and the risk for adenomas. A longer duration of alcohol consumption was associated with a higher risk for advanced adenomas (for >28 years of consumption: OR = 2.0, 95% CI: 1.10, 3.64) and 3 or more adenomas (OR = 2.19, 95% CI: 1.27, 3.76). In conclusion, cigarette smoking and alcohol consumption play roles in colorectal carcinogenesis, and the association differs by the clinical features of the adenomas.
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Affiliation(s)
- Aesun Shin
- Colorectal Cancer Branch, National Cancer Center Hospital, 323 Ilsanro Ilsandong-gu, Goyang-si, Geyonggi-do 410-769, Republic of Korea
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Sun ZJ, Huang YH, Wu JS, Yang YC, Chang YF, Lu FH, Chang CJ. The association of serum lipids with the histological pattern of rectosigmoid adenoma in Taiwanese adults. BMC Gastroenterol 2011; 11:54. [PMID: 21575164 PMCID: PMC3112117 DOI: 10.1186/1471-230x-11-54] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/20/2010] [Accepted: 05/15/2011] [Indexed: 11/10/2022] Open
Abstract
BACKGROUND The mortality rate of colorectal cancer ranks third behind lung and hepatic cancer in Taiwan. Colorectal cancer mostly arises from adenomatous polyps of left colon. The aim of our study was to examine the association of serum lipids with the histological pattern of rectosigmoid adenoma. METHODS There were 2,506 eligible examinees aged 20 and above who underwent sigmoidoscopy as a screening examination in National Cheng Kung University Hospital between January 2003 and October 2006. They were classified into three groups: tubular adenoma (333 subjects), villous-rich (tubulovillous/villous) adenoma (53 subjects) and normal (2,120 subjects). We defined high total cholesterol (TC) as a level ≧200 mg/dl, low high-density lipoprotein cholesterol (HDL-C) as a level <40 mg/dL, and high triglyceride (TG) as a level ≧200 mg/dl according to the third report of the National Cholesterol Education Program expert panel on detection, evaluation, and treatment of high blood cholesterol in adults. Adenoma histology was classified as tubular, tubulovillous and villous according to the proportion of villous part. RESULTS Among the study population, 333 subjects (13.3%) had tubular adenomas and 53 subjects (2.1%) had villous-rich adenomas. The odds ratio (OR) for villous-rich adenoma in subjects with TG≧200 mg/dL compared to those with TG < 200 mg/dL was 3.20 (95% confidence interval [CI]:1.71-6.01), after adjusting for age, gender, general obesity, central obesity, diabetes, hypertension, smoking, and alcohol consumption. If further taking high TC and low HDL-C into consideration, the OR was 4.42 (95% CI:2.03-9.63). CONCLUSIONS Our study showed that subjects with high serum TG tended to have a higher risk of tubulovillous/villous adenoma in rectosigmoid colon. Therefore, reducing the serum TG level might be one method to prevent the incidence of colorectal cancer.
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Affiliation(s)
- Zih-Jie Sun
- Department of Family Medicine, National Cheng Kung University College of Medicine and Hospital, Dou-Liou Branch, No.345, Zhuangjing Rd., Douliou City, Yunlin County 640, Taiwan
| | - Ying-Hsiang Huang
- Department of Family Medicine, National Cheng Kung University Hospital, No.138, Shengli Rd., East Dist., Tainan City 701, Taiwan
| | - Jin-Shang Wu
- Department of Family Medicine, National Cheng Kung University Hospital, No.138, Shengli Rd., East Dist., Tainan City 701, Taiwan
| | - Yi-Ching Yang
- Department of Family Medicine, National Cheng Kung University Hospital, No.138, Shengli Rd., East Dist., Tainan City 701, Taiwan
| | - Ying-Fang Chang
- Department of Family Medicine, National Cheng Kung University Hospital, No.138, Shengli Rd., East Dist., Tainan City 701, Taiwan
| | - Feng-Hwa Lu
- Department of Family Medicine, National Cheng Kung University Hospital, No.138, Shengli Rd., East Dist., Tainan City 701, Taiwan
| | - Chih-Jen Chang
- Department of Family Medicine, National Cheng Kung University Hospital, No.138, Shengli Rd., East Dist., Tainan City 701, Taiwan
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Ray G, Henson DE, Schwartz AM. Cigarette smoking as a cause of cancers other than lung cancer: an exploratory study using the Surveillance, Epidemiology, and End Results Program. Chest 2010; 138:491-9. [PMID: 20154072 DOI: 10.1378/chest.09-1909] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/01/2022] Open
Abstract
BACKGROUND Cigarette smoking is causally related to several cancers, particularly lung cancer, yet for some cancers there are inconsistent associations. This study investigates the association of smoking with other cancers by correlating them with the regional incidence rates for lung cancer, which was used as a proxy for cigarette smoking. This ecologic approach relating cigarette smoking to cancer using a large database avoids the limitations and bias present in case-control and cohort studies. METHODS Based on the assumption that regions with a high rate of lung cancer also have a high rate of cigarette smoking, our original hypothesis is that these high-intensity regions will also have high rates of other cancers if they are associated with cigarette smoking. Linear regression and correlation analysis of regional incidence rates for lung cancer, obtained from the Surveillance, Epidemiology, and End Results (SEER) Program, were plotted with incidence rates of other cancers to determine the association between lung cancer and the other cancers. RESULTS Cancers that have a strong correlation with cigarette smoking in the literature also demonstrate a strong correlation with lung cancer. These cancers included urinary bladder, laryngeal, esophageal, colorectal, and kidney cancer. A number of cancers showed a weak association with cigarette smoking, such as pancreatic and liver cancer. Other cancers showed no correlation, such as ovarian and prostate cancer. CONCLUSIONS Cancers that respectively showed a strong or absent correlation with lung cancer in the SEER Program were similarly strongly or weakly correlated with cigarette smoking in the literature. Cancers with borderline correlations show ambiguous results or confounding variables in the literature.
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Affiliation(s)
- Gabrielle Ray
- Department of Epidemiology and Biostatistics, School of Public Health and Health Services, George Washington University, Washington, DC 20037, USA
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Lifestyle factors, obesity and the risk of colorectal adenomas in EPIC-Heidelberg. Cancer Causes Control 2009; 20:1397-408. [DOI: 10.1007/s10552-009-9366-3] [Citation(s) in RCA: 39] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/28/2008] [Accepted: 05/06/2009] [Indexed: 12/13/2022]
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Abstract
It is estimated that almost 1.5 million people in the USA are diagnosed with cancer every year. However, due to the substantial effect of modifiable lifestyle factors on the most prevalent cancers, it has been estimated that 50% of cancer is preventable. Physical activity, weight loss, and a reduction in alcohol use can strongly be recommended for the reduction of breast cancer risk. Similarly, weight loss, physical activity, and cessation of tobacco use are important behavior changes to reduce colorectal cancer risk, along with the potential benefit for the reduction of red meat consumption and the increase in folic acid intake. Smoking cessation is still the most important prevention intervention for reducing lung cancer risk, but recent evidence indicates that increasing physical activity may also be an important prevention intervention for this disease. The potential benefit of lifestyle change to reduce prostate cancer risk is growing, with recent evidence indicating the importance of a diet rich in tomato-based foods and weight loss. Also, in the cancers for which there are established lifestyle risk factors, such as physical inactivity for breast cancer and obesity for colorectal cancer, there is emerging information on the role that genetics plays in interacting with these factors, as well as the interaction of combinations of lifestyle factors. Integration of genetic information into lifestyle factors can help to clarify the causal relationships between lifestyle and genetic factors and assist in better identifying cancer risk, ultimately leading to better-informed choices about effective methods to enhance health and prevent cancer.
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Affiliation(s)
- Yvonne M Coyle
- Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA
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Omata F, Brown WR, Tokuda Y, Takahashi O, Fukui T, Ueno F, Mine T. Modifiable risk factors for colorectal neoplasms and hyperplastic polyps. Intern Med 2009; 48:123-8. [PMID: 19182421 DOI: 10.2169/internalmedicine.48.1562] [Citation(s) in RCA: 44] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/06/2022] Open
Abstract
PURPOSE Obesity, smoking and alcohol are modifiable putative risk factors for colorectal neoplasms (CRN) and hyperplastic polyps (HP). The aim of this study was to evaluate the strength of association between these modifiable risk factors and colorectal polyps. METHODS These risk factors were assessed by using a questionnaire completed by the patient prior to colonoscopy. Eight hundred-seventy consecutive patients satisfying inclusion criteria who had undergone a complete colonoscopy were divided into 4 groups: CRN (n=194), HP (n=132), CRN and HP (n=42) and control (neither CRN nor HP; n=586). Multiple logistic regression was performed. RESULTS The ORs [95%CI] of both CRN and HP for incremental body mass index expressed in 2 categories (>or=22, >or=25) were 2.12 [1.00, 4.50] and 1.41 [0.53, 3.77], respectively. The ORs [95%CI] of CRN and HP for heavy smoking of over 20 pack-years were 1.66 [1.05, 2.64] and 1.67 [1.01, 2.77], respectively. The ORs of CRN and HP for habitual alcohol drinking (median ethanol intake 32 g/day and interquartile range 18-40 g/day) were 1.31 [0.86, 1.98] and 1.91 [1.06, 3.47], respectively. CRN and HP were correlated with each other (p=0.0043, chi-square test). Aging was a significant risk factor for all three groups of colorectal polyps. CONCLUSION These findings are especially important since smoking and alcohol consumption are modifiable risk factors. Heavy smokers should be encouraged to quit to reduce their risk of CRN and HP. Habitual drinkers should be warned of the risk of HP. HP can be a marker of coincidence of CRN.
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Affiliation(s)
- Fumio Omata
- Gastroenterology Center, St Luke's International Hospital, Tokyo, Japan.
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Ishibe N, Freedman AN, Michalek AM, Iacobuziodonahue C, Mettlin CJ, Petrelli NJ, Asirwatham JE, Hamilton SR. Expression of p27Kip1and bcl-2, cigarette smoking, and colorectal cancer risk. Biomarkers 2008; 5:225-34. [DOI: 10.1080/135475000230389] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/16/2022]
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Botteri E, Iodice S, Raimondi S, Maisonneuve P, Lowenfels AB. Cigarette smoking and adenomatous polyps: a meta-analysis. Gastroenterology 2008; 134:388-95. [PMID: 18242207 DOI: 10.1053/j.gastro.2007.11.007] [Citation(s) in RCA: 222] [Impact Index Per Article: 13.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/31/2007] [Accepted: 10/25/2007] [Indexed: 12/12/2022]
Abstract
BACKGROUND & AIMS Through the past 2 decades, a consistent association between cigarette smoking and colorectal adenomatous polyps, recognized precursor lesions of colorectal cancer, has been shown. We performed a meta-analysis to provide a quantitative pooled risk estimate of the association, focusing on the different characteristics of the study populations, study designs, and clinical feature of the polyps. METHODS We performed a comprehensive literature search of studies linking cigarette smoking and adenomas. We used random effects models to evaluate pooled relative risks and performed dose-response, heterogeneity, publication bias, and sensitivity analyses. RESULTS Forty-two independent observational studies were included in the analysis. The pooled risk estimates for current, former, and ever smokers in comparison with never smokers were 2.14 (95% confidence interval [CI], 1.86-2.46), 1.47 (95% CI, 1.29-1.67), and 1.82 (95% CI, 1.65-2.00), respectively. The association was stronger for high-risk adenomas than for low-risk adenomas. Studies in which all controls underwent full colonoscopy showed a higher risk compared with studies in which some or all controls underwent partial colon examination. CONCLUSIONS This meta-analysis provides strong evidence of the detrimental effect of cigarette smoking on the development of adenomatous polyps. Smoking is important for both formation and aggressiveness of adenomas.
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Affiliation(s)
- Edoardo Botteri
- Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy.
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Küry S, Buecher B, Robiou-du-Pont S, Scoul C, Sébille V, Colman H, Le Houérou C, Le Neel T, Bourdon J, Faroux R, Ollivry J, Lafraise B, Chupin LD, Bézieau S. Combinations of cytochrome P450 gene polymorphisms enhancing the risk for sporadic colorectal cancer related to red meat consumption. Cancer Epidemiol Biomarkers Prev 2007; 16:1460-7. [PMID: 17627011 DOI: 10.1158/1055-9965.epi-07-0236] [Citation(s) in RCA: 63] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023] Open
Abstract
Susceptibility to sporadic colorectal cancers (CRC) is generally thought to be the sum of complex interactions between environmental and genetic factors, all of which contribute independently, producing only a modest effect on the whole phenomenon. However, to date, most research has concealed the notion of interaction and merely focused on dissociate analyses of risk factors to highlight associations with CRC. By contrast, we have chosen a combinative approach here to explore the joint effects of several factors at a time. Through an association study based on 1,023 cases and 1,121 controls, we examined the influence on CRC risk of environmental factors coanalyzed with combinations of six single nucleotide polymorphisms located in cytochrome P450 genes (c.-163A>C and c.1548T>C in CYP1A2, g.-1293G>C and g.-1053C>T in CYP2E1, c.1294C>G in CYP1B1, and c.430C>T in CYP2C9). Whereas separate analyses of the SNPs showed no effect on CRC risk, three allelic variant combinations were found to be associated with a significant increase in CRC risk in interaction with an excessive red meat consumption, thereby exacerbating the intrinsic procarcinogenic effect of this dietary factor. One of these three predisposing combinations was also shown to interact positively with obesity. Provided that they are validated, our results suggest the need to develop robust combinative methods to improve genetic investigations into the susceptibility to CRC.
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Affiliation(s)
- Sébastien Küry
- Laboratoire d'Etude de l'ADN, Faculté de Médecine de Nantes, 1 rue Gaston Veil, 44035 Nantes Cedex, France.
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16
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Sun CL, Yuan JM, Koh WP, Yu MC. Green tea, black tea and colorectal cancer risk: a meta-analysis of epidemiologic studies. Carcinogenesis 2006; 27:1301-9. [PMID: 16638787 DOI: 10.1093/carcin/bgl024] [Citation(s) in RCA: 129] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/21/2023] Open
Abstract
Experimental studies have supported tea as a chemopreventive agent for colorectal cancer. No quantitative summary of the epidemiologic evidence on tea and colorectal cancer risk has ever been performed. The current meta-analysis included 25 papers conducted in 11 countries across three continents (North America, Asia and Europe). Summary odds ratios (ORs) for highest versus non/lowest tea consumption levels were calculated based on fixed and random effects models. The meta-regression and stratified methods were used to examine heterogeneity across studies. For green tea, the combined results from eight studies indicated a reduced risk of colorectal cancer with intake [summary OR = 0.82, 95% confidence interval (CI) = 0.69-0.98]. The protective effect is mainly found among the three case-control studies of colon cancer (summary OR = 0.74, 95% CI = 0.60-0.93). Results from studies of rectal cancer irrespective of study design (case-control versus cohort) (summary OR = 0.99, 95% CI = 0.71-1.37) and cohort studies of colon cancer (summary OR = 0.99, 95% CI = 0.79-1.24) were compatible with the null hypothesis. For black tea, the summary OR derived from 20 studies was 0.99 (95% CI = 0.87-1.13). There is wide divergence in results across the 20 individual studies; formal tests for homogeneity across studies revealed statistically significant differences in findings across all studies (P < 0.001), amongst the 7 cohort studies (P = 0.002), and amongst the 13 case-control studies (P < 0.001). Despite the strong evidence from in vitro and non-human in vivo studies in support of green and black tea as potential chemopreventive agents against colorectal cancer, available epidemiologic data are insufficient to conclude that either tea type may protect against colorectal cancer in humans.
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Affiliation(s)
- Can-Lan Sun
- The Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA
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17
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Gondal G, Grotmol T, Hofstad B, Bretthauer M, Eide TJ, Hoff G. Lifestyle-related risk factors and chemoprevention for colorectal neoplasia: experience from the large-scale NORCCAP screening trial. Eur J Cancer Prev 2005; 14:373-9. [PMID: 16030428 DOI: 10.1097/00008469-200508000-00010] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
The objective of this study was to evaluate the potential beneficial effects of non-steroidal anti-inflammatory drugs (NSAIDs) and/or acetylsalicylic acid (ASA) and hormone replacement therapy (HRT) on colorectal neoplasia, and to compare their effects with those of lifestyle-related risk factors in 12 960 individuals who underwent flexible sigmoidoscopy screening examination. The association between these factors and colonic neoplasia was assessed by logistic regression analysis. NSAIDs and/or ASA intake were associated with decreased risk of distal low grade adenoma (DLGA) (adjusted odds ratio (OR) 0.80, P trend=0.02) in men. The duration of HRT was inversely related to the risk of DLGA (OR 0.89, P trend=0.08). Current smoking increased the risk of DLGA and distal advanced neoplasia (DAN) in both men (OR 2.50, P<0.01) and women (OR 2.30, P<0.01). There was a significant positive trend for increasing risk of DLGA (OR 1.16, P<0.01) and DAN (OR 1.20, P=0.02) with increasing use of alcohol among men, but not among women. Prescription of NSAIDs and/or ASA for chronic conditions may not be expected to have a substantial preventive effect on colorectal neoplasia in comparison with the adverse effect of smoking and alcohol. This may be explained by an increased risk of colorectal neoplasia for patients with conditions for which NSAIDs or ASA are being prescribed.
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Affiliation(s)
- G Gondal
- Cancer Registry of Norway, Institute of Population-based Cancer Research, Montebello, N-0310 Oslo, Norway
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18
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Paskett ED, Reeves KW, Pineau B, Albert PS, Caan B, Hasson M, Iber F, Kikendall JW, Lance P, Shike M, Slattery ML, Weissfeld J, Kahle L, Schatzkin A, Lanza E. The Association Between Cigarette Smoking and Colorectal Polyp Recurrence (United States). Cancer Causes Control 2005; 16:1021-33. [PMID: 16184467 DOI: 10.1007/s10552-005-0298-2] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/15/2004] [Accepted: 04/29/2005] [Indexed: 02/06/2023]
Abstract
OBJECTIVE Although evidence exists linking smoking to precancerous colorectal adenomatous polyps, few studies have examined the association between cigarette smoking and recurrence of colorectal polyps. This association was investigated prospectively with data from the Polyp Prevention Trial. METHODS Cigarette smoking data were collected through baseline interviews. The study was completed by 1872 men and women with presence of adenomas at baseline colonoscopy. Multiple logistic regression analysis was used to examine the association between cigarette smoking and polyp recurrence (adenomatous and hyperplastic) up to four years from baseline. RESULTS Adenoma recurrence was not related to cigarette smoking. Current smokers had increased odds of hyperplastic polyps at follow-up compared to never smokers (OR 2.88, 95% CI 2.06-4.01). Current smoking was associated with subsequent distal (OR 3.44, 95% CI 2.38-4.95) and rectal (OR 3.53, 95% CI 2.15-5.78) hyperplastic polyps, but not subsequent proximal hyperplastic polyps. Cigarette smoking was associated with subsequent multiple and small size (4 mm) hyperplastic polyps. Significant linear trends were observed between development of subsequent hyperplastic polyps and all smoking variables. CONCLUSIONS Although no association with recurrent adenomas was observed, cigarette smoking was significantly associated with hyperplastic polyp development, except for those in the proximal colon. This prospective study confirms that cigarette smoking has a significant effect on the development of hyperplastic colorectal polyps.
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Affiliation(s)
- Electra D Paskett
- Division of Population Sciences, Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210-1240, USA.
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19
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Ye YN, Liu ESL, Shin VY, Wu WKK, Cho CH. Contributory role of 5-lipoxygenase and its association with angiogenesis in the promotion of inflammation-associated colonic tumorigenesis by cigarette smoking. Toxicology 2004; 203:179-88. [PMID: 15363593 DOI: 10.1016/j.tox.2004.06.004] [Citation(s) in RCA: 54] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/02/2004] [Revised: 06/03/2004] [Accepted: 06/04/2004] [Indexed: 01/03/2023]
Abstract
Our previous study shows that cigarette smoking can promote inflammation-associated adenoma formation in the mouse colon, but the underlying mechanism remains unknown. Several studies suggest that there is a link between 5-lipoxygenase (5-LOX) and carcinogenesis in humans and animals. In the present study, we aims to investigate whether the promoting action of cigarette smoke on inflammation-associated colon cancer formation is associated with 5-LOX activation in mice. Results showed that exposure to the mainstream smoke of unfiltered cigarettes enhanced the 5-LOX protein expression in the inflammation-associated colonic adenomas. It was accompanied with an up-regulation of matrix metalloproteinase-2 (MMP-2) and vascular endothelial growth factor (VEGF). Both are the key angiogenic factors for tumorigenesis. 5-LOX inhibitors decreased the incidence of colonic adenoma formation and reduced angiogenesis, MMP-2 activity and VEGF protein expression in the colons of these animals. Taken together, these results strongly suggest that cigarette smoke can induce 5-LOX expression which plays an important role in activation of MMP-2 and VEGF to induce angiogenic process and promotion of inflammation-associated adenoma formation in mice.
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Affiliation(s)
- Yi-Ni Ye
- Department of Pharmacology, Faculty of Medicine, Zhejiang University, Hangzhou, China
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20
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Abstract
BACKGROUND Gastrointestinal cancer is one of the leading causes of cancer mortality in the world. Therefore, numerous efforts are being made to find chemoprotective substances able to reduce its incidence. Amongst these, green tea, one of the most popular beverages world-wide, has been reported to provide protective effects against gastrointestinal cancer. AIM To critically evaluate all epidemiological studies reporting an association between green tea consumption and a reduced risk of gastrointestinal cancer. METHODS Epidemiological studies of green tea consumption in relation to gastrointestinal cancer or preneoplastic lesions were identified through computerized literature searches using the following databases: Medline (Pubmed), Embase, Amed, CISCOM, Phytobase and Cochrane Library. Only epidemiological studies indicating the type of tea (green tea) and the site of either cancer or precancerous lesions (stomach or intestine) were included. No language restrictions were imposed. RESULTS Twenty-one epidemiological investigations met our inclusion/exclusion criteria. CONCLUSION These studies seemed to suggest a protective effect of green tea on adenomatous polyps and chronic atrophic gastritis formations. By contrast, there was no clear epidemiological evidence to support the suggestion that green tea plays a role in the prevention of stomach and intestinal cancer.
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Affiliation(s)
- F Borrelli
- Department of Experimental Pharmacology, University of Naples Federico II, Naples, Italy.
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21
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Toyomura K, Yamaguchi K, Kawamoto H, Tabata S, Shimizu E, Mineshita M, Ogawa S, Lee KY, Kono S. Relation of cigarette smoking and alcohol use to colorectal adenomas by subsite: the self-defense forces health study. Cancer Sci 2004; 95:72-6. [PMID: 14720330 PMCID: PMC11159628 DOI: 10.1111/j.1349-7006.2004.tb03173.x] [Citation(s) in RCA: 48] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/31/2003] [Revised: 11/13/2003] [Accepted: 11/18/2003] [Indexed: 12/11/2022] Open
Abstract
While smoking has consistently been shown to be related to increased risk of colorectal adenomas, few studies have addressed the association between smoking and site-specific colorectal adenomas. The reported association between alcohol use and colorectal adenomas has been inconsistent. We evaluated risks of adenomas at the proximal colon, distal colon, and rectum in relation to cigarette smoking and alcohol use, and their interaction. Subjects were 754 cases with histologically proven colorectal adenomas and 1547 controls with normal colonoscopy among male officials of the Self-Defense Forces (SDF) undergoing total colonoscopy at two SDF hospitals. Statistical adjustment was made for hospital, rank, body mass index, physical activity, and either smoking or alcohol drinking. Cigarette smoking was significantly associated with an increased risk of adenomas, regardless of the location of the adenomas, but the increased risk associated with smoking was more pronounced for rectal adenomas. Alcohol use was associated with moderately increased risks of distal colon and rectal adenomas, but not of proximal colon adenomas. Cigarette smoking, but not alcohol drinking, was associated with greater increases in the risk of large adenomas and of multiple adenomas across the colorectum. There was no measurable interaction of cigarette smoking and alcohol drinking on colorectal adenomas. The findings corroborate an increased risk of colorectal adenomas associated with smoking and a weak association between alcohol use and colorectal adenomas. Further studies are needed to confirm whether smoking is more strongly related to rectal adenomas, large adenomas, or multiple adenomas.
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Affiliation(s)
- Kengo Toyomura
- Department of Preventive Medicine, Faculty of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan.
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22
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23
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Tiemersma EW, Bunschoten A, Kok FJ, Glatt H, de Boer SY, Kampman E. Effect ofSULT1A1 andNAT2 genetic polymorphism on the association between cigarette smoking and colorectal adenomas. Int J Cancer 2003; 108:97-103. [PMID: 14618622 DOI: 10.1002/ijc.11533] [Citation(s) in RCA: 48] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]
Abstract
Cigarette smoke contains polycyclic hydrocarbons and arylamines that may both be activated by sulfotransferase, encoded by SULT1A1. A genetic polymorphism leads to an Arg213His substitution, thereby decreasing enzyme activity and stability and might thus modify the association between smoking and colorectal adenomas. We investigated this in a Dutch case-control study. Additionally, we evaluated potential roles of epoxide hydrolase (EPHX), N-acetyltransferases (NAT1 and NAT2) and glutathione S-transferases (GSTM1 and GSTT1). The data analysis included 431 adenoma cases and 432 polyp-free controls (54% women; mean age, 54.6 years) enrolled at endoscopy in 8 Dutch hospitals between 1997 and 2000. All participants provided data on smoking habits and blood for DNA isolation. Genotyping was performed using appropriate polymerase chain reaction-restriction fragment length polymorphism procedures. Multivariate models included age, sex, endoscopy indication, consumption of snacks and alcohol and, if appropriate, daily smoking dose or smoking duration. Smoking increased colorectal adenoma risk, most importantly by duration. Smoking for more than 25 years more than doubled adenoma risk (OR = 2.4, 95% CI = 1.4-4.1) compared to never smoking. Combinations of SULT1A1 fast sulfation (*1/*1) and of NAT2 slow acetylation with smoking resulted in a 4 times higher risk of adenomas compared to never smokers with other inherited gene variants, although there was no statistically significant effect modification. We found no clear effects of the other genetic polymorphisms on the association between smoking and adenomas. We conclude that smoking increases risk of colorectal adenomas and that SULT1A1 and NAT2 only modestly modify this association.
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Affiliation(s)
- Edine W Tiemersma
- Division of Human Nutrition and Epidemiology, Wageningen University, Wageningen, The Netherlands
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24
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Abstract
Primary prevention of colonic adenomas and cancer through dietary interventions or chemoprevention has great appeal. This article discusses primary prevention goals and promising nutritional or chemopreventive strategies. There is substantial observational evidence that diets high in total calories and fat and or low in fruits and vegetables or total fiber as well as low levels of physical activity are related to the risk of colonic neoplasia. Similar observational data indicate that diets high in specific nutrients such as antioxidant vitamins or calcium may be protective. The article describes some of the newer chemopreventive agents and reviews the data linking diet and lifestyle to colorectal cancer risk, focusing on interventions that have also been studied in prospective clinical trials. Finally the evidence supporting the role of non-steroidal anti-inflammatory drugs for the chemoprevention of CRC is reviewed and the status of several other promising newer agents that are entering human trials is summarized.
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Affiliation(s)
- David Gatof
- Division of Gastroenterology, University of Colorado Health Sciences Center, University of Colorado School of Medicine B158, 4200 E. Ninth Avenue, Denver, CO 80262, USA
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25
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Bardou M, Montembault S, Giraud V, Balian A, Borotto E, Houdayer C, Capron F, Chaput JC, Naveau S. Excessive alcohol consumption favours high risk polyp or colorectal cancer occurrence among patients with adenomas: a case control study. Gut 2002; 50:38-42. [PMID: 11772965 PMCID: PMC1773084 DOI: 10.1136/gut.50.1.38] [Citation(s) in RCA: 52] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
BACKGROUND AND AIMS Excessive alcohol consumption is a risk factor for developing colorectal adenomas. This study aimed to investigate the influence of excessive alcohol consumption on the occurrence of high risk polyps (adenoma > or = 10 mm, villous component, high grade dysplasia) or colorectal cancer among patients with at least one colonic adenoma. PATIENTS AND METHODS Three groups of patients with at least one colorectal adenoma were included in a case control study: 401 heavy drinkers (group HD, mean daily alcohol intake 117 (SD 4) g/day for a mean duration of 22 (SD 0.6) years), aged 57 (0.5) years (78% men); 152 patients suffering from irritable bowel syndrome (IBS), aged 61 (0.9) years (57% male); and 108 patients with a family history (FH) of colorectal adenoma or cancer, aged 55 (1) years (64% male). Exclusion criteria were: anaemia, haematochezia, personal history of colorectal adenoma or cancer, and for groups HD and IBS a family history of colorectal adenoma and/or cancer. Relative risks were estimated by the odds ratio (OR) using a logistic regression model and were expressed with 95% confidence interval (CI). RESULTS After age and sex adjustment, the likelihood of having an adenoma > or = 10 mm was higher in group HD than in the IBS group (OR 1.8, 95% CI (1.2-2.7)) and the likelihood of having high risk adenomas or cancer was higher in group HD compared with the IBS group (OR 1.6, 95% CI (1.2-2.1)) and the FH group although this was not significant (OR 1.6, 95% CI (0.97-2.6) (p=0.081); 90% CI (1.03-2.4)). After age and sex adjustment, the likelihood of having an adenoma with high grade dysplasia or cancer was higher in group HD than in the IBS group (OR 1.7, 95% CI (1.02-2.8)) or group FH, although this was not significant (OR 3.7, 95% CI (0.98-15) (p=0.076); 90% CI (1.10-12.47)). CONCLUSION In patients with at least one colorectal adenoma, excessive alcohol consumption increases the likelihood of developing high risk adenomas or colorectal cancer.
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Affiliation(s)
- M Bardou
- Hepatogastroenterology Unit, Antoine Béclére Hospital, 157, rue de la Porte de Trivaux F-92141 Clamart Cedex, France.
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26
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Abstract
Regardless of the type and dose of beverage involved, alcohol facilitates the development of gastroesophageal reflux disease by reducing the pressure of the lower esophageal sphincter and esophageal motility. Fermented and nondistilled alcoholic beverages increase gastrin levels and acid secretion. Succinic and maleic acid contained in certain alcoholic drinks also stimulate acid secretion. Low alcohol doses accelerate gastric emptying, whereas high doses delay emptying and slow bowel motility. Alcohol facilitates the development of superficial gastritis and chronic atrophic gastritis--though it has not been shown to cause peptic ulcer. Alcoholic beverages, fundamentally wine, have important bactericidal effects upon Helicobacter pylori and enteropathogenic bacteria. The main alcohol-related intestinal alterations are diarrhea and malabsorption, with recovery after restoring a normal diet. Alcohol facilitates the development of oropharyngeal, esophageal, gastric, and colon cancer. Initial research suggests that wine may be comparatively less carcinogenic.
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Affiliation(s)
- L Bujanda
- Department of Gastroenterology, San Eloy Hospital, Baracaldo, Spain
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27
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Mak KM, Lieber CS. Blood group antigen expression in the rat colon II. Modulation by dietary ethanol consumption. THE ANATOMICAL RECORD 2000; 259:405-12. [PMID: 10903532 DOI: 10.1002/1097-0185(20000801)259:4<405::aid-ar40>3.0.co;2-k] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Abstract
In the accompanying article, we established that in the rat distal colon expression of H, B, and Le(b) blood group antigens by goblet cells is phenotypically fetal in nature. Because of the cocarcinogenic property of ethanol, the present study examined the effects of dietary ethanol consumption, fasting, and withdrawal on the expression of these antigens in the adult rat colon. To that effect, male adult Sprague-Dawley rats were pair-fed ethanol-containing or control Lieber-DeCarli liquid diets for 3 weeks. The effects of ethanol withdrawal were studied in rats fed the ethanol-containing diet for 3 weeks followed by the control diet for 1, 3, and 6 days. In rats fed the control diet, no antigen expression in the distal colon was observed, as expected. Ethanol feeding for 3 weeks resulted in a striking reappearance of H, B, and Le(b) antigens in goblet cells of the distal colon. In colonic crypts, a lower-to-upper crypt gradient of increasing numbers of positive goblet cells was present, suggesting that the induction of antigen expression paralleled the differentiation of goblet cells. After an overnight fast, the number of positive cells was significantly decreased. Withdrawal of ethanol for 1 day further decreased the number of positive goblet cells. The decrease was reflected by a downward shift in the number of positive cells per crypt column, which was more striking in the lower and mid-crypt segments than in the upper segment, suggesting that antigen expression was more labile in immature differentiating goblet cells than in mature ones. No antigen staining of goblet cells was detected after 3 and 6 days of ethanol withdrawal. Hence, expression of H, B, and Le(b) antigens by goblet cells of the distal colon can be modulated by ethanol consumption. Expression in the distal colon of A and Le(a) antigens, which did not exhibit a fetal phenotype, was not affected by ethanol feeding. In conclusion, because of the oncofetal phenotype of H, B, and Le(b) antigens, their reappearance in the distal colon may serve as a cytochemical marker for early recognition of epithelial changes of the colon in ethanol-related cocarcinogenesis before more overt manifestations of neoplasia.
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Affiliation(s)
- K M Mak
- Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center, Bronx, New York 10468, USA
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28
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Breuer-Katschinski B, Nemes K, Marr A, Rump B, Leiendecker B, Breuer N, Goebell H. Alcohol and cigarette smoking and the risk of colorectal adenomas. Dig Dis Sci 2000; 45:487-93. [PMID: 10749322 DOI: 10.1023/a:1005432804902] [Citation(s) in RCA: 22] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Abstract
Whether alcohol and tobacco can be considered as risk factors for the occurrence of adenomas remains inconclusive. A case-control study was carried out to examine these factors while taking into account possible confounding factors. One hundred eighty-two patients with colorectal adenomas and similar numbers of hospital and population controls were compared as to intake of alcohol and various nutrients including smoking and drug intake. There was a positive association between cigarette smoking and adenoma risk compared with hospital controls, the RR being 2.3 (1.1-4.6). Overall alcohol intake was no risk factor in hospital controls, but drinking liquor was associated with an increased risk, the RR being 4.1 (1.3-13.4) and was especially marked in males [RR 10.2 (2.3-46.2)]. Compared with population controls, there was no increased RR associated with smoking or alcohol intake. None of the risk factors was positively associated with disease risk in those with small or large adenomas. These findings suggest that alcohol and tobacco play no major role in the formation or growth of adenomas.
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Affiliation(s)
- B Breuer-Katschinski
- Department of Gastroenterology, Center of Internal Medicine, University Hospital Essen, Germany
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29
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Abstract
The epidemiology and molecular biology of colorectal cancer are reviewed with a view to understanding their interrelationship. Risk factors for colorectal neoplasia include a positive family history, meat consumption, smoking, and alcohol consumption. Important inverse associations exist with vegetables, nonsteroidal anti-inflammatory drugs (NSAIDs), hormone replacement therapy, and physical activity. There are several molecular pathways to colorectal cancer, especially the APC (adenomatous polyposis coli)-beta-catenin-Tcf (T-cell factor; a transcriptional activator) pathway and the pathway involving abnormalities of DNA mismatch repair. These are important, both in inherited syndromes (familial adenomatous polyposis [FAP] and hereditary nonpolyposis colorectal cancer [HNPCC], respectively) and in sporadic cancers. Other less well defined pathways exist. Expression of key genes in any of these pathways may be lost by inherited or acquired mutation or by hypermethylation. The roles of several of the environmental exposures in the molecular pathways either are established (e.g., inhibition of cyclooxygenase-2 by NSAIDs) or are suggested (e.g., meat and tobacco smoke as sources of specific blood-borne carcinogens; vegetables as a source of folate, antioxidants, and inducers of detoxifying enzymes). The roles of other factors (e.g., physical activity) remain obscure even when the epidemiology is quite consistent. There is also evidence that some metabolic pathways, e.g., those involving folate and heterocyclic amines, may be modified by polymorphisms in relevant genes, e.g., MTHFR (methylenetetrahydrofolate reductase) and NAT1 (N-acetyltransferase 1) and NAT2. There is at least some evidence that the general host metabolic state can provide a milieu that enhances or reduces the likelihood of cancer progression. Understanding the roles of environmental exposures and host susceptibilities in molecular pathways has implications for screening, treatment, surveillance, and prevention.
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Affiliation(s)
- J D Potter
- Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA.
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30
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Nagata C, Shimizu H, Kametani M, Takeyama N, Ohnuma T, Matsushita S. Cigarette smoking, alcohol use, and colorectal adenoma in Japanese men and women. Dis Colon Rectum 1999; 42:337-42. [PMID: 10223753 DOI: 10.1007/bf02236350] [Citation(s) in RCA: 34] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
Abstract
PURPOSE The aim of this study was to examine the relationships between smoking and alcohol use and risk of colorectal adenoma. METHODS Information about smoking, alcohol use, and other lifestyle variables were obtained prospectively from 14,427 male and 17,125 female residents in a city of Gifu Prefecture, Japan, by a self-administered questionnaire in September, 1992. Colorectal adenomas were newly diagnosed in 181 men and 78 women in this cohort between January, 1993 and December, 1995 by colonoscopic examination at two major hospitals of the city. Gender-specific and site-specific relative risks and 95 percent confidence intervals adjusted for age and for age plus other potential confounding factors were calculated by using logistic regression models. RESULTS Thirty or more years of smoking was significantly associated with risk of adenoma in general compared with never having smoked in both men and women (relative risk, 1.60; 95 percent confidence interval, 1.02-2.62 and relative risk, 4.54; 95 percent confidence interval, 2.04-9.08, respectively). Effect of smoking was stronger in the proximal colon. After adjusting for age and carbohydrate intake, total alcohol intake was not associated with risk of adenoma in any site in the colon in men. Sake drinkers were at significantly increased risk of adenoma in general, but the dose-response relationship was not statistically significant. Risk of adenoma in the rectum was not significantly increased for those who consumed >30.3 g/day of ethanol (relative risk, 5.7). CONCLUSION These data suggest that smoking is a risk factor of adenoma in Japanese men and women. The role of alcohol, however, is less clear.
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Affiliation(s)
- C Nagata
- Department of Public Health, Gifu University School of Medicine, Japan
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31
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Nosova T, Jokelainen K, Kaihovaara P, Heine R, Jousimies-Somer H, Salaspuro M. Characteristics of aldehyde dehydrogenases of certain aerobic bacteria representing human colonic flora. Alcohol Alcohol 1998. [PMID: 9632053 DOI: 10.1111/j.1530-0277.1997.tb03795.x] [Citation(s) in RCA: 31] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022] Open
Abstract
We have proposed the existence of a bacteriocolonic pathway for ethanol oxidation resulting in high intracolonic levels of toxic and carcinogenic acetaldehyde. This study was aimed at determining the ability of the aldehyde dehydrogenases (ALDH) of aerobic bacteria representing human colonic flora to metabolize intracolonically derived acetaldehyde. The apparent Michaelis constant (Km) values for acetaldehyde were determined in crude extracts of five aerobic bacterial strains, alcohol dehydrogenase (ADH) and ALDH activities of these bacteria at conditions prevailing in the human large intestine after moderate drinking were then compared. The effect of cyanamide, a potent inhibitor of mammalian ALDH, on bacterial ALDH activity was also studied. The apparent Km for acetaldehyde varied from 6.8 (NADP+-linked ALDH of Escherichia coli IH 13369) to 205 microM (NAD+-linked ALDH of Pseudomonas aeruginosa IH 35342), and maximal velocity varied from 6 nmol/min/mg (NAD+-linked ALDH of Klebsiella pneumoniae IH 35385) to 39 nmol/min/mg (NAD+-linked ALDH of Pseudomonas aeruginosa IH 35342). At pH 7.4, and at ethanol and acetaldehyde concentrations that may be prevalent in the human colon after moderate drinking, ADH activity in four out of five bacterial strains were 10-50 times higher than their ALDH activity. Cyanamide inhibited only NAD+-linked ALDH activity of Pseudomonas aeruginosa IH 35342 at concentrations starting from 0.1 nmM. We conclude that ALDHs of the colonic aerobic bacteria are able to metabolize endogenic acetaldehyde. However, the ability of ALDHs to metabolize intracolonic acetaldehyde levels associated with alcohol drinking is rather low. Large differences between ADH and ALDH activities of the bacteria found in this study may contribute to the accumulation of acetaldehyde in the large intestine after moderate drinking. ALDH activities of colonic bacteria were poorly inhibited by cyanamide. This study supports the crucial role of intestinal bacteria in the accumulation of intracolonic acetaldehyde after drinking alcohol. Individual variations in human colonic flora may contribute to the risk of alcohol-related gastrointestinal morbidity.
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Affiliation(s)
- T Nosova
- Research Unit of Alcohol Diseases, University Central Hospital of Helsinki, Finland
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32
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Abstract
OBJECTIVE Investigate risk factors for colon polyp using multivariate analyses. DESIGN In a group responding to a 1992 mail survey, we assessed the association between physician-diagnosed colon polyp and possible risk factors reported primarily 10 years earlier. SETTING Survey respondents within the Cancer Prevention Study II. PARTICIPANTS Respondents, 72,868 men and 81,356 women, who reported no polyp diagnosis when questioned in 1982 at ages 40 to 64 years. MEASUREMENTS AND MAIN RESULTS The characteristics of 7,504 men (10.3%) and 5,111 women (6.3%) reporting a first colon polyp were compared with those of participants who did not report a polyp. After adjustments for age, family history of colorectal cancer, and other potential risk factors, polyp occurrence was associated with 1982 histories of smoking, former smoking, alcohol use of at least two drinks per day (odds ratios [ORs] from 1.5 to 1.1; all p < .005), and a body mass index > or = 28 kg/m2 (men's OR 1.06; 95% confidence interval [CI] 1.00, 1.13; women's OR 1.08; 95% CI 0.99, 1.17). Polyps were also associated with a diagnosis of gallbladder disease or gallstone at any time and with gallbladder surgery up to 1982 (OR from 2.7 to 1.3; all p < .001). Polyp occurrence was inversely associated with 1982 histories of high exercise level (men's OR 0.83; 95% CI 0.76, 0.91; women's OR 0.90; 95% CI 0.78, 1.03), frequent aspirin use in women (OR 0.85; 95% CI 0.77, 0.95), and high parity in women (OR 0.84; 95% CI 0.75, 0.94). Among participants lacking a clinically normal gallbladder, the polyp risks associated with smoking and high body mass index were reduced (p < .04 for interactions). CONCLUSIONS Despite the limitations and potential biases in these self-reported data, the risk factors described here may be useful for identifying persons at modestly increased risk of having a colon polyp. The effect-modifying role of gallbladder status deserves further investigation.
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Affiliation(s)
- H S Kahn
- Department of Epidemiology and Surveillance Research, American Cancer Society, Atlanta, GA 30329-4251, USA
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33
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Freedman AN, Michalek AM, Marshall JR, Mettlin CJ, Petrelli NJ, Zhang ZF, Black JD, Satchidanand S, Asirwatham JE. The relationship between smoking exposure and p53 overexpression in colorectal cancer. Br J Cancer 1996; 73:902-8. [PMID: 8611424 PMCID: PMC2075827 DOI: 10.1038/bjc.1996.180] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023] Open
Abstract
Although epidemiological studies of the relationship between cigarette smoking and colorectal cancer risk have been equivocal, a positive association is consistently found for colorectal adenoma development. We performed an epidemiological study to determine whether p53 protein overexpression, in tumours obtained at the time of resection, is associated with cigarette exposure in colorectal cancer. A total of 163 colorectal cancer cases and 326 healthy controls responded to a standardised questionnaire on colorectal cancer risk factors including detailed information on their history of cigarette smoking. All patients' tumours were analysed immunohistochemically for p53 overexpression using an avidin-biotin immunoperoxidase procedure and polyclonal anti-p53 antibody CM1. Comparison of colorectal cases with controls revealed an elevated risk for ex-smokers (OR = 1.34, 95% CI 0.85-2.12) and current smokers (OR = 1.13, 95% CI 0.63-2.02) when compared with non-smokers. No dose-response relationship was found for total pack-years of smoking (trend test: P = 0.19). However, a trend for total pack-years of smoking was found when p53-positive cases were compared with p53-negative cases suggesting aetiological, heterogeneity (trend test: P = 0.06). Estimating the individual relative risk of developing a p53-positive tumour relative to controls showed no associations for smoking status or total pack-years of smoking. However, when p53-negative cases were compared with controls, an elevated risk was found for ex-smokers (OR = 1.84, 95% CI 1.00-3.37) and current years of smoking (trend test: P = 0.03). Colorectal tumours developing through p53-positive dependent pathways were not associated with smoking exposure. A significant increase in risk was observed for the p53-negative independent pathway with smoking. p53 overexpression appears to be associated with smoking exposure in colorectal cancer.
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Affiliation(s)
- A N Freedman
- Department of Educational Affairs, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
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34
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Abstract
Epidemiologic evidence on the relation between nutrition and colorectal cancer is reviewed. Colon cancer varies approximately 20-fold internationally. Although there is clear evidence of genetic predisposition to colon cancer, much of this variation appears to be related to differences in dietary habits. At present, the data suggest that vegetables are associated with lower risk, and that fiber alone does not account for this association. Further, meat consumption is associated with increased risk but this, too, is not explained solely by its fat content. Several microconstituents of the diet may be associated with reduced risk--including folate and calcium--but phytochemicals of other sorts may be relevant. Mutagenic compounds, particularly heterocyclic amines, produced when protein is cooked, plausibly explain the meat association. The most consistent inverse association is with physical activity. Alcohol is associated, though inconsistently, with increased risk. Rectal cancer is less well studied but, at present, there are few data to suggest that the dietary risk factors are markedly different. Physical activity does not appear to be associated with a lower risk. Colorectal adenomatous polyps also appear to share the spectrum of risk factors seen with colon cancer, although, for adenomas, tobacco smoking is also a clear and consistent risk factor. There are a variety of links between the dietary epidemiology and physiology of colorectal neoplasia and the relevant pathologic and molecular changes. Other causal connections remain to be explicated.
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Affiliation(s)
- J D Potter
- Cancer Prevention Research Program, Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA
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35
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Todoroki I, Kono S, Shinchi K, Honjo S, Sakurai Y, Wakabayashi K, Imanishi K, Nishikawa H, Ogawa S, Katsurada M. Relationship of cigarette smoking, alcohol use, and dietary habits with sigmoid colon adenomas. Ann Epidemiol 1995; 5:478-83. [PMID: 8680611 DOI: 10.1016/1047-2797(95)00064-x] [Citation(s) in RCA: 22] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
Abstract
The relationship between cigarette smoking, alcohol use, and dietary factors and the risk of adenomas of the sigmoid colon was examined in male self-defense officials who received a preretirement health examination at three Self-Defense Forces hospitals in Japan. In the comparison between 228 patients with sigmoid adenomas and 1484 control subjects with normal colonoscopy findings (> or = 60 cm from the anus), a clear dose-response relationship was observed between cigarette smoking and risk of adenoma. After adjustment for rank, body mass index, alcohol use, and physical activity as well as for hospital and survey season, the odds ratios (and 95% confidence intervals (CIs)) for the categories of 0, 1 to 399, 400 to 799, and 800 or more cigarette-years were 1.0, 2.1 (1.2 to 3.5), 2.8 (1.8 to 4.3), and 3.5 (2.1 to 5.8), respectively. Current alcohol drinkers tended to have an increased risk, but without a dose-response relation. Among four types of alcoholic beverages (shochu, sake, beer, and whiskey), only whiskey showed a weak association with risk of adenoma. None of the 13 dietary items studied (including meat and rice consumption) was measurably associated with adenoma risk. The present findings provide additional evidence that cigarette smoking is a risk factor for colon adenomas. It is inconclusive regarding alcohol intake's association with adenoma risk.
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Affiliation(s)
- I Todoroki
- Department of Public Health, National Defense Medical College, Saitama, Japan
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36
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Honjo S, Kono S, Shinchi K, Wakabayashi K, Todoroki I, Sakurai Y, Imanishi K, Nishikawa H, Ogawa S, Katsurada M. The relation of smoking, alcohol use and obesity to risk of sigmoid colon and rectal adenomas. Jpn J Cancer Res 1995; 86:1019-26. [PMID: 8567391 PMCID: PMC5920634 DOI: 10.1111/j.1349-7006.1995.tb03015.x] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023] Open
Abstract
We conducted a case-control study, using 429 cases with histologically confirmed sigmoid adenoma, 75 cases with rectal adenoma, and 3101 controls showing normal colonoscopy at least up to 60 cm from the anus. The subjects were male Self-Defense Forces personnel aged 48-56 who received a retirement health examination including a routine sigmoid- or colonoscopy. Lifestyle characteristics were ascertained by a self-administered questionnaire. Smoking in the recent past (< or = 10 years preceding the colonoscopy) and smoking in the remote past (> 10 years before the colonoscopy) were both significantly associated with risk of sigmoid adenoma but not with rectal adenoma as a whole. After reciprocal adjustment for smoking in the two periods, only smoking in the recent past was associated with both sigmoid colon and rectal adenomas. Odds ratios (OR) of sigmoid adenoma (and 95% confidence interval) for the categories of 0, 1-150, 151-250 and > or = 251 cigarette-years were 1.0 (reference), 1.9 (1.3-2.8), 2.1 (1.4-3.0) and 3.0 (1.9-4.7), respectively (P for trend < 0.01), and those for rectal adenoma were 1.0 (reference), 1.2 (0.4 3.2), 3.5 (1.4-8.5) and 2.0 (0.6 6.7), respectively (P for trend = 0.03). Alcohol use was significantly positively associated with sigmoid adenoma, and insignificantly associated with rectal adenoma. Body mass index was significantly positively associated with sigmoid adenoma, especially large ones. No such association was found for rectal adenoma. These findings suggest that smoking, especially in the recent past, and alcohol use are common risk factors for sigmoid colon and rectal adenomas while obesity may be exclusively related to the growth of sigmoid adenoma.
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Affiliation(s)
- S Honjo
- Department of Public Health, National Defense Medical College, Saitama
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37
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Heineman EF, Zahm SH, McLaughlin JK, Vaught JB. Increased risk of colorectal cancer among smokers: results of a 26-year follow-up of US veterans and a review. Int J Cancer 1994; 59:728-38. [PMID: 7989109 DOI: 10.1002/ijc.2910590603] [Citation(s) in RCA: 111] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
To clarify the relationship between tobacco use and risk of colorectal cancer, we evaluated a cohort of 248,046 American veterans followed prospectively for 26 years. In comparison with veterans who had never used tobacco, the risk of death was significantly increased for colon cancer and rectal cancer among current and former cigarette smokers and among pipe or cigar smokers, controlling for social class and occupational physical activity. Rectal-cancer risk was also significantly elevated among users of chewing tobacco or snuff. For both sites, risk increased significantly with pack-years, earlier age at first use, and number of cigarettes. These results reinforce 2 recent reports of the association of cigarette smoking and colorectal cancer in men and women. Inconsistencies in the findings of earlier epidemiologic studies appear to be due in large part to differences in length of follow-up or in choice of controls. Studies with at least 20 years of follow-up or population-based controls have tended to find elevated risk with tobacco smoking, while those with shorter follow-up or hospital controls have not. This, plus the strength and consistency of the association of smoking and colon polyps, suggest that smoking may primarily affect an early stage in the development of colon cancer. If this association is causal, tobacco use may be responsible for 16% of colon-cancer and 22% of rectal-cancer deaths among these veterans.
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Affiliation(s)
- E F Heineman
- Epidemiology and Biostatistics Program, National Cancer Institute, Rockville, MD 20852
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38
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Abstract
The incidence rates of colon cancer are high in North America and northern Europe, lower in southern Europe, and much lower in Asia and Africa. It is widely believed that environmental factors, particularly dietary patterns, account for most of this marked variation in rates. Over the past decade, a large number of case-control and cohort studies have added a substantial body of evidence regarding our understanding of the causes of colon cancer. Although the data are not entirely consistent, several important risk factors have emerged. The epidemiological evidence that physical inactivity or excess energy intake relative to requirements increases risk of this malignancy is quite strong. Intake of red meat appears to increase risk, but protein-rich sources other than red meat probably do not elevate risk and may even reduce the occurrence of colon cancer. Dietary fat, at least that from sources other than red meat, does not appear to increase risk appreciably. High consumption of vegetables and fruits and the avoidance of highly refined sugar containing foods are likely to reduce risk of colon cancer, although the responsible constituents remain unclear. Alcohol intake may enhance risk of cancers of the distal colorectum, although the evidence is not entirely consistent. The influence of alcohol may be particularly strong when combined with a diet low in methionine and folate, suggesting that the effect of alcohol may be through antagonism of methyl-group metabolism. The combined effect of these dietary factors, as well as modifiable non-dietary factors such as cigarette smoking, suggest that the majority of cases of colon cancer are preventable.
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Affiliation(s)
- E Giovannucci
- Channing Laboratory, Department of Medicine, Harvard Medical School, Boston, MA 02115
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39
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Abstract
Many studies indicate that animals and humans burdened with excess iron are at increased risk of neoplasia at various sites. This review focuses on inquiries that involve iron and colorectal cancer. Relevant studies reported in the past decade are briefly described and evaluated. The studies in animal models and in relatively large groups of humans point to a positive association of excessive iron with colorectal oncogenesis. Phytic acid, a chelator of iron and zinc, may be useful in withholding iron from the carcinogenic process. Sufficient evidence is available to justify construction of long-term prospective studies in humans in which would be monitored (i) levels of iron and phytate intake, (ii) serum transferrin iron saturation and ferritin, (iii) fecal levels of iron and hydroxyl radicals, and (iv) appearance of colorectal polyps, adenomas and carcinomas.
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Affiliation(s)
- E D Weinberg
- Department of Biology, Indiana University, Bloomington 47405
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40
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Papavassiliou ED, Arvind P, Tsioulias GJ, Qiao L, Goldin E, Staiano-Coico L, Rigas B. The effect of ethanol on the expression of HLA class I genes in human colon adenocarcinoma cell lines. Cancer Lett 1994; 81:33-8. [PMID: 8019985 DOI: 10.1016/0304-3835(94)90161-9] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
The loss of HLA antigens by neoplastic cells may allow tumors to escape immune surveillance. We observed reduced expression of HLA antigens during human colon carcinogenesis. Since ethanol, which is associated with human colonic carcinogenesis, modulates the expression of HLA genes, we examined whether it affects the expression of HLA class I genes in human colon adenocarcinoma cell lines. Ethanol (1.7 x 10(-10) M to 1.7 x 10(-1) M), had no effect on the expression of HLA class I antigens on these colonocytes, the corresponding mRNA levels, or the expression of HLA constructs. Our findings do not support the hypothesis that ethanol may modulate the expression of HLA class I genes in human colon cancer cells.
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Affiliation(s)
- E D Papavassiliou
- Department of Medicine, Cornell University Medical College, New York, NY
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41
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Jacobson JS, Neugut AI, Murray T, Garbowski GC, Forde KA, Treat MR, Waye JD, Santos J, Ahsan H. Cigarette smoking and other behavioral risk factors for recurrence of colorectal adenomatous polyps (New York City, NY, USA). Cancer Causes Control 1994; 5:215-20. [PMID: 8061168 DOI: 10.1007/bf01830239] [Citation(s) in RCA: 37] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
Adenomatous polyps (hereinafter referred to as adenomas) are known precursors of colorectal cancer. Cigarette smoking has been associated with adenomas but not with colorectal cancer, while alcohol and fat intake have been associated with both adenomas and cancer in some studies. Approximately 30 percent of patients with resected adenomas develop another adenoma within three years. This case-control study explores the association of cigarette smoking with adenoma recurrence. Between April 1986 and March 1988, we administered a questionnaire to colonoscoped patients aged 35 to 84 years in three New York City (NY, USA) practices. We compared 186 recurrent polyp cases (130 males, 56 females) and 330 controls (187 males, 143 females) who had a history of polypectomy but normal follow-up colonoscopy, by cigarette-smoking pack-years adjusted for possible confounders. Risk for a metachronous or recurrent adenoma was significantly greater in the highest quartile of smokers than in never-smokers among both men (odds ratio [OR] = 1.8, 95 percent confidence interval [CI] = 1.0-3.4) and women (OR = 3.6, CI = 1.7-7.6). Adjustment for time since smoking cessation reduced risk only slightly, as did adjustment for dietary fat intake, which itself remained significant. No association was found between alcohol intake and risk of recurrence. Cigarette smokers appear to have an elevated risk of adenoma recurrence that is not eliminated entirely by smoking cessation. Intervention trials that use adenoma recurrence as an endpoint should take smoking into account.
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42
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Benito E, Cabeza E, Moreno V, Obrador A, Bosch FX. Diet and colorectal adenomas: a case-control study in Majorca. Int J Cancer 1993; 55:213-9. [PMID: 8370618 DOI: 10.1002/ijc.2910550208] [Citation(s) in RCA: 104] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023]
Abstract
A case-control study on dietary factors and colorectal adenomas was conducted in the island of Majorca, Spain, from April 1987 to February 1990. Subjects were interviewed using a food frequency questionnaire. Nutrient and caloric intake was estimated using local food composition tables. The risk of colorectal adenomas was related to the consumption of sugar and pastries. Consumption of vegetables was highly protective, irrespective of the cooking procedures. Analyses by nutrients identified as protective factors fiber from fruits and vegetables, magnesium and zinc, and vitamins C, B6 and folic acid. No excess risk was found for alcohol drinking, intake of saturated fats or animal protein. Of the non-dietary factors, sedentariness in the work-place and urban residence were the only risk factors identified.
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Affiliation(s)
- E Benito
- Unitat d'Epidemiologia i Registre de Càncer de Mallorca, Ciutat de Mallorca, Spain
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43
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Lee WC, Neugut AI, Garbowski GC, Forde KA, Treat MR, Waye JD, Fenoglio-Preiser C. Cigarettes, alcohol, coffee, and caffeine as risk factors for colorectal adenomatous polyps. Ann Epidemiol 1993; 3:239-44. [PMID: 8275195 DOI: 10.1016/1047-2797(93)90025-y] [Citation(s) in RCA: 54] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/29/2023]
Abstract
The possible association of colorectal adenomatous polyps, a precursor lesion for colorectal cancer, with cigarette smoking, alcohol consumption, and coffee and caffeine consumption was investigated in a case-control study. Between April 1986 and March 1988, 271 cases of patients with pathologically confirmed incident colorectal adenomatous polyps and 457 control subjects were collected from three colonoscopy practices in New York City. Information on exposure was obtained by structured interviews. After adjustment of age, statistically significant odds ratios (highest-lowest quartile) were found for cigarette smoking in males (2.2; 95% confidence interval (CI), 1.2 to 3.8) and coffee consumption in females (2.0%; 95% CI, 1.0 to 3.9). No significant associations were obtained for cigarette smoking in females, for coffee consumption in males, or for alcohol or caffeine consumption. After adjustments for alcohol, coffee, and caffeine consumption, the association of adenomas with cigarette smoking remained in males and significant associations were also observed in subcategory analysis for both left-side and right-side adenomatous polyps. Adjustment for cigarette smoking eliminated the association between colorectal adenomatous polyps and coffee consumption in females. Cigarette smoking appears to be a significant risk factor for colorectal adenomatous polyps in males.
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Affiliation(s)
- W C Lee
- Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032
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44
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Kune GA, Vitetta L. Alcohol consumption and the etiology of colorectal cancer: a review of the scientific evidence from 1957 to 1991. Nutr Cancer 1992; 18:97-111. [PMID: 1437657 DOI: 10.1080/01635589209514210] [Citation(s) in RCA: 137] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
The relationship between alcohol consumption and colorectal cancer in humans has been examined in 52 major studies in the past 35 years. An association was found in five of the seven correlational studies. An elevated risk was found in about half of the 31 case-control studies and, of these, in 9 of the 10 studies using community controls but in only 5 of the 17 studies using hospital controls (p = 0.008), suggesting that the absence of association when hospital controls are used is due to a high prevalence of alcohol consumption/alcohol-related illness in the hospital controls. Of the 14 cohort studies, an association with alcohol was found in 10, while in 3 of the 4 cohort studies in which an association was not found the alcohol data obtained were somewhat restricted. A positive dose-response effect was found in two of three cohort studies and in all four case-control studies with community controls in which this effect was examined. In both case-control and cohort studies, the association was found for females and males and for colon and rectal cancer. When the type of alcohol consumed was examined separately, beer was the principal type of at-risk alcoholic beverage, with much less risk for spirits and least risk for wine. Statistically significant elevations of risk were more often found in males than in females and slightly more frequently for rectal than for colon cancer and were related almost entirely to beer, rather than to wine or spirit, consumption. The alcohol risk was independent of the dietary risk in those studies that controlled for this factor. There was some confirmatory evidence for alcohol augmentation in rodent models of chemically induced carcinogenesis in six of nine studies. The hypotheses of alcohol as a direct and specific colorectal carcinogen include increased mucosal cell proliferation, the activation of intestinal procarcinogens, and the role of unabsorbed carcinogens, particularly in beer. Also, five of six other human studies showed an association between alcohol/beer consumption and adenomatous polyps, consistent with the hypothesis that alcohol stimulates the colorectal mucosa. General or indirect carcinogenic effects of alcohol include immunodepression, activation of liver procarcinogens, and changes in bile composition, as well as nitrosamine content of alcoholic beverages and increased tissue nitrosamine levels. With alcohol/beer consumption, the overall conclusion on present evidence is that alcohol, particularly beer consumption, is an etiologic factor for colon and rectal cancer for females and males.(ABSTRACT TRUNCATED AT 400 WORDS)
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Affiliation(s)
- G A Kune
- University of Melbourne, Victoria, Australia
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