Heavy drinking can cause a cancer linked to cigarette smoking -- study

A population study reveals the genetic factors that drive some people to drink.

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Heavy drinking is typically linked to ailments like addiction, stroke, and liver damage. Now, scientists say the practice may also heighten the risk of cancer more often associated with smoking — lung cancer. This finding suggests that binge drinking can sometimes lead to the disease, even if one never lights up a cigarette.

The population study analyzed the DNA of 173,216 individuals across the United Kingdom and the United States. It was published Wednesday in the journal Science Advances.

The study authors pinpoint genes potentially involved in alcohol use — revealing that people who drink heavily share some genetic variants. This research also adds to the evidence that heavy drinking can have dangerous health consequences. Genes can influence the risk of high alcohol consumption, and in turn, that consumption can lead to disease.

Andrew Thompson, study co-author and researcher at the University of Liverpool, tells Inverse that alcohol is a known carcinogen and is implicated in cancers of the liver, colon, rectum, breast, and neck. Meanwhile, evidence that alcohol can be linked to lung cancer, Thompsons says, has been “variable.”

That relationship has been muddled in part because heavy drinkers are also likely to smoke, Thompson explains. Parsing out how alcohol use influences lung cancer has been a challenge, but examining the DNA of heavy drinkers has pointed to a solution.

DNA dive

To shed light on this relationship and pin down the genetic factors at play, Thompson and his team analyzed the DNA of 125,249 people whose data was stored in the UK Biobank. The researchers combed the participants’ DNA for genetic variations called single nucleotide polymorphisms (SNPs).

The team also mined the data of 47,967 people from a United States study, to test their initial results. Both analyses revealed similar genetic pathways involved with alcohol consumption and determined links to compulsive behavior and addiction.

It's already established that alcohol can cause irreversible genetic damage.

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Subsequently, they evaluated worms in an effort to test how these SNPs, or alcohol-related genetic variations, functioned directly. In these experiments, the researchers removed the SNPs in question and saw “marked changes” in the way the worms responded to alcohol, suggesting these SNPs make a crucial difference.

Why SNPs matter

Humans carry millions of SNPs in their genes. While most don’t impact health or development, some can influence how effective drugs are, how people behave, and what diseases they may be likely to develop. If certain people with a disease such as Alzheimer’s or lupus share the same SNP, the SNP may be a signal for the susceptibility to that disease. In turn, SNPs provide guideposts for scientists to track diseases across families and populations.

For decades, scientists have tried to hammer out how SNPs influence alcohol use, with some success. For example: In 2015, researchers analyzed 17 twin and adoption studies that explored this relationship and found that genes were 50 percent responsible for alcohol use disorder.

However, previous studies didn’t reveal which specific genes are involved. That’s where this new paper comes in.

Complicated factors lead people to drink.


After analyzing the DNA of the participants, the researchers identified six SNPs associated with alcohol use. It’s a bit of a stretch to call these SNPs, “alcohol genes”, Thompson tells Inverse. But they add to the list of complicated factors driving people to drink.

He explains that these six SNPs may contribute to a “range of diseases” including, but not limited to, alcohol dependence, hypertension, and skeletal disorders.

They may also contribute to lung cancer. The team discovered there was a strong association between having these six SNPs, heavy self-reported drinking, and being diagnosed with lung cancer. This remained true even after the scientists controlled for the participant’s smoking habits.

The U.S. Department of Health and Human Services defines heavy alcohol use as binge drinking on five or more days in the past month.

Looking forward

Lung cancer is the leading cause of cancer deaths in the United States and the most common cancer worldwide. Understanding how drinking behavior (and the genes underpinning it) connect to lung health could help people avoid getting cancer in the first place.

However, the research has key limitations: The study hinged on how much participants reported drinking, which may underestimate how much alcohol they were actually consuming.

Furthermore, participants in the study were all white and middle-aged. How genes influence alcohol use, and subsequently cancer, in more diverse populations is unknown.

Next, Thompson and his team are studying patients with other addictions to see whether their genes are similar to those of heavy alcohol users. He hopes the research will illuminate new therapies for people dealing with alcohol dependence and other issues.

Taken together, he explains, this increased understanding of the biology that might contribute to heavy alcohol use can hopefully lead to the identification of “targets that can be taken forward for drug discovery, or drug repurposing in the treatment of alcohol dependence or broader substance use.”

High alcohol consumption is a risk factor for morbidity and mortality, yet few genetic loci have been robustly associated with alcohol intake. Here, we use U.K. Biobank (n = 125,249) and GERA (n = 47,967) datasets to determine genetic factors associated with extreme population-level alcohol consumption and examine the functional validity of outcomes using model organisms and in silico techniques. We identified six loci attaining genome-wide significant association with alcohol consumption after meta-analysis and meeting our criteria for replication: ADH1B (lead SNP: rs1229984), KLB (rs13130794), BTF3P13 (rs144198753), GCKR (rs1260326), SLC39A8 (rs13107325), and DRD2 (rs11214609). A conserved role in phenotypic responses to alcohol was observed for all genetic targets available for investigation (ADH1B, GCKR, SLC39A8, and KLB) in Caenorhabditis elegans. Evidence of causal links to lung cancer, and shared genetic architecture with gout and hypertension was also found. These findings offer insight into genes, pathways, and relationships for disease risk associated with high alcohol consumption.
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