Another mechanism whereby alcohol could facilitate metastasis of certain cancers may involve disruption of the integrity of the cells lining the blood vessels (i.e., vascular endothelium). Thus, studies found that exposure to 0.2 percent (weight per volume [w/v]) ethanol in vitro, which promotes angiogenesis and invasion, interferes with the integrity of the vascular endothelium by inducing endocytosis of VE-cadherin (Xu et al. 2012). This molecule is an important component of certain junctions between cells (i.e., cellular adherens junctions).
The contribution of NK cells to the inhibition of metastasis was evaluated in mice consuming 10 percent or 20 percent w/v ethanol for 4 weeks (Meadows et al. 1993a). Whereas consumption of 10 percent ethanol did not alter the NK cells’ ability to destroy other cells (i.e., decrease cytolytic activity), animals consuming 20 percent ethanol showed decreased NK cytolytic activity. And although experimental stimulation of NK cells could enhance their cytolytic activity 4.3-fold in the ethanol-drinking animals, compared with 2.6-fold in the control animals, overall cytolytic activity still was lower in the ethanol group than in the control group. Treatment of mice with an antibody against NK cells (i.e., anti-NK1.1 antibody) markedly decreased NK-cell cytolytic activity in both water- and ethanol-drinking animals. Experimental stimulation of NK cells decreased the number of lung metastases in the water-drinking and 10-percent ethanol groups, but not in the 20-percent ethanol group.
Hepatocellular Carcinoma
Alcohol research and control efforts supported by multiple governmental and non-governmental organizations (NGOs) internationally have found that the public health impact of harmful alcohol consumption is substantial. In 2016, it resulted in an estimated 5.1% of the global burden of disease and injury, and 5.3% of deaths (1). A large meta-analysis of 23 health outcomes showed that the number of daily alcohol beverages that minimized harm overall was 0 (95% uncertainty interval 0.00–0.08) (2). Another enzyme, called aldehyde dehydrogenase 2 (ALDH2), metabolizes toxic acetaldehyde to nontoxic substances.
Which Cancers Are Most at Risk From Drinking Alcohol?
After 8 weeks of ethanol administration or regular food, the mice were implanted with the tumor cells and also received one injection of the anti-CD4 antibody. Mice in the non–ethanol-fed control group injected with one dose of anti-CD4 antibody initially developed large tumors at 6 weeks, which significantly regressed thereafter. Compared with these control animals, the ethanol-fed mice exhibited significantly larger tumors at 6 weeks as well as a diminished ability to decrease their tumor size at 13 weeks. The findings suggest that this difference in the ability of the ethanol-fed mice to reduce their tumor burden results from an impaired immune system caused by chronic alcohol intake.
Acetaldehyde can inhibit the activity of DNA methyltransferase (DNMT) which is essential for normal DNA methylation; acetaldehyde can also reduce DNMT mRNA levels leading to less production of DNMT [25]. Acetaldehyde and ethanol may also inhibit the synthesis of S-adenosyl-L-methionine (SAMe) which is essential to DNA methylation [21]. Alcoholic beverage production, distribution, and consumption have been regulated throughout the world for centuries (53). However, the federal government retained power to regulate alcohol through control of foreign and inter-state commerce, federal taxes, federal property, and financial incentives. Many individuals of East Asian descent carry a version of the gene for ADH that codes for a “superactive” form of the enzyme. Among people of how do you smoke moon rocks Japanese descent, those who have this form of ADH have a higher risk of pancreatic cancer than those with the more common form of ADH (30).
Inactivation of NK cells by administration of anti-NK1.1 antibody significantly increased lung metastases in the water-drinking and 10-percent ethanol groups, but not in the 20-percent ethanol group. The effects of alcohol on in vitro invasion of surrounding tissue primarily have been studied in breast cancer and melanoma cells, with a variety of results. The evidence in melanoma suggests that ethanol can positively impact the extracellular membrane and augment expression of genes that suppress tumor metastasis, resulting in inhibition of metastasis. In addition, certain immune cells called natural killer (NK) cells seem to have some role in regulating the metastasis of breast cancers and melanomas. Clearly, more mechanistic research is needed in murine models to serve as a template for further examination of the complex interactions connecting alcohol to tumor growth, metastasis, and survival in humans. Lipotropic nutrients such as folate are key sources of the methyl groups necessary for DNA methylation and influence the availability of SAMe, which is also essential to DNA methylation [25].
A study published in 2023 found widespread mistaken beliefs that the risk varies by beverage type, with the lowest cancer risk assigned to wine. Another study published in 2021 showed that nearly 70% of people did not even know that alcohol was a cancer risk factor. Because cancer risk increases with the amount of ethanol consumed, all alcoholic beverages pose a risk. The study confirmed that most American adults aren’t aware of the link between alcohol consumption and cancer. It also found that, even among those who are aware, there’s a belief that it varies by the type of alcohol. For example, more participants were aware of the cancer risks from hard liquor and beer than about the risk from wine, with some participants believing wine lowers your cancer risk.
Alcohol and Cancer: Epidemiology and Biological Mechanisms
However, these bacteria have limited capacity to break acetaldehyde down further into its non-harmful compound acetate, thus the oral epithelia are further exposed to acetaldehyde [21,44]. Acetaldehyde concentrations in the saliva of drinkers are between 10 and 100 times higher than in the blood; this is further doubled in smokers who drink alcohol as tobacco smoke contains high levels of acetaldehyde [21]. Retinoids are important regulators against carcinogenesis as they can induce cell growth, cell differentiation, and apoptosis [31].
Alcohol and Cancer: Existing Knowledge and Evidence Gaps Across the Cancer Continuum
Particularly troublesome maverick house sober living is that so many younger people—those within the 15–39 age range of adolescents and young adults, or AYAs—reported heavy drinking, said Adam DuVall, M.D., of the University of Chicago Cancer Center, who specializes in treating blood cancers in children and AYAs. The fact that drinking alcohol can cause cancer has received increasing attention in the past few years. But the potential threat it poses to people with cancer and longer-term survivors has largely been overlooked, explained Tanya Agurs-Collins, Ph.D., of the Behavioral Research Program in NCI’s Division of Cancer Control and Population Sciences.
7. Reduced Function of the Immune System
- In one of the first experiments conducted in melanoma, 6- to 8-week-old female CDBA/2F1 mice consumed water or 20 percent alcohol for 52 weeks before being inoculated in a leg with the Cloudman 8-91 melanoma tumor (Ketcham et al. 1963).
- An early study (Capel et al. 1978) found that mice given 10 percent ethanol in drinking water for 2 weeks before inoculation with B16 melanoma into the thigh showed no altered tumor growth or metastasis compared with water-drinking controls.
- The same meta-analysis also found significant inverse associations for the risk of thyroid cancer, Hodgkin lymphoma and non-Hodgkin lymphoma [8].
- However, less is known regarding the role and interaction among alcohol consumption, immune modulation of tumor growth, blood vessel formation (i.e., angiogenesis), metastasis, and survival.
- In addition to its involvement in downstream ROS-producing pathways, it is hypothesised that IL-8 contributes to further accumulation of white blood cells (neutrophils, specifically) in the liver leading to acute inflammation.
- Alcohol drinking disorders can lead to liver fibrosis and cirrhosis (12)–an established cause of liver cancer.
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. There is a strong scientific consensus that alcohol drinking can cause several types of cancer (1, 2). In its Report on Carcinogens, the National Toxicology Program of the US Department of Health and Human Services lists consumption of alcoholic beverages as a known human carcinogen.
These changes in the vascular endothelium have been shown to allow for increased migration of human A549 lung adenocarcinoma cells, MDA-MB-231 breast cancer cells, and HCT116 colon cancer cells through single-cell layers of endothelial cells (Xu et al. 2012). Other studies in mice assessed the effects of acute and chronic alcohol consumption on tumor growth and metastasis using B16 melanoma and its more metastatic variants, B16F10 and B16BL6. An early study (Capel et al. 1978) found that mice given 10 percent ethanol in drinking water for 2 weeks before inoculation with B16 melanoma into the thigh showed no altered tumor growth or metastasis compared with water-drinking controls. In another study (Tan et al. 2007), tumor growth and angiogenesis were examined in C57BL/6 mice implanted subcutaneously with B16F10 melanoma cells. The mice had access to regular drinking water and to 1 percent ethanol in their drinking water for 12 hours each per day for 4 weeks, with tumor cells being implanted during the second week of ethanol administration.
Ethanol can also contribute to carcinogenesis through the induction of oxidative stress which is recognised as a key determinant of disease initiation [26]. Oxidative stress can be induced by activation of certain pathways which produce reactive oxygen species (ROS) such as superoxide anion and hydrogen peroxide. One pathway by which ethanol achieves this is through increased CYP2E1 activity which produces high quantities of ROS whilst oxidising ethanol to acetaldehyde [27]. Other sources of ROS during ethanol metabolism include the mitochondrial respiratory chain and some cytosolic games for substance abuse groups enzymes [28].
Addressing knowledge gaps related to alcohol-cancer communication has potential to increase awareness and affect alcohol consumption behavior. The researchers also found that an individual’s cancer risk increased with the amount of alcohol consumed. However, even drinking two or fewer alcoholic drinks per day—considered moderate drinking, according to the study—accounted for an estimated 14% of alcohol-related cancers. However, based on more recent, comprehensive studies, public health experts now generally agree that alcohol—including wine—does not have a so-called “cardioprotective” effect. Nevertheless, the research team also asked participants about the purported heart health benefits of alcohol, to see if it was related to their awareness about alcohol and cancer risk. Alcoholic drinks contain ethanol, which is a known carcinogen, and there are several ways in which it may cause cancer.
