For many years, public health research has found a link between high levels of alcohol consumption and many types of cancer. A recent study done on mice sheds additional light on how drinking and cancer may be connected.

In our body, alcohol is broken down by the combined action of several protein machines, or enzymes. The alcohol (specifically, the molecule called ethanol) is first converted by the enzyme alcohol dehydrogenase into acetaldehyde, a toxic compound and carcinogen (cancer-causing chemical). The acetaldehyde is then quickly processed by another enzyme aldehyde dehydrogenase into acetate (the central component of vinegar). Acetate is then further broken down into carbon dioxide and water.

Our body has a number of different aldehyde dehydrogenase enzymes, each encoded by a different gene. One of the most important of these enzymes for metabolizing alcohol is ALDH2. There is a certain genetic variant of ALDH2 that makes the enzyme less capable of breaking down acetaldehyde. This variant is most commonly found in people of East Asian descent – about one-third to one-half of Japanese, Korean, Vietnamese, and Han Chinese populations (but not some of the indigenous groups and ethnic minorities in China and Taiwan). The accumulation of acetaldehyde in the body as a result of this slower metabolism could lead to poorer tolerance of alcohol consumption and physical symptoms such as facial flushing – hence the expression “Asian flush.” This ALDH2 variant has also been found to be associated with increased incidence of esophageal and other cancers.

In this recent study, researchers in the UK used mice whose ALDH2 gene has been made completely nonfunctional, or “knocked out.” Additionally, they also knocked out a gene called FANCD2, which encodes an enzyme involved in repairing DNA damages (in humans, FANCD2 is one the genes that may be mutated in individuals with a hereditary condition called Fanconi anemia, who are more likely to develop cancers such as leukemia). After giving these mice high levels of alcohol, the scientists looked at the mice’s blood stem cells (which give rise to all the cells in the blood). They found significant levels of DNA damage, a major risk factor for cancer development.

There are some important caveats to consider before these research findings can be applied clinically. First of all, the study was performed in mice, particularly ones that were purposely engineered to be more prone to DNA damage and cancer. The researchers also did not look at whether actual cancer development increased in the alcohol-treated mice, only at mutations that may potentially cause cancer. Additionally, while the scientists examined the mice’s blood stem cells because they are plentiful and easily retrieved, the less-active ALDH2 variant in humans have not been found to be associated with increased levels of blood cancer. Nevertheless, this new research provides important insights into how high levels of alcohol consumption may lead to increased incidents of cancer.

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