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Alcohol May Trigger DNA Damage Leading to Breast-Cancer

by | Latest News, Research

Home Latest News Alcohol May Trigger DNA Damage Leading to Breast-Cancer

Alcohol, a known carcinogen, even in small doses can turn poisonous in some humans causing disease and has the potential to create cancer cells. There are several individuals that when imbibing alcohol, even on a social level, posses the inability to properly metabolize the chemicals in liquor. When alcohol is metabolized it produces a primary chemical, acetaldehyde; this primary metabolite has now shown signs of a possible implication for breast and liver cancers.
For quite some time now there has been a link between ingesting alcohol and particular types of cancer. This was first established in the 1980’s, however a recent study (results will be published in the December 2011 issue of Alcoholism; Clinical & Experimental Research) using human cells has established a link between alcohol metabolism and acetaldehyde-DNA damage. Phillip J. Brooks, program director in the Division of Metabolism and Health Effects at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) stated, “the existence of such a relationship did not prove that alcohol itself caused the cancers. More recent evidence, however has confirmed that alcohol – or more specifically, ethanol – is carcinogenic to human beings at several sites in the body.”
Alcohol-related esophageal cancer, as evidence suggests has displayed a connection to acetaldehyde-DNA damage as well; the chemical acetaldehyde is structurally similar to formaldehyde, as it breaks down in the human body it can cause a trigger within our chromosomes producing abnormalities within the cell structures. Normally, most individuals bodies posses the capability to quickly convert alcohol through the process of metabolization into acetate (a relatively harmless chemical), according to Brooks, however, “ thirty percent of East Asians are unable to metabolize alcohol to acetate due to a genetic variant in the aldehyde dehydrogenase 2 (ALDH2) gene, and have greatly elevated risks of esophageal cancer from alcohol drinking. This helped researchers establish the carcinogenicity of acetaldehyde in humans and its role in esophageal cancer.”
In respect to alcohol use and the implication of breast cancer and liver cancer, cells need the ability to divide or else they cannot replicate their genomic DNA. If a human’s genomic DNA is then damaged the replication process is halted. There was a collection of proteins discovered through studies done by Brooks and his colleagues that was found to be very important in the defense against breast cancer. “The Fanconi anemia-breast cancer (FA-BRCA) network is a collection of proteins that responds to DNA damage by coordinating DNA repair or helping the replication machinery to bypass the DNA damage, thereby allowing replication to continue.”
Human cells constructed to metabolize alcohol into the chemical acetaldehyde were exposed to concentrations that would equal levels found in the human body during a period of social drinking. The enzyme alcohol dehydrogenase 1B (ADH1B) is conveyed in human liver and breast tissue; while in the process of transforming the alcohol to acetaldehyde the result was an increase in the levels of acetaldehyde-DNA damage. The human cells then responded by activating the FA-BRCA network. Brooks commented “using alcohol concentrations designed to correspond to blood levels attained during social drinking remains to be shown whether our findings reflect what happens in the human body during alcohol drinking. Similarly, while our work is consistent with a role for acetaldehyde in alcohol related liver and breast cancer, more studies in animals and humans will be necessary to prove such a role.”
The make-up of our human cellular system is not built to handle the daily abuse that many subject it to by over consuming alcohol a proven carcinogenic to humans in the upper aero-digestive tract, liver and colorectal sites in the body.
It is very evident that more research needs to be undertaken. The hope is that this report will push for further investigation of the role of acetaldehyde-DNA damage in the implication of not only liver cancer, but the development of breast cancer.
Exploring the extent to which acetaldehyde resulting from alcohol metabolism and the activation of the FA-BRCA network in liver and breast cells will be an increasingly important area of investigation in the future considering the growth of social binge drinking especially among our adolescent population.
With the rise in particular types of cancer globally, we can only hope that with scientific research working towards distinguishing the relationship between the transformation of alcohol within the human body, the FA-BRA network and human health, people will wise up to the dangers caused by social binge drinking and how the misuse and abuse of liquor can create cell damage and the potential for cancer.