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Binge drinking with chronic alcohol use more destructive than previously thought

Date:
December 17, 2015
Source:
University of Missouri-Columbia
Summary:
Chronic alcohol use, when combined with repeated binge drinking, causes more damage to the liver than previously thought, new research shows.
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Excessive alcohol consumption is a global public health issue. In the United States, binge drinking is the most common form -- so common, in fact, that the Centers for Disease Control and Prevention reports approximately one in six adults binge drinks about four times each month. Now, a study by University of Missouri School of Medicine researchers shows that chronic alcohol use, when combined with repeated binge drinking, causes more damage to the liver than previously thought.

"Heavy binge drinking by those who habitually consume alcohol is the most common cause of liver damage in chronic alcoholic liver disease," said Shivendra Shukla, Ph.D., the Margaret Proctor Mulligan Professor of medical pharmacology and physiology at the MU School of Medicine and lead author of the study. "We know that this behavior causes large fatty deposits in the liver that ultimately impair the organ's ability to function properly. However, we wanted to understand the mechanism that causes this damage and the extent of the harm. Our research focused on different forms of alcohol abuse and the results of those behaviors."

Shukla's team studied mice to examine the extent of liver injury caused by chronic alcohol use, repeat binge episodes and a combination of both. During a four-week period, the team found that mice exposed to chronic alcohol use and repeated binge consumption exhibited the highest levels of liver damage.

"Either chronic alcohol use or acute repeat binge episodes caused moderate liver damage when compared to the control group not exposed to alcohol," Shukla said. "This outcome came as no surprise. However, in the mice exposed to both chronic use and repeat binge episodes, liver damage increased tremendously. Even more shocking was the extent of fatty deposits in the livers of those exposed to chronic plus binge alcohol. It was approximately 13 times higher than the control group."

The highly amplified fat accumulation was in part caused by metabolic changes within the liver. These changes not only significantly increased fatty liver deposits, but increased stress on the organ while decreasing the liver's ability to fight the stress.

Shukla also pointed out that chronic and excessive alcohol use should not be associated only with liver damage.

"Drinking alcohol excessively can create an inflammatory response to the liver and other organ systems in the body," Shukla said. "If those organs work at a lower level of function, then a whole host of physiological processes can be affected. It is important for us to understand the extent of damage caused by alcohol abuse, which also can lead to other health issues such as diabetes, cardiovascular disease and some forms of cancer."


Story Source:

Materials provided by University of Missouri-Columbia. Note: Content may be edited for style and length.


Journal Reference:

  1. Shivendra Shukla, Annayya Aroor, Ricardo Restrepo, Kusum Kharbanda, Jamal Ibdah. In Vivo Acute on Chronic Ethanol Effects in Liver: A Mouse Model Exhibiting Exacerbated Injury, Altered Metabolic and Epigenetic Responses. Biomolecules, 2015; 5 (4): 3280 DOI: 10.3390/biom5043280

Cite This Page:

University of Missouri-Columbia. "Binge drinking with chronic alcohol use more destructive than previously thought." ScienceDaily. ScienceDaily, 17 December 2015. <www.sciencedaily.com/releases/2015/12/151217111440.htm>.
University of Missouri-Columbia. (2015, December 17). Binge drinking with chronic alcohol use more destructive than previously thought. ScienceDaily. Retrieved December 22, 2024 from www.sciencedaily.com/releases/2015/12/151217111440.htm
University of Missouri-Columbia. "Binge drinking with chronic alcohol use more destructive than previously thought." ScienceDaily. www.sciencedaily.com/releases/2015/12/151217111440.htm (accessed December 22, 2024).

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