Analysis

Could alcohol be damaging to your DNA? - International Scientific Forum on Alcohol Research Critique 211

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The latest research to go under The ISFAR's microscope concerns an extensive basic scientific experiment in mice. The authors of the paper describe the features and mutational landscape of DNA damage caused by acetaldehyde, an endogenous and alcohol-derived metabolite. This damage results in DNA double-stranded breaks that, despite stimulating recombination repair, also cause chromosome rearrangements.

The ISFAR considers research into the effect on DNA of an alcohol-derived metabolite

The ISFAR considers research into the effect on DNA of an alcohol-derived metabolite

Furthermore, the authors identify how the choice of DNA-repair pathway and a stringent p53 response limit the transmission of aldehyde-induced mutations in stem cells.

ISFAR members considered this to be a well-done series of experiments that add additional data on the effects of aldehyde on cellular damage, which could potentially lead to an increased risk of cancer.

While interesting, these results in mice have limited applicability to the effects of alcohol in humans, as the study conditions do not correspond to that found in real life. For example, the levels of ethanol used to elicit the DNA changes were high and alcohol was directly injected into the animals, whereas in humans alcohol is orally absorbed and undergoes several types of metabolism that reduce maximum blood alcohol concentrations achieved.

Further, the animal model was based on mice that had been genetically manipulated in that particular genes had been selectively 'knocked out' to make them unable to metabolise aldehyde or to repair DNA damage; while this was necessary to study the effects in a basic scientific experiment, it is in contrast to what would occur under non-manipulated conditions of alcohol consumption in humans. 

Heavy drinking clearly increases the risk of upper aero-digestive cancers in humans. However, epidemiologic studies have generally not found an increase in the risk of hematologic cancers in humans, especially from moderate intake of alcohol, and the key damages shown in these experiments were to hematologic cells.

Thus, epidemiologic studies do not add further support to these mouse results, and suggest that cellular damage from aldehydes is probably not an important factor for most hematologic cancers in humans.

To read the full critique, click here.

These critiques are published with the permission of The International Scientific Forum on Alcohol Research.


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