Many studies have found a link between alcohol use and the risk of developing certain cancers. But it is not clear whether alcohol use after treatment might increase the risk of these cancers coming back (recurring). For example, alcohol can increase the levels of estrogens in the body, which might increase the risk for breast cancer recurrence. We found an elevated risk for all cancers among participants who recently quit drinking compared with those who sustained their level of drinking.
What happens to cancer risk after a person stops drinking alcohol?
They also used an assessment tool, called AUDIT-C, that was developed to study drinking behavior. Participants in the survey are a nationally representative sample of adults aged 18 and older. The nearly 4,000 people who took part in the survey were asked how much does drinking several types of alcohol (wine, beer, and liquor) affect the risk of getting cancer. The significantly greater risks seen in men carrying the low-alcohol tolerability ALDH2 gene variant who still drank regularly suggests that greater accumulation of acetaldehyde may directly increase cancer risk. The study team used DNA samples from approximately 150,000 participants (roughly 60,000 men and 90,000 women) in the China Kadoorie Biobank study and measured the frequency of the low-alcohol tolerability alleles for ALDH2 and ADH1B.
Other long-term health effects from drinking alcohol
Over the past few decades, however, several animal studies have indicated that alcohol can have a cocarcinogenic, or cancer-promoting, effect. This means that when alcohol is administered together with other known cancer-inducing agents (i.e., carcinogens), it promotes or accelerates cancer development. This effect was noted for several digestive tract cancers, specifically cancers of the esophagus and the nonglandular forestomach5 (Doll et al. 1999).
Data availability
It has been reported that ethanol treatment in ACI/N rats significantly increased MAM-initiated large bowel tumorigenesis [107]. Chronic ethanol feeding in rats treated with DMH has been shown to significantly increase the number of aberrant crypt foci in colons [108]. A mounting body of evidence suggest that cancer initiation and progression is closely linked to oxidative stress. The metabolism of ethanol leads to generation of ROS that serve as primary carcinogens due to their genotoxic effects on diverse cellular processes. ROS produced by CYP2E1 results in the accumulation of lipid peroxidation products such as malondialdehyde and 4-hydroxynonenal (4-HNE) which in turn forms exocyclic DNA adducts [85]. ROS can act as messengers in intracellular signaling pathways leading to the transformation of a normal cell to tumor cell [86].
To control for this possibility, the investigators included separate analyses for men and women in their statistical models, where feasible. However, gender explained a significant portion of the observed variability in study results only for esophageal and liver cancer, but not for other types of cancers. Another limitation of this and other meta-analyses is that alcohol consumption levels may have been systematically underreported in several studies, leading to biased RR estimates. In all, 229 studies (183 case-control studies and 46 cohort studies) met the eligibility criteria and were included in the meta-analysis. These studies, which reported a total of 115,199 cases, investigated alcohol’s effects on the risk for developing cancer at a total of 19 sites in the body or at all sites combined (see the table and figure for a summary of the studies and their findings for each of those sites).
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Singletary and colleagues (2001) found that incubation in 0.4 percent w/v ethanol increased cell proliferation in the estrogen receptor–positive MCF-7 and ZR75.1 breast cancer cells but not in the estrogen receptor–negative BT-20 and MDA-MB-231 cells. The effect of ethanol on MCF-7 cells also was correlated with increases in estrogen receptor alpha content. When the MCF-7 cells were cultured together with human skin fibroblasts in 0.4 percent ethanol for 72 hours, ethanol suppressed estrogen receptor alpha expression compared with untreated cells (Sanchez-Alvarez et al. 2013). Thus, the tumor micro-environment is important in determining estrogen-receptor status and the effects of alcohol on breast cancer. However, additional studies are warranted, because estrogen receptor–negative breast cancer generally is more aggressive, and patients have a worse prognosis than patients with estrogen receptor–positive breast cancer.
Experimental models have robustly demonstrated that dietary exposure to ethanol during puberty causes morphologic changes in mouse mammary glands, including increases in ductal branching and epithelial growth and breast density [40]. For other cancers of the digestive tract (e.g., stomach, pancreas, colon, and rectum), however, the results are controversial and remain elusive, possibly due to the differences in study design. However, substantial data confirming its role as tumor initiator and/or tumor progressor in patients with different cancer is still not well explained and requires extensive investigation. The association between various levels of alcohol consumption and an increased risk of liver cancer remains difficult to interpret even with the pooled data used in this meta-analysis. This difficulty results from the fact that, as discussed earlier, the association between alcohol consumption and liver cancer is only indirect.
- But the All of Us study, Dr. Cao and her colleagues explained, offered a unique opportunity to take a robust look at people in these groups in the United States.
- This indicates that when alcohol is administered along with other cancer-inducing agents (i.e., carcinogens), it promotes cancer development.
- The breakdown of ethanol in the body can also create high levels of acetaldehyde, which can damage DNA and cause liver, head and neck, and esophageal cancers.
- Statistically significant gender differences existed only for esophageal and liver cancer—where the alcohol-related risk was higher in women than in men—but not for other types of cancer.
- However, direct or indirect interactions of the tumors with their microenvironment can facilitate immune evasion so that the tumor is not detected by the immune system and thus can spread uncontrolled.
WCRF found an elevated risk of malignant melanoma per 10 g alcohol per day (RR 1.08 (95% CI 1.03–1.13)), but no effect on basal cell carcinoma (RR 1.04 (95% CI 0.99–1.10)) or squamous cell carcinoma (RR 1.03 (95% CI 0.97–1.09)) risk [7]. An increased risk of prostate cancer was observed for light and moderate oxycodone uses, side effects, dosages, precautions drinking in Bagnardi and colleagues’ meta-analysis but not in the dose-response analysis of one drink per day by WCRF [7,8]. Numerous epidemiological studies have consistently demonstrated a dose-response relationship between chronic alcohol consumption and increase in the risk for breast cancer [21,22].
But it has been difficult to establish whether alcohol directly causes cancer, or if it is linked to possible confounding factors (such as smoking and diet) that could generate biased results. It was also unclear whether alcohol is linked to other types of cancer, including lung and stomach cancers. The December 2020 NCI Workshop highlighted existing evidence on the alcohol-cancer link, and revealed opportunities to strengthen relevant scientific knowledge. Additionally, the workshop panel recognized that the health, including cancer, impact of increases in alcohol consumption resulting from the coronavirus pandemic (60) will need to be carefully assessed, particularly if these behaviors are sustained long-term. Another enzyme, called aldehyde dehydrogenase 2 (ALDH2), metabolizes toxic acetaldehyde to nontoxic substances. Some people, particularly those of East Asian descent, carry a variant of the gene for ALDH2 that encodes a defective form of the enzyme.
The accumulation of acetaldehyde has such unpleasant effects (including facial flushing and heart palpitations) that most people who have inherited the ALDH2 variant are unable to consume large amounts of alcohol and therefore have a low risk of developing alcohol-related cancers. Fifth, there might be unmeasured confounders, particularly those that would not be identified through routine health screening, such as stress or other mental the dangers of mixing trazodone and alcohol health factors. It is possible that participants whose alcohol consumption behaviors changed over time may also experience changes in smoking status or physical activity. However, the sensitivity analysis among nonsmokers showed consistent results, suggesting that confounding from concomitant health behavior changes was not significant. Alcohol and its metabolite acetaldehyde can drive cancer development through several pathways.
Within 20 years of quitting smoking, according to the CDC, a person’s risk of getting cancer of the mouth, throat, voice box, or pancreas, “drops to close of that of someone who does not smoke.” The CDC notes that by quitting smoking, a person’s chance of getting cancer of the mouth, throat, lungs or voice box decreases by half. In 2021, the most recent data available, nearly 1.8 million new cases of cancer were reported in the U.S. Alcohol-related deaths increased among all age groups (during 2020–2021) from just a few years earlier (2016–2017). These are increases of 27% among boys and men, and 35% among girls and women from just a few years earlier (2016–2017). Launched in 2018, All of Us captures information on participants’ lifestyle and other behaviors and personal background via comprehensive surveys.
Many of these pathways are interlinked and show the complexity and breadth of alcohol’s harmful potential. For example, inflammation can result in oxidative stress, but inflammation is a reaction by the immune system which is itself compromised by alcohol use. Furthermore, DNA damage can occur through exposure to acetaldehyde and ROS which are both produced through CYP2E1 activity, with acetaldehyde also a product of ADH activity. Other potential pathways have been proposed including the dysregulation of carnitine metabolism [49]. We have only covered carcinogenesis in this review, but alcohol likely alters, through these pathways and others, other functions in the body which render it more susceptible to other diseases and injuries, as discussed in other articles in this Special Issue.
The recommended limit is lower for women because of their smaller body size and because their bodies tend to break down alcohol more slowly. Reported in this paper was undertaken during a PhD studentship at the International Agency for Research on Cancer. Separately, this expert insight explains three strategies organizations can use to leverage oncology pharmacists and improve cancer care. Similarly, these ready-to-use slides outline the major structural shifts impacting cancer care, as well as the strategic decisions that oncology leaders will need to make.
Myeloid-derived suppressor cells (MDSC) and iNKT cells are key inhibitory cells that modulate CD8+ T cell function in mouse model of alcohol-induced tumors. Also, in these mice, immunotherapy targeting IL-15/IL-15Rα could be another strategy to boost CD8+ T cell function [164]. Targeting underlying molecular basis of interaction between alcohol and cancer cells, leading to the modulation of sphingosine-1-phosphate/receptor 1 (S1P/S1PR1) signaling pathway and impairment alcohol and the adolescent brain national institute on alcohol abuse and alcoholism niaaa of mature B cell circulation could be another promising approach. With continued research and validation of a combination of different strategies may produce more efficient therapeutic regimen for alcoholics with cancer. Although risk estimates were adjusted for tobacco smoking (considering cigarettes, cigars and pipes), some residual confounding may remain. An analysis among never smokers would rule out possible residual confounding due to tobacco smoking.