New study examines link between alcohol consumption and cancer

Ethanol can also contribute to carcinogenesis through the induction of oxidative stress which is recognised as a key determinant of disease initiation [26]. Oxidative stress can be induced by activation of certain pathways which produce reactive oxygen species (ROS) such as superoxide anion and hydrogen peroxide. One pathway by which ethanol achieves this is through increased CYP2E1 activity which produces high quantities of ROS whilst oxidising ethanol to acetaldehyde [27]. Other sources of ROS during ethanol metabolism include the mitochondrial respiratory chain and some cytosolic enzymes [28]. For example, alcohol – even in very small amounts – can irritate mouth sores caused by some cancer treatments, and can even make them worse.

Effects on other harmful chemicals

There is further hypothesis that alcohol consumption might activate the pathways of other carcinogenic agents; this could occur through the alcohol-induced activity of CYP2E1 which may metabolise pro-carcinogens in tobacco smoke and industrial chemicals [21]. It is also possible that ethanol might aid these carcinogens to penetrate cells, especially those of the mucosa of the upper aerodigestive tract [21,48], where tobacco and alcohol have a synergistic effect on the risk of cancer [11,12]. However, these bacteria have limited capacity to break acetaldehyde down further into its non-harmful compound acetate, thus the oral epithelia are further exposed to acetaldehyde [21,44]. Acetaldehyde concentrations in the saliva of drinkers are between 10 and 100 times higher than in the blood; this is further doubled in smokers who drink alcohol as tobacco smoke contains high levels of acetaldehyde [21]. More than 30 years ago, in 1988, the International Agency for Research on Cancer (IARC) classified alcoholic beverages as a group 1 carcinogen, the most severe classification [4].

Effects of Combined Alcohol and Tobacco Use

With alcohol consumption rising, particularly in rapidly developing countries such as China, there is an urgent need to understand how alcohol affects disease risks in different populations. Total protein carbonyl content was assessed as a measure of oxidatively damaged proteins. To this end, alcohol exposure significantly increased the accumulation of oxidatively damaged proteins in both differentiated and undifferentiated cells after 12 or 24 hours of exposure.

  1. Many studies have found a link between alcohol use and the risk of developing certain cancers.
  2. Overall, about 12,000 people in this group reported that they drink alcohol, and nearly 40% reported engaging in hazardous drinking—that is, repeated excessive alcohol use.
  3. The profile of damaged proteins observed in this study was similar to that observed in brain tissues of alcoholic individuals.
  4. In contrast, in triple-negative breast cancer, the cancer cells carry neither estrogen nor progesterone or HER2 receptors.


For alcohol-related diseases, these included higher sales taxes on alcohol, limits on where and when alcohol can be purchased, and restrictions on marketing to the public. The breakdown of alcohol can also produce reactive oxygen species, also known as free radicals. These molecules can damage DNA, and the gene changes that result can lead to a cell turning cancerous. The WHO researchers also created an interactive website where people can explore the results by country, cancer site, and other variables. For the study, the research team identified 15,199 participants who, between May 2018 and January 2022, reported a history of cancer on their initial survey.

Limitations and Strengths of the Meta-Analysis

“Drinking less is a great way to be healthier,” said Dr. Timothy Naimi, who directs the Canadian Institute for Substance Use Research at the University of Victoria in British Columbia. 4Statistically significant means that the observed result would occur by chance under hypothesized conditions less than a specified proportion of the time (usually 5 percent). 2Statistical analyses generally do not lead to a calculated, accurate result but instead provide an estimate of the result.

The RR for the disease in people without the variable (e.g., abstainers) is defined as 1.0. A RR among the people with the variable (e.g., drinkers) of greater than 1.0 indicates that the variable increases the risk for the disease. The curves shown know the difference between ethanol and alcohol here were obtained by fitting certain statistical models to the data from several studies (i.e., a meta-analysis). Blue dotted lines indicate 95-percent confidence intervals; that is, the range of RR that is 95 percent likely to show a true RR.

In the study, many people being treated for cancer and longer-term cancer survivors reported regularly drinking alcohol—many moderately, but some also heavily and often. According to the study’s findings, male long-term survivors and younger people being treated for cancer were among those who were particularly likely to be heavy or frequent drinkers. The plant secondary compound resveratrol, found in grapes used to make red wine and some other plants, has been investigated for many possible health effects, including cancer prevention. However, researchers have found no association between moderate consumption of red wine and the risk of developing prostate cancer (32) or colorectal cancer (33). Alcohol and its metabolite acetaldehyde can drive cancer development through several pathways. Many of these pathways are interlinked and show the complexity and breadth of alcohol’s harmful potential.

This balance depends on the age, gender, and baseline disease rates among the members of a given population. Consequently, any definite risk-benefit assessment for moderate alcohol drinking requires much more far-reaching analyses that are beyond the scope of this article but that in the future may provide important information from a public health perspective. Other studies in mice assessed the effects of acute and chronic alcohol consumption on tumor growth and metastasis using B16 melanoma and its more metastatic variants, B16F10 and B16BL6. An early study (Capel et al. 1978) found that mice given 10 percent ethanol in drinking water for 2 weeks before inoculation with B16 melanoma into the thigh showed no altered tumor growth or metastasis compared with water-drinking controls. In another study (Tan et al. 2007), tumor growth and angiogenesis were examined in C57BL/6 mice implanted subcutaneously with B16F10 melanoma cells.

For female breast cancer, the meta-analysis described here confirms the existence of a strong dose-risk relationship between alcohol consumption level and breast cancer risk. It is possible, however, that for breast cancer and other types of cancer related to disturbances in female hormone levels, alcohol may act by altering the metabolism and blood levels of female hormones, such as estrogen (Longnecker 1994). Moreover, a recent study suggests that the association may be limited to women with a family history of breast cancer (Vachon et al. xanax side effects 2001). In all, 229 studies (183 case-control studies and 46 cohort studies) met the eligibility criteria and were included in the meta-analysis. Animal models have yielded some insights into the effects of alcohol on tumor growth, survival, and metastasis of different cancers, including breast cancer, lung cancer, liver cancer, and melanoma. However, because cancer is a collection of many different diseases and subtypes, each cancer or cancer subtype might not respond similarly to alcohol, as is evident from the research discussed here.

The importance of these findings is unknown, although patients with tumors that did not express MIF had a worse prognosis than patients that did. Tumor metastasis is the ability of tumor cells to spread from their original site to other sites in the body and to re-establish growth, a new blood supply, and tumor colonies at the new location. (1) Cells that escape from a primary solid tumor invade into the surrounding normal tissue by passing through the basement membrane and extracellular salvia drug overview matrix (ECM). Several factors are involved in the invasion process, including the ability to activate enzymes called matrix metalloproteinases (MMP), which are important for the tumor cells to degrade basement membranes and underlying stroma. (2) The escaped cells reach the blood either directly by actively passing through endothelial cells that line the blood vessels or passively through the lymphatic system, which ultimately carries the tumor cells to the blood.

What’s more, the combination of drinking and smoking might indirectly increase the risk of cancer, with alcohol acting as a kind of solvent for the carcinogenic chemicals in tobacco. It’s the first time, Rumgay says, that research has quantified the risks of different levels of drinking. “Our study highlights the contribution of even relatively low levels of alcohol to the risk of new cancer cases,” says Rumgay.

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