Alcohol consumption can elevate cancer risk through mechanisms such as DNA damage, hormonal changes, and oxidative stress, with risks increasing alongside consumption levels.
Alcohol consumption has long been associated with an increased risk of several cancers, including mouth, throat, liver, breast, and colon cancers. Despite alcohol being classified as a carcinogen nearly 40 years ago by the World Health Organization’s International Agency for Research on Cancer (IARC), public awareness of this risk remains low.1
According to Surgeon General Vivek Murthy, MD, MBA, alcohol is responsible for approximately 100,000 cancer cases and 20,000 cancer deaths annually in the country. But how exactly does consuming alcohol increase the risk of cancer?
When the body metabolizes alcohol, it converts it into acetaldehyde, a toxic compound classified as a group 1 carcinogen by the IARC.2 Acetaldehyde directly damages DNA by forming adducts, or altered structures that interfere with DNA replication and repair. This damage increases the likelihood of mutations, which can lead to cancer.
Individuals with deficiencies in the ALDH2 enzyme, which breaks down acetaldehyde, are at an even greater risk. In 2018, researchers found that in mice lacking the ALDH2 enzyme, even a single dose of ethanol caused significant DNA damage in blood stem cells, including deletions, breaks, and chromosome rearrangements, which can lead to cancer.3 They also revealed that while the body uses repair mechanisms to minimize this damage, faults in these processes increase susceptibility, suggesting that reducing alcohol consumption can also lower cancer risk.
Alcohol consumption can also elevate hormone levels, particularly estrogen, which is closely linked to breast cancer development.4 It can also increase insulin levels, which promote cell proliferation and create conditions favorable for tumor growth.
According to the Breast Cancer Research Foundation, women who consume 1 alcoholic drink per day—considered moderate consumption—face a 7% to 10% higher risk compared with non-drinkers, while those who have 2 to 3 alcoholic drinks have about a 20% increased risk.5
Alcohol consumption can elevate hormone levels, particularly estrogen. | Image credit: monticellllo – stock.adobe.com
Alcohol acts as a solvent, enhancing the absorption of carcinogens like those found in tobacco.6 This mechanism is particularly relevant for cancers of the mouth, throat, and esophagus, which are exposed to both alcohol and harmful chemicals from cigarettes.
According to an NIH fact sheet, the combined use of alcohol and tobacco results in a multiplicative risk for oral and pharyngeal cancers.7 This means smoking and drinking together increases the risk of cancer even more than the combined risks of smoking or drinking on their own.
Reactive oxygen species (ROS) are highly reactive molecules naturally produced during normal metabolic processes, but excessive levels can wreak havoc on the body’s cells.8 Alcohol consumption significantly increases ROS production, particularly in the liver, by disrupting the body’s ability to regulate these compounds. This occurs through multiple mechanisms such as alcohol metabolism, which generates molecules that promote formation of ROS, stimulation of ROS-producing enzymes like cytochrome P450s, and reductions in antioxidant levels that would normally neutralize ROS.
Alcohol also alters the balance of certain metals in the body, further accelerating ROS production. The resulting oxidative stress damages DNA, proteins, and lipids, contributing to cell injury and playing a central role in the development of alcoholic liver disease and possible liver cancer.
Nutritional deficiencies caused by heavy alcohol consumption play a significant role in alcohol-associated carcinogenesis. Chronic alcohol use interferes with the absorption of essential nutrients, including vitamins A, C, and E, as well as folate, which are critical for DNA repair and cellular health.7 These deficiencies leave the body more vulnerable to carcinogenic damage.
Additionally, alcohol-induced folate deficiency inhibits gene regulation processes, while zinc deficiency disrupts vitamin A metabolism and reduces detoxifying enzymes, leading to increased cell proliferation and heightened cancer risk in tissues like the esophagus and liver.9
References
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