Hard liquor, not beer or wine, may explain trends in cirrhosis mortality

September 13, 1999

Scientists have noted a new clue to an epidemiological mystery surrounding the link between alcohol and cirrhosis. Although cirrhosis has long been associated with heavy drinking, US cirrhosis mortality trends have not always corresponded well with the nation's total alcohol consumption including beer, wine, and hard liquor.

Now, UCSF researchers have reported that the trend of hard liquor consumption by itself closely follows the long-term pattern of cirrhosis mortality. Their paper is published in the current issue of the British Medical Journal. Cirrhosis mortality in the United States experienced a long-term increase after World War II, peaked in 1973, then steadily declined to half its peak rate by 1994. Total alcohol consumption - as measured by combining the alcohol (ethanol) contributions of beer, wine, and liquor - also increased over the post-war era. But consumption peaked and turned downward around 1980, a half dozen years after cirrhosis mortality started falling.

"Why cirrhosis peaked when it did and why it commenced its long-term decline is unknown and has been a long-standing mystery," said Ron Roizen, UCSF sociologist in the department of social and behavioral science and lead author of the study. "Excluding beer and wine and only looking at hard alcohol was a remarkably simple thing for us to have previously overlooked."

Looking at data between 1949 and 1994, the researchers found that the consumption pattern of hard liquor in the US showed a reasonably close match to cirrhosis deaths. They evaluated their observed long-term correlation against two sharp, short-term declines in hard liquor consumption. In 1942-43, when wartime needs diverted all ethanol production to the making of synthetic rubber and explosives, per capita consumption fell 22 percent. A similar drop occurred in 1946-47 when post-war consumption levels commenced.

These short-term "natural experiments" generated mixed results, said Roizen. The 1942-43 drop in spirits consumption was soon followed by a marked dip in cirrhosis mortality but the 1946-47 drop was not. Measurement problems associated with wartime and immediate post-war consumer behavior, including hoarding of scarce goods, make these tests suggestive rather than definitive, said Roizen.

"Our results serve as a clue, not an explanation, for the mysterious peak and decline of cirrhosis mortality," said Roizen.

The observed long-term correlation was effectively anticipated in a 1967 paper published in the American Journal of Public Health by noted epidemiologist Milton Terris. Based on a three-country analysis of cirrhosis and alcohol consumption trends, Terris concluded that per capita beer consumption had no association with cirrhosis mortality trends. Since wine contributes only one-eighth of US alcohol consumption, Terris' exclusion of beer implied that hard liquor would be strongly associated with cirrhosis mortality trends. The new UCSF paper confirms Terris' 30-year-old implied prediction.

The researchers caution that correlations between population data are not equivalent to data about individual drinking behavior and cirrhosis risk. "Our findings do not show that drinking hard liquor leads to cirrhosis and drinking beer and wine does not," said Roizen. "The reported relationship does, however, open the door to exploring beverage-specific links between alcohol consumption and cirrhosis."

In addition to Roizen, co-authors of the paper are William C. Kerr, PhD, UCSF assistant research economist in the department of social and behavior sciences; and Kaye Fillmore, PhD, UCSF adjunct professor of social and behavioral sciences.
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NOTE TO REPORTERS: A copy of the article can be found at http://www.bmj.com/cgi/content/full/319/7211/666

University of California - San Francisco

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