Ditching Boozy Beverages Tied to Lower Risk of Alcohol-Related Cancers

Increased alcohol consumption was associated with a higher risk for alcohol-related cancers, as well as all cancers, while quitting and reducing drinking were linked with lower risks, a large Korean population-based study showed.

Among over 4.5 million adults, non-drinkers who started to drink had an associated higher risk of alcohol-related cancers compared with those who did not drink, even at mild levels of alcohol intake and with an apparent dose-response relationship:

• Mild levels (adjusted HR 1.03, 95% CI 1.00-1.06)
• Moderate levels (aHR 1.10, 95% CI 1.02-1.18)
• Heavy levels (aHR 1.34, 95% CI 1.23-1.45)

This study “highlights that there is no safe level of alcohol consumption in terms of cancer risk,” said Dong Wook Shin, MD, MBA, DrPH, of Samsung Medical Center in Seoul, and colleagues, writing in JAMA Network Open. “Alcohol cessation and reduction should be reinforced for the prevention of cancer.”

Those with mild drinking levels who stopped drinking did appear to have a lower risk of alcohol-related cancers, including cancers of the head and neck, esophagus, colorectum, liver, larynx, and female breast (aHR 0.96, 95% CI 0.92-0.99), versus those who sustained their drinking levels.

Of note, those with moderate (aHR 1.07, 95% CI 1.03-1.12) or heavy (aHR 1.07, 95% CI 1.02-1.12) drinking levels who stopped drinking had a higher all-cancer incidence than those who sustained drinking levels, though this increase in risk disappeared when quitting was sustained.

Shin and team suggested that this could be explained by the “sick quitter phenomenon” — the idea that people could have stopped consuming alcohol after feeling symptoms and/or other adverse health effects.

Overall, reducing heavy drinking levels was associated with decreased cancer risk compared with sustained heavy drinking, whether individuals reduced to moderate levels (alcohol-related cancer: aHR 0.91, 95% CI 0.86-0.97; all cancers: aHR 0.96, 95% CI 0.92-0.99) or mild levels (alcohol-related cancer: aHR 0.92, 95% CI 0.86-0.98; all cancers: aHR 0.92, 95% CI 0.89-0.96).

In an accompanying commentary, Neal D. Freedman, PhD, MPH, and Christian C. Abnet, PhD, MPH, both of the National Cancer Institute, noted that while a dose-response association has been reported between alcohol consumption and cancer risk, little data are available on the impact of increasing, decreasing, or cessation of alcohol use.

“Not only would such information provide additional support for the role of alcohol in cancer development, but it would also inform public health guidance,” they wrote. “It is within this context that [the authors] provide evidence suggesting that cancer risk can be meaningfully altered by changing the amount of alcoholic beverages consumed.”

For this study, Shin and colleagues included 4,513,746 participants (mean age 53.6 years, 51.5% men) who had available data on their drinking status from two biennial health screenings in 2009 and 2011.

Alcohol consumption level was self-reported by participants in health screening questionnaires, and was categorized into none (0 g/day), mild (<15 g/day), moderate (15-29.9 g/day), and heavy (30 g/day) drinking.

Participants were followed for a median of 6.4 years, yielding a total of 28,090,140 person-years. During this period, there were 215,676 cancer events (7.7 per 1,000 person-years), 37.2% of which were alcohol-related cancers.

Freedman and Abnet noted that one of the study’s limitations was the fact that the authors were unable to assess ALDH2 gene status among participants. Since the ALDH2*2 allele is more common among East Asian populations and is associated with both cancer risk and alcohol intake, they suggested that “studies assessing changing alcohol use in other racial and ethnic groups are needed.”

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