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Alcohol Consumption and Cancer Risk

Understanding Possible Causal Mechanisms for Breast and Colorectal Cancers

Evidence Reports/Technology Assessments, No. 197

Investigators: , MD, MPH, , PhD, , BA, , PhD, MPH, , PhD, and , MD, SM, FACP.

ECRI Institute Evidence-based Practice Center
Rockville (MD): Agency for Healthcare Research and Quality (US); .
Report No.: 11-E003

Structured Abstract

Objectives:

The purpose of this report is to systematically examine the possible causal mechanism(s) that may explain the association between alcohol (ethanol) consumption and the risk of developing breast and colorectal cancers.

Data Sources:

We searched 11 external databases, including PubMed and EMBASE, for studies on possible mechanisms. These searches used Medical Subject Headings and free text words to identify relevant evidence.

Review Methods:

Two reviewers independently screened search results, selected studies to be included, and reviewed each trial for inclusion. We manually examined the bibliographies of included studies, scanned the content of new issues of selected journals, and reviewed relevant gray literature for potential additional articles.

Results:

Breast Cancer. Five human and 15 animal studies identified in our searches point to a connection between alcohol intake and changes in important metabolic pathways that when altered may increase the risk of developing breast cancer. Alterations in blood hormone levels, especially elevated estrogen-related hormones, have been reported in humans. Several cell line studies suggest that the estrogen receptor pathways may be altered by ethanol. Increased estrogen levels may increase the risk of breast cancer through increases in cell proliferation and alterations in estrogen receptors. Human studies have also suggested a connection with prolactin and with biomarkers of oxidative stress. Of 15 animal studies, six reported increased mammary tumorigenesis (four administered a co-carcinogen and two did not). Other animal studies reported conversion of ethanol to acetaldehyde in mammary tissue as having a significant effect on the progression of tumor development. Fifteen cell line studies suggested the following mechanisms:

  • increased hormonal receptor levels
  • increased cell proliferation
  • a direct stimulatory effect
  • DNA adduct formation
  • increase cyclic adenosine monophosphate (cAMP)
  • change in potassium channels
  • modulation of gene expression.

Colorectal Cancer. One human tissue study, 19 animal studies (of which 12 administered a co-carcinogen and seven did not), and 10 cell line studies indicate that ethanol and acetaldehyde may alter metabolic pathways and cell structures that increase the risk of developing colon cancer. Exposure of human colonic biopsies to acetaldehyde suggests that acetaldehyde disrupts epithelial tight junctions.

Among 19 animal studies the mechanisms considered included:

  • mucosal damage after ethanol consumption
  • increased degradation of folate
  • stimulation of rectal carcinogenesis
  • increased cell proliferation
  • increased effect of carcinogens.

Ten cell line studies suggested:

  • folate uptake modulation
  • tumor necrosis factor modulation
  • inflammation and cell death
  • DNA adduct formation
  • cell differentiation
  • modulation of gene expression.

One study used a combination of animal and cell line and suggested intestinal cell proliferation and disruption of cellular signals as possible mechanisms.

Conclusions:

Based on our systematic review of the literature, many potential mechanisms by which alcohol may influence the development of breast or colorectal cancers have been explored but the exact connection or connections remain unclear. The evidence points in several directions but the importance of any one mechanism is not apparent at this time.

Contents

540 Gaither Road, Rockville, MD 20850; www​.ahrq.gov

Prepared for: Agency for Healthcare Research and Quality, U.S. Department of Health and Human Services1, Contract Number: 290-2007-10063-I, Prepared by: ECRI Institute Evidence-based Practice Center, Plymouth Meeting, PA

Suggested citation:

Oyesanmi O, Snyder D, Sullivan N, Reston J, Treadwell J, Schoelles KM. Alcohol Consumption and Cancer Risk: Understanding Possible Causal Mechanisms for Breast and Colorectal Cancers. Evidence Report/Technology Assessment No. 197 (prepared by ECRI Institute Evidence-based Practice Center under Contract No. 290-2007-10063-I). AHRQ Publication No. 11-E003. Rockville, MD: Agency for Healthcare Resarch and Quality. November 2010.

This report is based on research conducted by the ECRI Institute Evidence-based Practice Center (EPC) under contract to the Agency for Healthcare Research and Quality (AHRQ), Rockville, MD (Contract No. 290-2007-10063-I). The findings and conclusions in this document are those of the author(s), who are responsible for its content, and do not necessarily represent the views of AHRQ. No statement in this report should be construed as an official position of AHRQ or of the U.S. Department of Health and Human Services.

The information in this report is intended to help clinicians, employers, policymakers, and others make informed decisions about the provision of health care services. This report is intended as a reference and not as a substitute for clinical judgment.

This report may be used, in whole or in part, as the basis for the development of clinical practice guidelines and other quality enhancement tools, or as a basis for reimbursement and coverage policies. AHRQ or U.S. Department of Health and Human Services endorsement of such derivative products may not be stated or implied.

No investigators have any affiliations or financial involvement (e.g., employment, consultancies, honoraria, stock options, expert testimony, grants or patents received or pending, or royalties) that conflict with material presented in this report.

1

540 Gaither Road, Rockville, MD 20850; www​.ahrq.gov

Bookshelf ID: NBK55953
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