Alcohol and its byproducts can also damage the liver, leading to inflammation and scarring (cirrhosis). As liver cells try to repair the damage, they can end up with mistakes in their DNA, which could lead to cancer. Once in the body, alcohol can be converted into acetaldehyde, a chemical that can damage the DNA inside cells and has been shown to cause cancer in lab animals. Public health campaigns about the cancer https://sober-home.org/alcohol-abuse-and-alcoholism-signs-symptoms-and/ risk posed by alcohol in England and Australia have been effective at raising awareness with their target audiences. Given the study’s findings, “there’s also a need to better understand why so many cancer survivors have such high alcohol consumption,” she continued. Dr. LoConte said that she has direct conversations with her patients about drinking and other behaviors that could affect their treatment.
of cancers found to be preventable with these lifestyle changes
The percentage and number of CD3+NK1.1+ invariant NKT cells was elevated in the blood of alcohol- consuming, B16BL6 melanoma-bearing mice especially at day 14 after tumor inoculation (Zhang et al. 2012). These cells have important regulatory functions and can either promote antitumor immune responses or inhibit them. Initially, these cells express a cytokine profile that favors antitumor immune responses (i.e., a high ratio of IFN-γ to IL-4). After repeated activation, however, these cells become anergic and switch to a cytokine profile that inhibits antitumor immune responses and favors tumor progression (i.e., a high ratio of IL-4 to IFN-γ) (Parekh et al. 2005). The invariant NKT cells from the alcohol-consuming, melanoma-bearing mice exhibit a high IL4/IFN-γ ratio, indicating that they express a cytokine profile favoring immune inhibition and tumor progression (Zhang et al. 2015). A large body of literature indicates that alcohol consumption modulates many aspects of the innate and adaptive immune systems.
2. Adaptive Immune Surveillance
In the study, many people being treated for cancer and longer-term cancer survivors reported regularly drinking alcohol—many moderately, but some also heavily and often. According to the study’s findings, male long-term survivors and younger people being treated for cancer were among those who were particularly likely to be heavy or frequent drinkers. The results remained the same when the data were adjusted for other cancer risk factors, such as smoking, diet, physical activity, body mass and family history of cancer.
Effects of Alcohol on Tumor Growth, Metastasis, Immune Response, and Host Survival
Animal studies strongly support a critical role of alcohol exposure at a young age on breast cancer development. 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.
Alcohol, Tumor Growth, Invasion, and Metastasis in Animal Models
Participants can also allow access to their electronic health records (with all identifying information removed), providing important insights on treatments received and other relevant health information. 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. The results, the study team argued, should be a wake-up call for all those involved in cancer care. But results from a new study suggest that this information may not be reaching people who fall into either of these two categories. Reported in this paper was undertaken during a PhD studentship at the International Agency for Research on Cancer.
- Both acetaldehyde and ethanol can impact DNA methylation which may lead to changes in the expression of oncogenes and tumour-suppressor genes [21].
- Other sources of ROS during ethanol metabolism include the mitochondrial respiratory chain and some cytosolic enzymes [28].
- At the moment, however, proven ways to help people with cancer limit drinking during or after completing treatment are extremely limited, Dr. DuVall said.
- However, the National Institute on Alcohol Abuse and Alcoholism defines a standard drink as 12 ounces of regular beer, 5 ounces of wine and 1.5 ounces of distilled spirits.
- Numerous reports have advocated a critical suppressive effect of alcohol on NK cell function.
In pregnant women, alcohol use, especially heavy drinking, may lead to birth defects or other problems with the fetus. Most people know about the short-term effects of drinking alcohol, such as its effects on mood, concentration, judgment, and coordination. Ethanol is the type of alcohol found in alcoholic drinks, whether they are beers, wines, liquors (distilled spirits), or other drinks. Alcoholic drinks contain different percentages of ethanol, but in general, a standard size drink of any type — 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80-proof liquor — contains about the same amount of ethanol (about half an ounce). A related study using the same alcohol-feeding regimen confirmed alcohol’s effects on growth and angiogenesis of E0771 inoculated into other female C57BL/6 mice (Lu et al. 2014). In that study, a molecule that can inhibit VEGF receptor 2 blocked alcohol’s stimulatory effect on tumor growth, indicating that alcohol acts via a VEGF pathway.
Compared to patients prescribed insulin, patients prescribed a GLP-1 agonist had a 65 percent lower risk of gallbladder cancer and 62 percent lower risk of a central nervous system tumor called meningioma. He also emphasized the role that certain viruses, such as HPV — which people can prevent through vaccination and cervical screening — play in cancer risk. “It’s a risk that you face every day, and that also means that the reduction of the risks can benefit you every day as well.” Genetics play a significant role in determining a person’s risk of developing alcohol-related cancers. Some of the highest proportions of alcohol-related cancers were found in Moldova and Romania, she said. But recent changes in taxing policy, which has increased the cost of alcohol in those countries, have caused a drop in alcohol sales.
People who choose to drink alcohol should limit their intake to no more than 2 drinks per day for men and 1 drink a day for women. Too much alcohol can add extra calories to the diet, which can contribute to weight gain in some people. Alcohol can raise the levels of estrogen, a hormone important in the growth and development of breast tissue. Alcohol may help other harmful chemicals, such as those in tobacco smoke, enter the cells lining the upper digestive tract more easily.
One early study (Capel et al. 1978) investigated the effect of alcohol exposure on the growth and metastasis of Lewis lung carcinoma. Male animals from a type of mouse strain called C57BL/6 were exposed to 10 percent ethanol in their drinking water for 2, 4, 5, or 8 weeks before tumor cells were implanted into their thighs. Furthermore, metastases were significantly reduced in the 2-week and 8-week ethanol groups but not in the 4-week and 5-week groups. Administration of ethanol for 2 weeks after tumor inoculation affected neither tumor growth nor metastasis. Exposure to ethanol before but not after tumor injection significantly decreased the tumor cell number. One of the strengths of this meta-analysis is that the investigators performed a separate analysis of studies that also reported estimates adjusted for tobacco use, which contributes to various forms of cancer, prominently lung cancer.
Overall, about 12,000 people in this group reported that they drink alcohol, and nearly 40% reported engaging in hazardous drinking—that is, repeated excessive alcohol use. Of those who may have been actively undergoing treatment for cancer, about 75% drank alcohol, many heavily. There has been a marked increase in alcohol consumption in low- and middle-income countries over the last decade. Consumption of country liquor predominates in rural areas, whereas Indian-made foreign liquor is the preferred alcoholic beverage in urban areas.
This treatment increased invasion of the estrogen receptor–positive MCF-7 and T47D breast cancer cells as well as the estrogen receptor–negative HS578T, MDA- MB231, and MDA-MB435 cells. Similarly, incubation for 48 hours in 0.1 percent and 0.2 percent w/v ethanol stimulated https://sober-home.org/ invasion of estrogen receptor–negative SKBR3 and estrogen receptor–positive BT474 breast cancer cells. In contrast, ethanol exposure did not affect invasion of HB2, an immortalized normal human breast tissue cell line, or estrogen receptor–negative BT20 breast cancer cells.
For example, a Canadian container label intervention demonstrated a 10% greater increase in knowledge of alcohol as a carcinogen in the intervention vs. the comparison group two months post-intervention (40). Another study found that using multiple and diverse information sources can reduce alcohol use intentions as compared to reliance on a single source (41). Retinoids are important regulators against carcinogenesis as they can induce cell growth, cell differentiation, and apoptosis [31].
Several studies using animal cancer models indicate tumor-specific differences in the effect of alcohol on tumor growth and metastasis. These models included various types of breast cancer, melanoma, lung cancer, colon cancer, and liver cancer (i.e., hepatocellular carcinoma). For cancer specifically, an estimated 4.1% of all new cases globally in 2020 (3), and from 2013 through 2016, 4.8% of all cases annually in the U.S., were attributable to alcohol consumption (4). Current evidence suggests that “[t]here is no threshold of alcohol consumption below which cancer risk does not increase, at least for some cancers ” (5), and cancer prevention guidelines indicate that it is best not to drink alcohol (5, 6). Despite the large body of scientific evidence on the topic, the full cancer burden due to alcohol remains uncertain because for many cancer (sub)types associations with risk and survivorship are inconsistent or there are few studies. Moreover, most U.S. adults are unaware of the alcohol-cancer link (7), and the interrelationships of alcohol control regulations and cancer risk is unclear.
It may lead to the development of HCC either through direct (genotoxic) or indirect mechanisms (development of cirrhosis) [6]. The relationship between alcohol and liver disease correlates with the amount of alcohol consumed over a lifetime and the overall dose-response relationship between alcohol consumption and the risk of liver cancer is linear [41]. The most probable mechanism underlying alcohol-related liver carcinogenicity is through development of liver cirrhosis, although other events such as hepatitis B infection [19], genetic mutations [21] or altered hepatic metabolism of carcinogens may also play a role [13].
Similarly, spontaneous metastasis to the lung was significantly inhibited in mice injected with melanoma at 1, 4, 6.5, and 10 weeks of consuming 20 percent ethanol. One of the ways in which the body defends itself against tumor cells involves their destruction by NK cells. The investigators also analyzed alcohol’s effects on NK-cell activity, finding that neither acute injection nor dietary administration of ethanol in these experiments affected NK-cell activity against MADB106 cells when determined in an in vitro assay (Yirmiya et al. 1992).
Analysis of the tumors indicated an increase in VEGF mRNA and VEGF protein, as well as increased tumor angiogenesis. Moreover, another marker of angiogenesis, VEGF-R1 (Flt-1), also was found in a greater number of tumor cells and endothelial cells in the surrounding tissue from the ethanol group compared with the control group. A series of studies have been carried out in animals and cancer patients to delineate the effects of alcohol on T cell function. In one study, the role of ethanol and CD4+ T cells in controlling tumor growth was examined by implanting 201T human lung adenocarcinoma cell line into the lung of ethanol-fed BALB/c mice that also received anti-CD4 antibody [155]. In another study, alcohol consuming mice that were inoculated with B16BL6 melanoma showed marked reduction in the number of CD8+ T cells that specifically recognize a melanoma-specific antigen (i.e., gp100) compared with water-drinking control mice [156]. Alcohol consumption has been established as a leading cause of chronic liver diseases and HCC.
Alcohol also reduces the body’s ability to absorb certain cancer-protective nutrients, including vitamins A, C, D, E and folate. Anton said that while the body is resilient, too much damage from heavy alcohol consumption can limit cells’ ability to repair themselves and hinder the immune system from recognizing cells that are behaving abnormally. That recommendation “was intended to prevent people from becoming alcoholics,” psychologist Tim Stockwell, PhD, of the University of Victoria noted in a recent article in Scientific American.